Contact Us / Request a Quote Download Manuals
Advanced Cell Diagnostics Advanced Cell Diagnostics

Search form

Please sign in
  • Log In
  • Register
  • How to Order
  • What to Buy
0 My Cart
X

You have no items in your shopping cart.

Menu
X
  • Products +
    RNAscope™/BaseScope™/ miRNAscope™
    +
    • Assay Selection Guide
    Target Probes
    +
    • All About Probes
    • Catalog Probes
    • Probe Sets
    • New Probe Request
    Manual Assays
    +
    RNAscope™ Chromogenic
    • Overview
    • RNAscope™ 2.5 HD Assay-Brown
    • RNAscope™ 2.5 HD Assay-Red
    • RNAscope™ 2.5 HD Duplex Assay
    RNAscope™ Multiplex Fluorescent
    • Overview
    • RNAscope™ HiPlex v2 Assay
    • RNAscope™ Multiplex Fluorescent V2
    BaseScope™
    • Overview
    • BaseScope™ Assay Red
    • BaseScope™ Duplex Assay
    miRNAscope™
    • Overview
    • miRNAscope™ Assay red
    • RNAscope™ Plus smRNA-RNA Assay
    DNAscope™
    • Overview
    • DNAscope™ Duplex Assay
    Automated Assays
    +
    For Lunaphore COMET™
    • RNAscope™ HiPlex Pro for COMET™
    For Leica systems
    • Overview
    • RNAscope™ 2.5 LS Assay-Brown
    • RNAscope™ 2.5 LS Assay-Red
    • RNAscope™ 2.5 LS Duplex Assay
    • RNAscope™ Multiomic LS Assay
    • RNAscope™ 2.5 LS Fluorescent Multiplex Assay
    • RNAscope™ 2.5 LSx Reagent Kit-BROWN
    • RNAscope™ 2.5 LSx Reagent Kit-RED
    • BaseScope™ LS Reagent Kit – RED
    • miRNAscope LS Reagent Kit Red
    • RNAscope™ Plus smRNA-RNA LS Assay
    Roche DISCOVERY ULTRA system
    • Overview
    • RNAscope™ VS Universal HRP
    • RNAscope™ VS Universal AP
    • RNAscope™ VS Duplex Assay
    • BaseScope™ VS Reagent Kit – RED
    RNA-Protein Co-Detection Assay
    +
    • RNAscope HiPlex-IMC™ Co-Detection
    • Integrated Codetection Assay
    • Sequential RNA Protein Detection
    Software
    +
    • Overview
    • Aperio RNA ISH Algorithm
    • HALO® image analysis platform
    Controls & Accessories
    +
    • RNAscope™
    • BaseScope™
    • miRNAscope™
    • Accessories
    How to Order
    +
    • Ordering Instructions
    • What to Buy
  • Services +
    Professional Assay Services
    +
    • Our Services
    • Multiomic Services
    • Biomarker Assay Development
    • Cell & Gene Therapy Services
    • Clinical Assay Development
    • Tissue Bank & Sample Procurement
    • Image Analysis
    Benefits
    +
    • Your Benefits
    • Certified Providers
    How to Order
    +
    • Ordering Process
    • Contact Services
  • Areas of Research +
    Most Popular
    +
    • COVID-19 Coronavirus
    • Single Cell Analysis
    • Whole-Mount
    • Anatomic Pathology Panels
    • Neuroscience
    • Inflammation
    • Gene Therapy/AAV
    • Stem Cell
    • Immuno-oncology
    • Liver Research
    • Cardiovascular & Skeletal Muscle Research
    Cell & Gene Therapy
    +
    • Gene Therapy
    • Gene Therapy/AAV
    • siRNA/ASO
    • Cell Therapy
    Cancer
    +
    • Breast Cancer
    • EGFRvIII Splice Variant
    • HPV Related Cancer
    • Immuno-oncology
    • Lung Cancer
    • PDx
    • Prostate Cancer
    • Point Mutation
    • CDR3 for TCR
    Viral
    +
    • COVID-19 Coronavirus
    • HIV & SIV
    • Infectious Disease
    • Zika Virus
    Pathways
    +
    • AKT
    • JAK STAT
    • WNT B-Catenin
    Neuroscience
    +
    Neuroscience
    • Neural Development
    • Neuronal Cell Types
    • Learning and Memory
    • G-protein-coupled Receptors & Ion Channels
    • Post-mortem Brain Tissue
    Other
    +
    • Circular RNA
    • Gene Fusions
    • HT Transcript Validation
    • Long Non-coding RNA
    • RNAseq Validation
    • Single Cell Analysis
    • Splice Variant
    • miRNA
    RNA & Protein
    +
    • Antibody Challenges
    • Dual ISH + IHC Methods
    • No Antibodies
    • RNA & Protein Analysis
    Customer Innovations
    +
    • Dual RNA+DNA ISH
    • Very old FFPE ISH
    • Wholemount ISH
    Animal Models
    +
    • Any Species
    • Mouse Model
    • Preclincal Safety
  • Technology +
    Overview
    +
    • How it Works
    • Data Image Gallery
    • Technology Video
    • Webinars
    RNA Detection
    +
    • Why RNA?
    • RNA ISH and IHC
    Pretreatment Options
    +
    • RNAscope™ Pretreatment
    • PretreatPro™
    Spotlights
    +
    • Researchers Spotlights
    • RNA & DNA
    • WISH
    • FFPE
    • Testimonials
    Publications, Guides & Posters
    +
    • Search publications
    • RNAscope™ Reference Guide
    • RNAscope™ Data Analysis Guide
    • Download RNAscope™ Posters
  • Support +
    Overview
    +
    • Get Started
    • How to Order
    • Distributors
    • Contact Support
    Troubleshooting
    +
    • Troubleshooting Guide
    • FAQs
    • User Manuals, SDS and Product Inserts
    • Documents and Downloads
    Imaging Resource
    +
    • Image Analysis
    • Image Registration Software
    • QuPath
    • HALO® image analysis platform
    Learn More
    +
    • Webinars
    • Training Videos
  • Partners +
    Partners
    +
    • Overview
    Partners Directory
    +
    Automation Partners
    • Leica Biosystem
    • Roche Diagnostics
    Workflow Partners
    • NanoString
    Software Partners
    • indica labs
    Become a Partner
    +
    • Learn How
  • Diagnostics +
    Diagnostics
    +
    • Diagnostics
    • Literature
    • Diagnostics ASR Probes
    • Diagnostics CE-IVD Probes
    • Diagnostics CE-IVD Detection
    • Companion Diagnostics
  • Image Calendar +
    Image Calendar
    +
    • Image Contest
    • Data Image Gallery
Search

Probes for INS

ACD can configure probes for the various manual and automated assays for INS for RNAscope Assay, or for Basescope Assay compatible for your species of interest.

  • Probes for INS (0)
  • Kits & Accessories (0)
  • Support & Documents (0)
  • Publications (55)
  • Image gallery (0)
Refine Probe List

Content for comparison

Gene

  • TBD (1413) Apply TBD filter
  • Lgr5 (151) Apply Lgr5 filter
  • SARS-CoV-2 (136) Apply SARS-CoV-2 filter
  • Gad1 (90) Apply Gad1 filter
  • vGlut2 (80) Apply vGlut2 filter
  • HPV E6/E7 (78) Apply HPV E6/E7 filter
  • Slc17a6 (77) Apply Slc17a6 filter
  • Axin2 (74) Apply Axin2 filter
  • SLC32A1 (74) Apply SLC32A1 filter
  • FOS (73) Apply FOS filter
  • Sst (65) Apply Sst filter
  • TH (63) Apply TH filter
  • VGAT (58) Apply VGAT filter
  • Gad2 (54) Apply Gad2 filter
  • tdTomato (54) Apply tdTomato filter
  • DRD2 (53) Apply DRD2 filter
  • Slc17a7 (52) Apply Slc17a7 filter
  • GLI1 (51) Apply GLI1 filter
  • PVALB (47) Apply PVALB filter
  • egfp (46) Apply egfp filter
  • ZIKV (46) Apply ZIKV filter
  • DRD1 (42) Apply DRD1 filter
  • GFAP (39) Apply GFAP filter
  • COL1A1 (38) Apply COL1A1 filter
  • Crh (37) Apply Crh filter
  • Chat (37) Apply Chat filter
  • V-nCoV2019-S (37) Apply V-nCoV2019-S filter
  • Pomc (34) Apply Pomc filter
  • PDGFRA (33) Apply PDGFRA filter
  • Il-6 (33) Apply Il-6 filter
  • Cre (33) Apply Cre filter
  • AGRP (32) Apply AGRP filter
  • PECAM1 (32) Apply PECAM1 filter
  • Npy (32) Apply Npy filter
  • Wnt5a (31) Apply Wnt5a filter
  • CXCL10 (31) Apply CXCL10 filter
  • (-) Remove GLP1R filter GLP1R (31)
  • Sox9 (29) Apply Sox9 filter
  • CD68 (28) Apply CD68 filter
  • Penk (28) Apply Penk filter
  • PD-L1 (28) Apply PD-L1 filter
  • ACTA2 (27) Apply ACTA2 filter
  • SHH (27) Apply SHH filter
  • VGluT1 (27) Apply VGluT1 filter
  • OLFM4 (26) Apply OLFM4 filter
  • GFP (26) Apply GFP filter
  • Rbfox3 (25) Apply Rbfox3 filter
  • MALAT1 (24) Apply MALAT1 filter
  • SOX2 (24) Apply SOX2 filter
  • Ccl2 (24) Apply Ccl2 filter

Product

  • RNAscope Multiplex Fluorescent Assay (8) Apply RNAscope Multiplex Fluorescent Assay filter
  • RNAscope Fluorescent Multiplex Assay (7) Apply RNAscope Fluorescent Multiplex Assay filter
  • RNAscope 2.0 Assay (6) Apply RNAscope 2.0 Assay filter
  • RNAscope 2.5 HD Red assay (6) Apply RNAscope 2.5 HD Red assay filter
  • RNAscope (5) Apply RNAscope filter
  • RNAscope 2.5 LS Assay (5) Apply RNAscope 2.5 LS Assay filter
  • RNAscope 2.5 VS Assay (4) Apply RNAscope 2.5 VS Assay filter
  • RNAscope 2.5 HD Duplex (1) Apply RNAscope 2.5 HD Duplex filter
  • RNAscope HiPlex v2 assay (1) Apply RNAscope HiPlex v2 assay filter
  • RNAscope HiPlex12 Reagents Kit (1) Apply RNAscope HiPlex12 Reagents Kit filter
  • RNAscope Multiplex Fluorescent v2 (1) Apply RNAscope Multiplex Fluorescent v2 filter

Research area

  • Neuroscience (19) Apply Neuroscience filter
  • Cancer (14) Apply Cancer filter
  • Stem Cells (11) Apply Stem Cells filter
  • Other (7) Apply Other filter
  • HPV (4) Apply HPV filter
  • diabetes (2) Apply diabetes filter
  • Metabolism (2) Apply Metabolism filter
  • Other: Metabolism (2) Apply Other: Metabolism filter
  • Development (1) Apply Development filter
  • Endocrinology (1) Apply Endocrinology filter
  • Obesity (1) Apply Obesity filter
  • Other: Metbolism (1) Apply Other: Metbolism filter
  • Other: Methods (1) Apply Other: Methods filter
  • Sensory Neurons (1) Apply Sensory Neurons filter
  • Theraputic Development (1) Apply Theraputic Development filter
  • vasopressin (1) Apply vasopressin filter

Category

  • Publications (55) Apply Publications filter
Localization of cells expressing SGLT1 mRNA in the yolk sac and small intestine of broilers

Poultry Science

2018 Aug 01

Zhang H, Li H, Kidrick J, Wong EA.
PMID: - | DOI: 10.3382/ps/pey343

The uptake of glucose is mediated mainly by the sodium-glucose cotransporter, SGLT1. Previous studies using quantitative PCR showed that SGLT1 mRNA was induced in the yolk sac and in the small intestine prior to hatch. However, PCR analysis did not allow for the localization of cells expressing SGLT1 mRNA. The objective of this study was to use in situ hybridization to identify cells in the yolk sac and small intestine that expressed SGLT1 mRNA during the transition from late embryogenesis to early post-hatch. Expression of SGLT1 mRNA in yolk sac epithelial cells was low from embryonic d 11 to 17, peaked at embryonic d 19, and declined at day of hatch. In the small intestine, cells expressing SGLT1 mRNA were present not only along the intestinal villi but also in the crypts. There was greater expression of SGLT1 mRNA in the intestinal epithelial cells that line the villus than in the olfactomedin 4-expressing stem cells located in the crypts. The latter result suggests that stem cells have the ability to import glucose. Expression of SGLT1 mRNA in the intestine increased from embryonic d 19 to day of hatch and then maintained a high level of expression from d 1 to d 7 post-hatch. For both the yolk sac and small intestine, the temporal pattern of SGLT1 mRNA expression detected by in situ hybridization was consistent with the pattern revealed by PCR.

Effect of GLP1R agonists taspoglutide and liraglutide on primary thyroid C-cells from rodent and man.

Journal of molecular endocrinology, 50(3), 325–336.

Boess F, Bertinetti-Lapatki C, Zoffmann S, George C, Pfister T, Roth A, Lee SM, Thasler WE, Singer T, Suter L (2013).
PMID: 23463748 | DOI: 10.1530/JME-12-0186.

Glucagon-like peptide 1 (GLP1) analogs have been associated with an increased incidence of thyroid C-cell hyperplasia and tumors in rodents. This effect may be due to a GLP1 receptor (GLP1R)-dependent mechanism. As the expression of GLP1R is much lower in primates than in rodents, the described C-cell proliferative lesions may not be relevant to man. Here, we aimed to establish primary thyroid cell cultures of rat and human to evaluate the expression and function of GLP1R in C-cells. In our experiments, GLP1R expression was observed in primary rat C-cells (in situ hybridization) but was not detected in primary human C-cells (mRNA and protein levels). The functional response of the cultures to the stimulation with GLP1R agonists is an indirect measure of the presence of functional receptor. Liraglutide and taspoglutide elicited a modest increase in calcitonin release and in calcitonin expression in rat primary thyroid cultures. Contrarily, no functional response to GLP1R agonists was observed in human thyroid cultures, despite the presence of few calcitonin-positive C-cells. Thus, the lack of functional response of the human cultures adds to the weight of evidence indicating that healthy human C-cells have very low levels or completely lack GLP1R. In summary, our results support the hypothesis that the GLP1R agonist-induced C-cell responses in rodents may not be relevant to primates. In addition, the established cell culture method represents a useful tool to study the physiological and/or pathological roles of GLP1 and GLP1R agonists on normal, non-transformed primary C-cells from rats and man.
Prognostic significance of stromal GREM1 expression in colorectal cancer

Human Pathology

2016 Dec 30

Jang BG, Kim HS, Chang WY, Bae JM, Oh HJ, Wen X, Jeong S, Cho NY, Kim WH, Kang GH.
PMID: - | DOI: 10.1016/j.humpath.2016.12.018

Cancer associated fibroblasts (CAFs) are the dominant cell population in the cancer stroma. Gremlin 1 (GREM1), an antagonist of the bone morphogenetic protein pathway, is expressed by CAFs in a variety of human cancers. However, its biological significance for cancer patients is largely unknown. We applied RNA in situ hybridization (ISH) to evaluate the prognostic value of stromal GREM1 expression in a large cohort of 670 colorectal cancers (CRCs). Overall GREM1 expression in CRCs was lower than that of the matched normal mucosa, and GREM1 expression had a strong positive correlation with BMI1 and inverse correlations with EPHB2 and OLFM4. RNA ISH localized the GREM expression to smooth muscle cells of the muscularis mucosa, fibroblasts around crypt bases and in the submucosal space of a normal colon. In various colon polyps, epithelial GREM1 expression was exclusively observed in traditional serrated adenomas. In total, 44% of CRCs were positive for stromal GREM1, which was associated with decreased lymphovascular invasion, a lower cancer stage, and nuclear β-catenin staining. Stromal GREM1 was significantly associated with improved recurrence-free and overall survival, although it was not found to be an independent prognostic marker in multivariate analyses. In addition, for locally advanced stage II and III CRCs, it was associated with better, stage-independent clinical outcomes. In summary, CRCs are frequently accompanied by GERM1-expressing fibroblasts, which are closely associated with low lymphovascular invasion and a better prognosis, suggesting stromal GREM1 as a potential biomarker and possible candidate for targeted therapy in the treatment of CRCs.

Distribution of LGR5+ Cells and Associated Implications during the Early Stage of Gastric Tumorigenesis.

PLoS One, 8(12):e82390.

Jang BG, Lee BL, Kim WH. (2013).
PMID: 24340024 | DOI: 10.1371/journal.pone.0082390.

Lgr5 was identified as a promising gastrointestinal tract stem cell marker in mice. Lineage tracing indicates that Lgr5(+) cells may not only be the cells responsible for the origin of tumors; they may also be the so-called cancer stem cells. In the present study, we investigated the presence of Lgr5(+) cells and their biological significance in normal human gastric mucosa and gastric tumors. RNAscope, a newly developed RNA in situ hybridization technique, specifically labeled Lgr5(+) cells at the basal glands of the gastric antrum. Notably, the number of Lgr5(+) cells was remarkably increased in intestinal metaplasia. In total, 76% of gastric adenomas and 43% of early gastric carcinomas were positive for LGR5. Lgr5(+) cells were found more frequently in low-grade tumors with active Wnt signaling and an intestinal gland type, suggesting that LGR5 is likely involved in the very early stages of Wnt-driven tumorigenesis in the stomach. Interestingly, similar to stem cells in normal tissues, Lgr5(+) cells were often restricted to the base of the tumor glands, and such Lgr5(+) restriction was associated with high levels of intestinal stem cell markers such as EPHB2, OLFM4, and ASCL2. Thus, our findings show that Lgr5(+) cells are present at the base of the antral glands in the human stomach and that this cell population significantly expands in intestinal metaplasias. Furthermore, Lgr5(+) cells are seen in a large number of gastric tumors ; their frequent basal arrangements and coexpression of ISC markers support the idea that Lgr5(+) cells act as stem cells during the early stage of intestinal-type gastric tumorigenesis.
Area postrema neurons mediate interleukin-6 function in cancer-associated cachexia

bioRxiv : the preprint server for biology

2023 Jan 14

Sun, Q;van de Lisdonk, D;Ferrer, M;Gegenhuber, B;Wu, M;Tollkuhn, J;Janowitz, T;Li, B;
PMID: 36711916 | DOI: 10.1101/2023.01.12.523716

Interleukin-6 (IL-6) has been long considered a key player in cancer-associated cachexia 1-15 . It is believed that sustained elevation of IL-6 production during cancer progression causes brain dysfunctions, which ultimately result in cachexia 16-20 . However, how peripheral IL-6 influences the brain remains poorly understood. Here we show that neurons in the area postrema (AP), a circumventricular structure in the hindbrain, mediate the function of IL-6 in cancer-associated cachexia in mice. We found that circulating IL-6 can rapidly enter the AP and activate AP neurons. Peripheral tumor, known to increase circulating IL-6 1-5,15,18,21-23 , leads to elevated IL-6 and neuronal hyperactivity in the AP, and causes potentiated excitatory synaptic transmission onto AP neurons. Remarkably, neutralization of IL-6 in the brain of tumor-bearing mice with an IL-6 antibody prevents cachexia, reduces the hyperactivity in an AP network, and markedly prolongs lifespan. Furthermore, suppression of Il6ra , the gene encoding IL-6 receptor, specifically in AP neurons with CRISPR/dCas9 interference achieves similar effects. Silencing of Gfral-expressing AP neurons also ameliorates the cancer-associated cachectic phenotypes and AP network hyperactivity. Our study identifies a central mechanism underlying the function of peripheral IL-6, which may serve as a target for treating cancer-associated cachexia.
Central NPFF signalling is critical in the regulation of glucose homeostasis

Molecular metabolism

2022 Jun 09

Zhang, L;Koller, J;Gopalasingam, G;Qi, Y;Herzog, H;
PMID: 35691527 | DOI: 10.1016/j.molmet.2022.101525

Neuropeptide FF (NPFF) group peptides belong to the evolutionary conserved RF-amide peptide family. While they have been assigned a role as pain modulators, their roles in other aspects of physiology have received much less attention. NPFF peptides and their receptor NPFFR2 have strong and localized expression within the dorsal vagal complex that has emerged as the key centre for regulating glucose homeostasis. Therefore, we investigated the role of the NPFF system in the control of glucose metabolism and the histochemical and molecular identities of NPFF and NPFFR2 neurons.We examined glucose metabolism in Npff-/- and wild type (WT) mice using intraperitoneal (i.p.) glucose tolerance and insulin tolerance tests. Body composition and glucose tolerance was further examined in mice after 1-week and 3-week of high-fat diet (HFD). Using RNAScope double ISH, we investigated the neurochemical identity of NPFF and NPFFR2 neurons in the caudal brainstem, and the expression of receptors for peripheral factors in NPFF neurons.Lack of NPFF signalling in mice leads to improved glucose tolerance without significant impact on insulin excursion after the i.p. glucose challenge. In response to an i.p. bolus of insulin, Npff-/- mice have lower glucose excursions than WT mice, indicating an enhanced insulin action. Moreover, while HFD has rapid and potent detrimental effects on glucose tolerance, this diet-induced glucose intolerance is ameliorated in mice lacking NPFF signalling. This occurs in the absence of any significant impact of NPFF deletion on lean or fat masses, suggesting a direct effect of NPFF signalling on glucose metabolism. We further reveal that NPFF neurons in the subpostrema area (SubP) co-express receptors for peripheral factors involved in glucose homeostasis regulation such as insulin and GLP1. Furthermore, Npffr2 is expressed in the glutamatergic NPFF neurons in the SubP, and in cholinergic neurons of the dorsal motor nucleus of the vagus (DMV), indicating that central NPFF signalling is likely modulating vagal output to innervated peripheral tissues including those important for glucose metabolic control.NPFF signalling plays an important role in the regulation of glucose metabolism. NPFF neurons in the SubP are likely to receive peripheral signals and mediate the control of whole-body glucose homeostasis via centrally vagal pathways. Targeting NPFF and NPFFR2 signalling may provide a new avenue for treating type 2 diabetes and obesity.
Adhesion receptor ADGRG2/GPR64 is in the GI-tract selectively expressed in mature intestinal tuft cells

Molecular metabolism

2021 Apr 05

Grunddal, KV;Tonack, S;Egerod, KL;Thompson, JJ;Petersen, N;Engelstoft, MS;Vagne, C;Keime, C;Gradwohl, G;Offermanns, S;Schwartz, TW;
PMID: 33831593 | DOI: 10.1016/j.molmet.2021.101231

GPR64/ADGRG2 is an orphan Adhesion G protein-coupled receptor (ADGR) known to be mainly expressed in the parathyroid gland and epididymis. This investigation aimed to delineate the cellular expression of GPR64 throughout the body with focus on the gastrointestinal (GI) tract. Transgenic Gpr64mCherry reporter mice were histologically examined throughout the body and reporter protein expression in intestinal tuft cells was confirmed by specific cell ablation. The GPCR repertoire of intestinal Gpr64mCherry-positive tuft cells was analyzed by quantitative RT-PCR analysis and in situ hybridization. The Gpr64mCherry was crossed into the general tuft cell reporter Trpm5GFP to generate small intestinal organoids for time-lapse imaging. Intestinal tuft cells were isolated from small intestine, FACS-purified and transcriptionally compared using RNA-seq analysis. Expression of the Gpr64mCherry reporter was identified in multiple organs and specifically in olfactory microvillous cells, enteric nerves, and importantly in respiratory and GI tuft cells. In the small intestine, cell ablation targeting Gpr64-expressing epithelial cells eliminated tuft cells. Transcriptional analysis of small intestinal Gpr64mCherry -positive tuft cells confirmed expression of Gpr64 and the chemo-sensors Sucnr1, Gprc5c, Drd3, and Gpr41/Ffar3. Time-lapse studies of organoids from Trpm5GFP:Gpr64mCherry mice revealed sequential expression of initially Trpm5GFP and subsequently also Gpr64mCherry in maturing intestinal tuft cells. RNA-seq analysis of small intestinal tuft cells based on these two markers demonstrated a dynamic change in expression of transcription factors and GPCRs from young to mature tuft cells. GPR64 is expressed in chemosensory epithelial cells across a broad range of tissues; however, in the GI tract, GPR64 is remarkably selectively expressed in mature versus young immunoregulatory tuft cells.
Glucagon-like peptide-1 acutely affects renal blood flow and urinary flow rate in spontaneously hypertensive rats despite significantly reduced renal expression of GLP-1 receptors.

Physiol Rep.

2017 Dec 12

Ronn J, Jensen EP, Wewer Albrechtsen NJ, Holst JJ, Sorensen CM.
PMID: 29233907 | DOI: 10.14814/phy2.13503

Glucagon-like peptide-1 (GLP-1) is an incretin hormone increasing postprandial insulin release. GLP-1 also induces diuresis and natriuresis in humans and rodents. The GLP-1 receptor is extensively expressed in the renal vascular tree in normotensive rats where acute GLP-1 treatment leads to increased mean arterial pressure (MAP) and increased renal blood flow (RBF). In hypertensive animal models, GLP-1 has been reported both to increase and decrease MAP. The aim of this study was to examine expression of renal GLP-1 receptors in spontaneously hypertensive rats (SHR) and to assess the effect of acute intrarenal infusion of GLP-1. We hypothesized that GLP-1 would increase diuresis and natriuresis and reduce MAP in SHR. Immunohistochemical staining and in situ hybridization for the GLP-1 receptor were used to localize GLP-1 receptors in the kidney. Sevoflurane-anesthetized normotensive Sprague-Dawley rats and SHR received a 20 min intrarenal infusion of GLP-1 and changes in MAP, RBF, heart rate, dieresis, and natriuresis were measured. The vasodilatory effect of GLP-1 was assessed in isolated interlobar arteries from normo- and hypertensive rats. We found no expression of GLP-1 receptors in the kidney from SHR. However, acute intrarenal infusion of GLP-1 increased MAP, RBF, dieresis, and natriuresis without affecting heart rate in both rat strains. These results suggest that the acute renal effects of GLP-1 in SHR are caused either by extrarenal GLP-1 receptors activating other mechanisms (e.g., insulin) to induce the renal changes observed or possibly by an alternative renal GLP-1 receptor.

Profiling of G Protein-Coupled Receptors in Vagal Afferents Reveals Novel Gut-to-Brain Sensing Mechanisms

Molecular Metabolism

2018 Apr 03

Egerod KL, Petersen N ,Timshel PN, Rekling JC, Wang Y, Liu Q, Schwartz TW, Gautron L.
PMID: - | DOI: 10.1016/j.molmet.2018.03.016

Abstract

Objectives

G protein-coupled receptors (GPCRs) act as transmembrane molecular sensors of neurotransmitters, hormones, nutrients, and metabolites. Because unmyelinated vagalafferents richly innervate the gastrointestinal mucosa, gut-derived molecules may directly modulate the activity of vagal afferents through GPCRs. However, the types of GPCRs expressed in vagal afferents are largely unknown. Here, we determined the expression profile of all GPCRs expressed in vagal afferents of the mouse, with a special emphasis on those innervating the gastrointestinal tract.

Methods

Using a combination of high-throughput quantitative PCR, RNA sequencing, and in situhybridization, we systematically quantified GPCRs expressed in vagal unmyelinated Nav1.8-expressing afferents.

Results

GPCRs for gut hormones that were the most enriched in Nav1.8-expressing vagal unmyelinated afferents included NTSR1, NPY2R, CCK1R, and to a lesser extent, GLP1R, but not GHSR and GIPR. Interestingly, both GLP1R and NPY2R were coexpressed with CCK1R. In contrast, NTSR1 was coexpressed with GPR65, a marker preferentially enriched in intestinal mucosal afferents. Only few microbiome-derived metabolite sensors such as GPR35 and, to a lesser extent, GPR119 and CaSR were identified in the Nav1.8-expressing vagal afferents. GPCRs involved in lipid sensing and inflammation (e.g. CB1R, CYSLTR2, PTGER4), and neurotransmitters signaling (CHRM4, DRD2, CRHR2) were also highly enriched in Nav1.8-expressing neurons. Finally, we identified 21 orphan GPCRs with unknown functions in vagal afferents.

Conclusion

Overall, this study provides a comprehensive description of GPCR-dependent sensing mechanisms in vagal afferents, including novel coexpression patterns, and conceivably coaction of key receptors for gut-derived molecules involved in gut-brain communication.

Identification of cells expressing OLFM4 and LGR5 mRNA by in situ hybridization in the yolk sac and small intestine of embryonic and early post-hatch chicks.

Poult Sci.

2017 Nov 15

Zhang H, Wong EA.
PMID: 29155957 | DOI: 10.3382/ps/pex328

The chicken yolk sac (YS) and small intestine are essential for nutrient absorption during the pre-hatch and post-hatch periods, respectively. Absorptive enterocytes and secretory cells line the intestinal villi and originate from stem cells located in the intestinal crypts. Similarly, in the YS, there are absorptive and secretory cells that presumably originate from a stem cell population. Leucine-rich repeat containing G protein-coupled receptor 5 (Lgr5) and olfactomedin 4 (Olfm4) are 2 widely used markers for intestinal stem cells. The objective of this study was to map the distribution of putative stem cells expressing LGR5 and OLFM4 mRNA in the chicken small intestine from the late embryonic period to early post hatch and the YS during embryogenesis. At embryonic d 11, 13, 15, 17, and 19, the YS was collected (n = 3), and small intestine was collected at embryonic d 19, d of hatch (doh), and d 1, 4, and 7 post hatch (n = 3). Cells expressing OLFM4 and LGR5 mRNA were identified by in situ hybridization. In the YS, cells expressing only LGR5 and not OLFM4 mRNA were localized to the vascular endothelial cells lining the blood vessels. In the small intestine, cells in the intestinal crypt expressed both LGR5 and OLFM4 mRNA. Staining for OLFM4 mRNA was more intense than LGR5 mRNA, demonstrating that Olfm4 is a more robust marker for stem cells than Lgr5. At embryonic d 19 and doh, cells staining for OLFM4 mRNA were already present in the rudimentary crypts, with the greatest staining in the duodenal crypts. The intensity of OLFM4 mRNA staining increased from doh to d 7 post hatch. Dual label staining at doh for the peptide transporter PepT1 and Olfm4 revealed a population of cells above the crypts that did not express Olfm4 or PepT1 mRNA. These cells are likely progenitor transit amplifying cells. Thus, avians and mammals share similarity in the ontogeny of stem cells in the intestinal crypts.

Heterozygosity of chaperone Grp78 reduces intestinal stem cell regeneration potential and protects against adenoma formation.

Cancer Res.

2018 Sep 19

van Lidth de Jeude JF, Spaan CN, Meijer BJ, Smit WL, Soeratram TTD, Wielenga MCB, Westendorp BF, Lee AS, Meisner S, Vermeulen JLM, Wildenberg ME, van den Brink GR, Muncan V, Heijmans J.
PMID: 30232220 | DOI: 10.1158/0008-5472.CAN-17-3600

Deletion of endoplasmic reticulum (ER) resident chaperone Grp78 results in activation of the unfolded protein response and causes rapid depletion of the entire intestinal epithelium. Whether modest reduction of Grp78 may affect stem cell fate without compromising intestinal integrity remains unknown. Here we employ a model of epithelial-specific, heterozygous Grp78 deletion by use of VillinCreERT2-Rosa26ZsGreen/LacZ-Grp78+/fl mice and organoids. We examine models of irradiation and tumorigenesis both in vitro and in vivo. Although we observed no phenotypic changes in Grp78 heterozygous mice, Grp78 heterozygous organoid growth was markedly reduced. Irradiation of Grp78 heterozygous mice resulted in less frequent regeneration of crypts compared to non-recombined (wild-type) mice, exposing reduced capacity for self-renewal upon genotoxic insult. We crossed mice to Apc mutant animals for adenoma studies and found that adenomagenesis in Apc heterozygous-Grp78 heterozygous mice was reduced compared to Apc heterozygous controls (1.43 vs. 3.33; P < 0.01). In conclusion, epithelium specific Grp78 heterozygosity compromises epithelial fitness under conditions requiring expansive growth such as adenomagenesis or regeneration after γ-irradiation. These results suggest that Grp78 may be a therapeutic target in prevention of intestinal neoplasms without affecting normal tissue.

GLP-1 modulates the supramammillary nucleus-lateral hypothalamic neurocircuit to control ingestive and motivated behavior in a sex divergent manner.

Molecular Metabolism

2018 Nov 27

López-Ferreras L, Eerola K, Mishra D, Shevchouk OT, Richard JE, Nilsson FH, Hayes MR, Skibicka KP.
PMID: - | DOI: 10.1016/j.molmet.2018.11.005

Objective

The supramammillary nucleus (SuM) is nestled between the lateral hypothalamus (LH) and the ventral tegmental area (VTA). This neuroanatomical position is consistent with a potential role of this nucleus to regulate ingestive and motivated behavior. Here neuroanatomical, molecular, and behavior approaches are utilized to determine whether SuM contributes to ingestive and food-motivated behavior control.

Methods

Through the application of anterograde and retrograde neural tract tracing with novel designer viral vectors, the current findings show that SuM neurons densely innervate the LH in a sex dimorphic fashion. Glucagon-like peptide-1 (GLP-1) is a clinically targeted neuro-intestinal hormone with a well-established role in regulating energy balance and reward behaviors. Here we determine that GLP-1 receptors (GLP-1R) are expressed throughout the SuM of both sexes, and also directly on SuM LH-projecting neurons and investigate the role of SuM GLP-1R in the regulation of ingestive and motivated behavior in male and female rats.

Results

SuM microinjections of the GLP-1 analogue, exendin-4, reduced ad libitum intake of chow, fat, or sugar solution in both male and female rats, while food-motivated behaviors, measured using the sucrose motivated operant conditioning test, was only reduced in male rats. These data contrasted with the results obtained from a neighboring structure well known for its role in motivation and reward, the VTA, where females displayed a more potent response to GLP-1R activation by exendin-4. In order to determine the physiological role of SuM GLP-1R signaling regulation of energy balance, we utilized an adeno-associated viral vector to site-specifically deliver shRNA for the GLP-1R to the SuM. Surprisingly, and in contrast to previous results for the two SuM neighboring sites, LH and VTA, SuM GLP-1R knockdown increased food seeking and adiposity in obese male rats without altering food intake, body weight or food motivation in lean or obese, female or male rats.

Conclusion

Taken together, these results indicate that SuM potently contributes to ingestive and motivated behavior control; an effect contingent on sex, diet/homeostatic energy balance state and behavior of interest. These data also extend the map of brain sites directly responsive to GLP-1 agonists, and highlight key differences in the role that GLP-1R play in interconnected and neighboring nuclei.

Pages

  • 1
  • 2
  • 3
  • 4
  • 5
  • next ›
  • last »
X
Description
sense
Example: Hs-LAG3-sense
Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe.
Intron#
Example: Mm-Htt-intron2
Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection
Pool/Pan
Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G)
A mixture of multiple probe sets targeting multiple genes or transcripts
No-XSp
Example: Hs-PDGFB-No-XMm
Does not cross detect with the species (Sp)
XSp
Example: Rn-Pde9a-XMm
designed to cross detect with the species (Sp)
O#
Example: Mm-Islr-O1
Alternative design targeting different regions of the same transcript or isoforms
CDS
Example: Hs-SLC31A-CDS
Probe targets the protein-coding sequence only
EnEmProbe targets exons n and m
En-EmProbe targets region from exon n to exon m
Retired Nomenclature
tvn
Example: Hs-LEPR-tv1
Designed to target transcript variant n
ORF
Example: Hs-ACVRL1-ORF
Probe targets open reading frame
UTR
Example: Hs-HTT-UTR-C3
Probe targets the untranslated region (non-protein-coding region) only
5UTR
Example: Hs-GNRHR-5UTR
Probe targets the 5' untranslated region only
3UTR
Example: Rn-Npy1r-3UTR
Probe targets the 3' untranslated region only
Pan
Example: Pool
A mixture of multiple probe sets targeting multiple genes or transcripts

Enabling research, drug development (CDx) and diagnostics

Contact Us
  • Toll-free in the US and Canada
  • +1877 576-3636
  • 
  • 
  • 
Company
  • Overview
  • Leadership
  • Careers
  • Distributors
  • Quality
  • News & Events
  • Webinars
  • Patents
Products
  • RNAscope or BaseScope
  • Target Probes
  • Controls
  • Manual assays
  • Automated Assays
  • Accessories
  • Software
  • How to Order
Research
  • Popular Applications
  • Cancer
  • Viral
  • Pathways
  • Neuroscience
  • Other Applications
  • RNA & Protein
  • Customer Innovations
  • Animal Models
Technology
  • Overview
  • RNA Detection
  • Spotlight Interviews
  • Publications & Guides
Assay Services
  • Our Services
  • Biomarker Assay Development
  • Cell & Gene Therapy Services
  • Clinical Assay Development
  • Tissue Bank & Sample Procurement
  • Image Analysis
  • Your Benefits
  • How to Order
Diagnostics
  • Diagnostics
  • Companion Diagnostics
Support
  • Getting started
  • Contact Support
  • Troubleshooting Guide
  • FAQs
  • Manuals, SDS & Inserts
  • Downloads
  • Webinars
  • Training Videos

Visit Bio-Techne and its other brands

  • bio-technie
  • protein
  • bio-spacific
  • rd
  • novus
  • tocris
© 2025 Advanced Cell Diagnostics, Inc.
  • Terms and Conditions of Sale
  • Privacy Policy
  • Security
  • Email Preferences
  • 
  • 
  • 

For Research Use Only. Not for diagnostic use. Refer to appropriate regulations. RNAscope is a registered trademark; and HybEZ, EZ-Batch and DNAscope are trademarks of Advanced Cell Diagnostics, Inc. in the United States and other countries. All rights reserved. ©2025 Advanced Cell Diagnostics, Inc.

 

Contact Us / Request a Quote
Download Manuals
Request a PAS Project Consultation
Order online at
bio-techne.com
OK
X
Contact Us

Complete one of the three forms below and we will get back to you.

For Quote Requests, please provide more details in the Contact Sales form below

  • Contact Sales
  • Contact Support
  • Contact Services
  • Offices

Advanced Cell Diagnostics

Our new headquarters office starting May 2016:

7707 Gateway Blvd.  
Newark, CA 94560
Toll Free: 1 (877) 576-3636
Phone: (510) 576-8800
Fax: (510) 576-8798

 

Bio-Techne

19 Barton Lane  
Abingdon Science Park
Abingdon
OX14 3NB
United Kingdom
Phone 2: +44 1235 529449
Fax: +44 1235 533420

 

Advanced Cell Diagnostics China

20F, Tower 3,
Raffles City Changning Office,
1193 Changning Road, Shanghai 200051

021-52293200
info.cn@bio-techne.com
Web: www.acdbio.com/cn

For general information: Info.ACD@bio-techne.com
For place an order: order.ACD@bio-techne.com
For product support: support.ACD@bio-techne.com
For career opportunities: hr.ACD@bio-techne.com

See Distributors
×

You have already Quick ordered an Item in your cart . If you want to add a new item , Quick ordered Item will be removed form your cart. Do You want to continue?

OK Cancel
Need help?

How can we help you?