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.
Diabetes.
2016 Dec 01
Burmeister MA, Ayala JE, Smouse H, Landivar-Rocha A, Brown JD, Drucker DJ, Stoffers DA, Sandoval DA, Seeley RJ, Ayala JE.
PMID: 27908915 | DOI: 10.2337/db16-1102
Pharmacological activation of the hypothalamic glucagon-like peptide-1 (GLP-1) receptor (GLP-1R) promotes weight loss and improves glucose tolerance. This demonstrates that the hypothalamic GLP-1R is sufficient but does not show whether it is necessary for the effects of exogenous GLP-1R agonists (GLP-1RA) or endogenous GLP-1 on these parameters. To address this, we crossed mice harboring floxed Glp1r alleles to mice expressing Nkx2.1-Cre to knock down Glp1r expression throughout the hypothalamus (GLP-1RKDΔNkx2.1cre). We also generated mice lacking Glp1r expression specifically in two GLP-1RA-responsive hypothalamic feeding nuclei/cell types, the paraventricular nucleus (GLP-1RKDΔSim1cre) and proopiomelanocortin neurons (GLP-1RKDΔPOMCcre). Chow -fed GLP-1RKDΔNkx2.1cre mice exhibited increased food intake and energy expenditure with no net effect on body weight. When fed a high fat diet (HFD), these mice exhibited normal food intake but elevated energy expenditure, yielding reduced weight gain. None of these phenotypes were observed in GLP-1RKDΔSim1creand GLP-1RKDΔPOMCcre mice. The acute anorectic and glucose tolerance effects of peripherally-dosed GLP-1RA exendin-4 and liraglutide were preserved in all mouse lines. Chronic liraglutide treatment reduced body weight in chow-fed GLP-1RKDΔNkx2.1cre mice, but this effect was attenuated upon HFD feeding. In sum, classical homeostatic control regions are sufficient but not individually necessary for the effects of GLP-1RA on nutrient homeostasis.
J Cell Sci.
2019 Apr 11
Pirapaharan DC, Olesen JB, Andersen TL, Christensen SB, Kjærsgaard-Andersen P, Delaisse JM, Søe K.
PMID: 30975918 | DOI: 10.1242/jcs.229351
Osteoblast-lineage cells in bone human were recently shown to colonize eroded bone surfaces and to closely interact with osteoclasts. They proved identical with reversal cells and are believed to differentiate into bone forming osteoblasts thereby coupling resorption and formation. However, they also exert catabolic activity that contributes to osteoclastic bone resorption, but this has not received much attention. Herein, we used co-cultures of primary human osteoblast-lineage cells and human osteoclasts derived from peripheral blood monocytes to investigate whether a catabolic activity of osteoblast-lineage cells may impact on osteoclastic bone resorption. Through a combination of immunofluorescence, in-situ hybridization, and time-lapse we show that MMP-13 expressing osteoblast-lineage cells are attracted to and closely interact with bone resorbing osteoclasts. This close interaction results in a strong and significant increase in the bone resorptive activity of osteoclasts - especially those making trenches. Importantly, we show that osteoclastic bone resorption becomes sensitive to inhibition of matrix metalloproteinases in the presence, but not in the absence, of osteoblast-lineage cells. We propose that this may be due to the direct action of osteoblast-lineage-derived MMP-13 on bone resorption.
JCI insight
2022 Dec 15
Sieber, P;Schäfer, A;Lieberherr, R;Caimi, SL;Lüthi, U;Ryge, J;Bergmann, JH;Le Goff, F;Stritt, M;Blattmann, P;Renault, B;Rammelt, P;Sempere, B;Freti, D;Studer, R;White, ES;Birker-Robaczewska, M;Boucher, M;Nayler, O;
PMID: 36520540 | DOI: 10.1172/jci.insight.154719
Sci Rep.
2018 Jul 09
Salinas CBG, Lu TT, Gabery S, Marstal K, Alanentalo T, Mercer AJ, Cornea A, Conradsen K, Hecksher-Sørensen J, Dahl AB, Knudsen LB, Secher A.
PMID: 29985439 | DOI: 10.1038/s41598-018-28496-6
Light Sheet Fluorescence Microscopy (LSFM) of whole organs, in particular the brain, offers a plethora of biological data imaged in 3D. This technique is however often hindered by cumbersome non-automated analysis methods. Here we describe an approach to fully automate the analysis by integrating with data from the Allen Institute of Brain Science (AIBS), to provide precise assessment of the distribution and action of peptide-based pharmaceuticals in the brain. To illustrate this approach, we examined the acute central nervous system effects of the glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide. Peripherally administered liraglutide accessed the hypothalamus and brainstem, and led to activation in several brain regions of which most were intersected by projections from neurons in the lateral parabrachial nucleus. Collectively, we provide a rapid and unbiased analytical framework for LSFM data which enables quantification and exploration based on data from AIBS to support basic and translational discovery.
Cell Metab.
2018 Nov 21
Li C, Navarrete J, Liang-Guallpa J, Lu C, Funderburk SC, Chang RB, Liberles SD, Olson DP, Krashes MJ.
PMID: 30472090 | DOI: 10.1016/j.cmet.2018.10.016
Understanding the neural framework behind appetite control is fundamental to developing effective therapies to combat the obesity epidemic. The paraventricular hypothalamus (PVH) is critical for appetite regulation, yet, the real-time, physiological response properties of PVH neurons to nutrients are unknown. Using a combination of fiber photometry, electrophysiology, immunohistochemistry, and neural manipulation strategies, we determined the population dynamics of four molecularly delineated PVH subsets implicated in feeding behavior: glucagon-like peptide 1 receptor (PVHGlp1r), melanocortin-4 receptor (PVHMc4r), oxytocin (PVHOxt), and corticotropin-releasing hormone (PVHCrh). We identified both calorie- and state-dependent sustained activity increases and decreases in PVHGlp1r and PVHCrh populations, respectively, while observing transient bulk changes of PVHMc4r, but no response in PVHOxt, neurons to food. Furthermore, we highlight the role of PVHGlp1r neurons in orchestrating acute feeding behavior, independent of the anti-obesity drug liraglutide, and demonstrate the indispensability of PVHGlp1r and PVHMc4r, but not PVHOxt or PVHCrh neurons, in body weight maintenance.
Thrombosis and haemostasis
2022 Dec 03
Ye, M;Ni, Q;Wang, H;Wang, Y;Yao, Y;Li, Y;Wang, W;Yang, S;Chen, J;Lv, L;Zhao, Y;Xue, G;Guo, X;Zhang, L;
PMID: 36462769 | DOI: 10.1055/s-0042-1757875
Scientific reports
2022 Mar 30
Minatoguchi, S;Saito, S;Furuhashi, K;Sawa, Y;Okazaki, M;Shimamura, Y;Kaihan, AB;Hashimoto, Y;Yasuda, Y;Hara, A;Mizutani, Y;Ando, R;Kato, N;Ishimoto, T;Tsuboi, N;Esaki, N;Matsuyama, M;Shiraki, Y;Kobayashi, H;Asai, N;Enomoto, A;Maruyama, S;
PMID: 35354870 | DOI: 10.1038/s41598-022-09331-5
Molecular metabolism
2021 Nov 26
Costa, A;Ai, M;Nunn, N;Culotta, I;Hunter, J;Boudjadja, MB;Valencia-Torres, L;Aviello, G;Hodson, DJ;Snider, BM;Coskun, T;Emmerson, PJ;Luckman, SM;D'Agostino, G;
PMID: 34844019 | DOI: 10.1016/j.molmet.2021.101407
Neurotoxicology and teratology
2021 Apr 20
Graham, DL;Madkour, HS;Noble, BL;Schatschneider, C;Stanwood, GD;
PMID: 33864929 | DOI: 10.1016/j.ntt.2021.106984
ACR open rheumatology
2021 May 01
Jones, K;Angelozzi, M;Gangishetti, U;Haseeb, A;de Charleroy, C;Lefebvre, V;Bhattaram, P;
PMID: 33931959 | DOI: 10.1002/acr2.11255
Basic Res Cardiol.
2018 Jun 04
Mouton AJ, DeLeon-Pennell KY, Rivera Gonzalez OJ, Flynn ER, Freeman TC, Saucerman JJ, Garrett MR, Ma Y, Harmancey R, Lindsey ML.
PMID: 29868933 | DOI: 10.1007/s00395-018-0686-x
In response to myocardial infarction (MI), cardiac macrophages regulate inflammation and scar formation. We hypothesized that macrophages undergo polarization state changes over the MI time course and assessed macrophage polarization transcriptomic signatures over the first week of MI. C57BL/6 J male mice (3-6 months old) were subjected to permanent coronary artery ligation to induce MI, and macrophages were isolated from the infarct region at days 1, 3, and 7 post-MI. Day 0, no MI resident cardiac macrophages served as the negative MI control. Whole transcriptome analysis was performed using RNA-sequencing on n = 4 pooled sets for each time. Day 1 macrophages displayed a unique pro-inflammatory, extracellular matrix (ECM)-degrading signature. By flow cytometry, day 0 macrophages were largely F4/80highLy6Clow resident macrophages, whereas day 1 macrophages were largely F4/80lowLy6Chigh infiltrating monocytes. Day 3 macrophages exhibited increased proliferation and phagocytosis, and expression of genes related to mitochondrial function and oxidative phosphorylation, indicative of metabolic reprogramming. Day 7 macrophages displayed a pro-reparative signature enriched for genes involved in ECM remodeling and scar formation. By triple in situ hybridization, day 7 infarct macrophages in vivo expressed collagen I and periostin mRNA. Our results indicate macrophages show distinct gene expression profiles over the first week of MI, with metabolic reprogramming important for polarization. In addition to serving as indirect mediators of ECM remodeling, macrophages are a direct source of ECM components. Our study is the first to report the detailed changes in the macrophage transcriptome over the first week of MI.
Biochimica et biophysica acta. Molecular basis of disease
2022 Jun 27
Ha, S;Yang, Y;Kim, BM;Kim, J;Son, M;Kim, D;Yu, HS;Im, D;Chung, HY;Chung, KW;
PMID: 35772632 | DOI: 10.1016/j.bbadis.2022.166474
Description | ||
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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 | |
EnEm | Probe targets exons n and m | |
En-Em | Probe 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 |
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