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.
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Stem Cells
2022 Jan 19
Figeac, F;Tencerova, M;Ali, D;Andersen, T;Appadoo, D;Kerckhofs, G;Ditzel, N;Kowal, J;Rauch, A;Kassem, M;
| DOI: 10.1093/stmcls/sxab011
The mechanisms of obesity and type 2 diabetes (T2D)-associated impaired fracture healing are poorly studied. In a murine model of T2D reflecting both hyperinsulinemia induced by high fat diet (HFD) and insulinopenia induced by treatment with streptozotocin (STZ), we examined bone healing in a tibia cortical bone defect. A delayed bone healing was observed during hyperinsulinemia as newly formed bone was reduced by - 28.4±7.7% and was associated with accumulation of marrow adipocytes at the defect site +124.06±38.71%, and increased density of SCA1+ (+74.99± 29.19%) but not Runx2 +osteoprogenitor cells. We also observed increased in reactive oxygen species production (+101.82± 33.05%), senescence gene signature (≈106.66± 34.03%) and LAMIN B1 - senescent cell density (+225.18± 43.15%), suggesting accelerated senescence phenotype. During insulinopenia, a more pronounced delayed bone healing was observed with decreased newly formed bone to -34.9± 6.2% which was inversely correlated with glucose levels (R 2=0.48, p<0.004) and callus adipose tissue area (R 2=0.3711, p<0.01). Finally, to investigate the relevance to human physiology, we observed that sera from obese and T2D subjects had disease state-specific inhibitory effects on osteoblast related gene signatures in human bone marrow stromal cells which resulted in inhibition of osteoblast and enhanced adipocyte differentiation. Our data demonstrate that T2D exerts negative effects on bone healing through inhibition of osteoblast differentiation of skeletal stem cells and induction of accelerated bone senescence and that the hyperglycaemia per se and not just insulin levels is detrimental for bone healing.
PLoS biology
2021 Dec 21
Herder, V;Dee, K;Wojtus, JK;Epifano, I;Goldfarb, D;Rozario, C;Gu, Q;Da Silva Filipe, A;Nomikou, K;Nichols, J;Jarrett, RF;Stevenson, A;McFarlane, S;Stewart, ME;Szemiel, AM;Pinto, RM;Masdefiol Garriga, A;Davis, C;Allan, J;Graham, SV;Murcia, PR;Boutell, C;
PMID: 34932557 | DOI: 10.1371/journal.pbio.3001065
The pandemic spread of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiological agent of Coronavirus Disease 2019 (COVID-19), represents an ongoing international health crisis. A key symptom of SARS-CoV-2 infection is the onset of fever, with a hyperthermic temperature range of 38 to 41°C. Fever is an evolutionarily conserved host response to microbial infection that can influence the outcome of viral pathogenicity and regulation of host innate and adaptive immune responses. However, it remains to be determined what effect elevated temperature has on SARS-CoV-2 replication. Utilizing a three-dimensional (3D) air-liquid interface (ALI) model that closely mimics the natural tissue physiology of SARS-CoV-2 infection in the respiratory airway, we identify tissue temperature to play an important role in the regulation of SARS-CoV-2 infection. Respiratory tissue incubated at 40°C remained permissive to SARS-CoV-2 entry but refractory to viral transcription, leading to significantly reduced levels of viral RNA replication and apical shedding of infectious virus. We identify tissue temperature to play an important role in the differential regulation of epithelial host responses to SARS-CoV-2 infection that impact upon multiple pathways, including intracellular immune regulation, without disruption to general transcription or epithelium integrity. We present the first evidence that febrile temperatures associated with COVID-19 inhibit SARS-CoV-2 replication in respiratory epithelia. Our data identify an important role for tissue temperature in the epithelial restriction of SARS-CoV-2 independently of canonical interferon (IFN)-mediated antiviral immune defenses.
Molecular Pathology Demonstration of SARS-CoV-2 in Cytotrophoblast from Placental Tissue with Chronic Histiocytic Intervillositis, Trophoblast Necrosis and COVID-19
Journal of developmental biology
2021 Aug 25
Schwartz, DA;Bugatti, M;Santoro, A;Facchetti, F;
PMID: 34449643 | DOI: 10.3390/jdb9030033
A subset of placentas from pregnant women having the SARS-CoV-2 infection have been found to be infected with the coronavirus using molecular pathology methods including immunohistochemistry and RNA in situ hybridization. These infected placentas can demonstrate several unusual findings which occur together-chronic histiocytic intervillositis, trophoblast necrosis and positive staining of the syncytiotrophoblast for SARS-CoV-2. They frequently also have increased fibrin deposition, which can be massive in some cases. Syncytiotrophoblast is the most frequent fetal-derived cell type to be positive for SARS-CoV-2. It has recently been shown that in a small number of infected placentas, villous stromal macrophages, termed Hofbauer cells, and villous capillary endothelial cells can also stain positive for SARS-CoV-2. This report describes a placenta from a pregnant woman with SARS-CoV-2 that had chronic histiocytic intervillositis, trophoblast necrosis, increased fibrin deposition and positive staining of the syncytiotrophoblast for SARS-CoV-2. In addition, molecular pathology testing including RNAscope and immunohistochemistry for SARS-CoV-2 and double-staining immunohistochemistry using antibodies to E-cadherin and GATA3 revealed that cytotrophoblast cells stained intensely for SARS-CoV-2. All of the cytotrophoblast cells that demonstrated positive staining for SARS-CoV-2 were in direct physical contact with overlying syncytiotrophoblast that also stained positive for the virus. The pattern of cytotrophoblast staining for SARS-CoV-2 was patchy, and there were chorionic villi having diffuse positive staining of the syncytiotrophoblast for SARS-CoV-2, but without staining of cytotrophoblast. This first detailed description of cytotrophoblast involvement by SARS-CoV-2 adds another fetal cell type from infected placentas that demonstrate viral staining.
Hepatology communications
2023 Feb 01
Wang, D;Li, M;Ling, J;Chen, S;Zhang, Q;Liu, Z;Huang, Y;Pan, C;Lin, Y;Shi, Z;Zhang, P;Zheng, Y;
PMID: 36724124 | DOI: 10.1097/HC9.0000000000000021
Endothelial cell (EC) function declines with age and contributes to the development of many vascular-related disease processes. Currently, the effects of aging on the molecular regulatory mechanisms of liver ECs have not been fully elucidated. Here, we employed single-cell RNA sequencing to map the transcriptome of ECs and analyzed their relationship with aging. We identified 8 different EC subtypes, interestingly, 2 of which were specially expressed in aged mice ECs namely aged capillary ECs (Aged ECs) and pro-inflammation capillary ECs (Proinfla.ECs). Double immunostaining for an EC marker (Cd31) and a marker of these specialized EC phenotypes confirmed the single-cell RNA sequencing data. Gene ontology analysis revealed that Aged ECs and Proinfla.ECs were associated with inflammatory response. Then we found that liver proliferating capillary ECs (Prolife.ECs) were most affected by senescence. Single-cell transcript analysis suggests that Prolife.ECs and angiogenic capillary ECs may form a poor microenvironment that promotes angiogenesis and tumorigenesis. Pseudo-temporal trajectories revealed that Prolife.ECs have different differentiation pathways in young and aged mice. In aged mice, Prolife.ECs could specifically differentiate into an unstable state, which was mainly composed of angiogenic capillary ECs. Intercellular communication revealed inflammatory activation in old group. Overall, this work compared the single-cell RNA profiles of liver ECs in young and aged mice. These findings provide a new insight into liver aging and its molecular mechanisms, and further exploration of Aged ECs and Proinfla.ECs may help to elucidate the molecular mechanisms associated with senescence.
bioRxiv : the preprint server for biology
2022 Feb 01
Jiang, L;Driedonks, TAP;Jong, WSP;Dhakal, S;van den Berg van Saparoea, HB;Sitaras, I;Zhou, R;Caputo, C;Littlefield, K;Lowman, M;Chen, M;Lima, G;Gololobova, O;Smith, B;Mahairaki, V;Richardson, MR;Mulka, KR;Lane, AP;Klein, SL;Pekosz, A;Brayton, CF;Mankowski, JL;Luirink, J;Villano, JS;Witwer, KW;
PMID: 35132418 | DOI: 10.1101/2021.06.28.450181
Several vaccines have been introduced to combat the coronavirus infectious disease-2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Current SARS-CoV-2 vaccines include mRNA-containing lipid nanoparticles or adenoviral vectors that encode the SARS-CoV-2 Spike (S) protein of SARS-CoV-2, inactivated virus, or protein subunits. Despite growing success in worldwide vaccination efforts, additional capabilities may be needed in the future to address issues such as stability and storage requirements, need for vaccine boosters, desirability of different routes of administration, and emergence of SARS-CoV-2 variants such as the Delta variant. Here, we present a novel, well-characterized SARS-CoV-2 vaccine candidate based on extracellular vesicles (EVs) of Salmonella typhimurium that are decorated with the mammalian cell culture-derived Spike receptor-binding domain (RBD). RBD-conjugated outer membrane vesicles (RBD-OMVs) were used to immunize the golden Syrian hamster ( Mesocricetus auratus ) model of COVID-19. Intranasal immunization resulted in high titers of blood anti-RBD IgG as well as detectable mucosal responses. Neutralizing antibody activity against wild-type and Delta variants was evident in all vaccinated subjects. Upon challenge with live virus, hamsters immunized with RBD-OMV, but not animals immunized with unconjugated OMVs or a vehicle control, avoided body mass loss, had lower virus titers in bronchoalveolar lavage fluid, and experienced less severe lung pathology. Our results emphasize the value and versatility of OMV-based vaccine approaches.
Brain : a journal of neurology
2022 Jul 29
Lee, MH;Perl, DP;Steiner, J;Pasternack, N;Li, W;Maric, D;Safavi, F;Horkayne-Szakaly, I;Jones, R;Stram, MN;Moncur, JT;Hefti, M;Folkerth, RD;Nath, A;
PMID: 35788639 | DOI: 10.1093/brain/awac151
The underlying mechanisms by which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leads to acute and long-term neurological manifestations remains obscure. We aimed to characterize the neuropathological changes in patients with coronavirus disease 2019 and determine the underlying pathophysiological mechanisms. In this autopsy study of the brain, we characterized the vascular pathology, the neuroinflammatory changes and cellular and humoral immune responses by immunohistochemistry. All patients died during the first wave of the pandemic from March to July 2020. All patients were adults who died after a short duration of the infection, some had died suddenly with minimal respiratory involvement. Infection with SARS-CoV-2 was confirmed on ante-mortem or post-mortem testing. Descriptive analysis of the pathological changes and quantitative analyses of the infiltrates and vascular changes were performed. All patients had multifocal vascular damage as determined by leakage of serum proteins into the brain parenchyma. This was accompanied by widespread endothelial cell activation. Platelet aggregates and microthrombi were found adherent to the endothelial cells along vascular lumina. Immune complexes with activation of the classical complement pathway were found on the endothelial cells and platelets. Perivascular infiltrates consisted of predominantly macrophages and some CD8+ T cells. Only rare CD4+ T cells and CD20+ B cells were present. Astrogliosis was also prominent in the perivascular regions. Microglial nodules were predominant in the hindbrain, which were associated with focal neuronal loss and neuronophagia. Antibody-mediated cytotoxicity directed against the endothelial cells is the most likely initiating event that leads to vascular leakage, platelet aggregation, neuroinflammation and neuronal injury. Therapeutic modalities directed against immune complexes should be considered.
SARS-CoV2 infects pancreatic beta cells in vivo and induces cellular and subcellular disruptions that reflect beta cell dysfunction
Research square
2021 Jul 20
Millette, K;Cuala, J;Wang, P;Marks, C;Woo, V;Hayun, M;Kang, H;Martin, M;Dhawan, S;Chao, L;Fraser, S;Junge, J;Lewis, M;Georgia, S;
PMID: 34312617 | DOI: 10.21203/rs.3.rs-592374/v1
Increasing evidence of new-onset diabetes during the COVID19 pandemic indicates that the SARS-CoV2 virus may drive beta-cell dysfunction leading to diabetes, but it is unclear if it is a primary or secondary effect. Here, we present evidence of SARS-CoV-2 infection of pancreatic beta cells in vivo using a robust and reproducible non-human primates model of mild to moderate COVID19 pathogenesis. Pancreas from SARS-CoV-2 infected subjects were positive for the SARS-CoV2 spike protein by immunohistochemistry and structures indicative of viral replication were evident by electron microscopy. Total beta cell area was decreased in SARS-CoV-2-infected pancreas, attributable to beta cell atrophy. Beta cell granularity was decreased. These histologic phenotypes persisted beyond the duration of the clinical disease course. Detailed electron microscopy of SARS-CoV-2 infected beta-cells revealed ultrastructural hallmarks of beta cell stress that are seen in islets of patients with Type 2 diabetes, including disrupted mitochondria and dilated endoplasmic reticulum. To assess the metabolic status of beta cells from SARS-CoV-2-infected subjects, we used fluorescence life-time imaging to measure the ratio of free and bound NADH as a surrogate of glycolytic and oxidative metabolism. We report an increase in free NADH levels, suggesting that beta cells from SARS-CoV-2-infected subjects adopt a more glycolytic metabolic profile. Taken together, we conclude that SARS-CoV-2 infection induces beta cell stress that may compromise beta-cell function beyond the duration of the disease course. This raises the possibility that the beta cell stress and injury may have clinical implications of the long-term future health of patients that have recovered from COVID19.
Acta neuropathologica communications
2023 May 22
Seeker, LA;Bestard-Cuche, N;Jäkel, S;Kazakou, NL;Bøstrand, SMK;Wagstaff, LJ;Cholewa-Waclaw, J;Kilpatrick, AM;Van Bruggen, D;Kabbe, M;Baldivia Pohl, F;Moslehi, Z;Henderson, NC;Vallejos, CA;La Manno, G;Castelo-Branco, G;Williams, A;
PMID: 37217978 | DOI: 10.1186/s40478-023-01568-z
The myelinated white matter tracts of the central nervous system (CNS) are essential for fast transmission of electrical impulses and are often differentially affected in human neurodegenerative diseases across CNS region, age and sex. We hypothesize that this selective vulnerability is underpinned by physiological variation in white matter glia. Using single nucleus RNA sequencing of human post-mortem white matter samples from the brain, cerebellum and spinal cord and subsequent tissue-based validation we found substantial glial heterogeneity with tissue region: we identified region-specific oligodendrocyte precursor cells (OPCs) that retain developmental origin markers into adulthood, distinguishing them from mouse OPCs. Region-specific OPCs give rise to similar oligodendrocyte populations, however spinal cord oligodendrocytes exhibit markers such as SKAP2 which are associated with increased myelin production and we found a spinal cord selective population particularly equipped for producing long and thick myelin sheaths based on the expression of genes/proteins such as HCN2. Spinal cord microglia exhibit a more activated phenotype compared to brain microglia, suggesting that the spinal cord is a more pro-inflammatory environment, a difference that intensifies with age. Astrocyte gene expression correlates strongly with CNS region, however, astrocytes do not show a more activated state with region or age. Across all glia, sex differences are subtle but the consistent increased expression of protein-folding genes in male donors hints at pathways that may contribute to sex differences in disease susceptibility. These findings are essential to consider for understanding selective CNS pathologies and developing tailored therapeutic strategies.
Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases
2022 Mar 23
Almamlouk, R;Kashour, T;Obeidat, S;Bois, MC;Maleszewski, JJ;Omrani, OA;Tleyjeh, R;Berbari, E;Chakhachiro, Z;Zein-Sabatto, B;Gerberi, D;Tleyjeh, IM;Cardiac Autopsy in COVID-19 Study Group, ;
PMID: 35339672 | DOI: 10.1016/j.cmi.2022.03.021
Many post-mortem studies addressing the cardiovascular effects of COVID-19 provided valuable information but were limited by their small sample size.The aim of this systematic review is to better understand the various aspects of the cardiovascular complications of COVID-19 by pooling data from a large number of autopsy studies.We searched online databases Ovid EBM Reviews, Ovid Embase, Ovid Medline, Scopus and Web of Science for the concepts of autopsy or histopathology combined with COVID-19 published between database inception to February 2021. We also searched for unpublished manuscripts using the medRxiv services operated by Cold Spring Harbor Laboratory.Articles were considered eligible for inclusion if they reported human post-mortem cardiovascular findings among individuals with confirmed SARS-CoV-2 infection.Studies were individually assessed for risk of selection bias, detection bias and reporting bias.Median prevalence of different autopsy findings with associated interquartile ranges.This review cohort contained 50 studies including 548 hearts. The median age of the deceased was 69 years. The most prevalent acute cardiovascular findings were myocardial necrosis (median=100.0%, IQR 20-100%, number of studies=9, number of patients=64) and myocardial edema (median=55.5%, IQR 19.5-92.5%, number of studies=4, number of patients=46). Median reported prevalence's of extensive, focal active and multifocal myocarditis were all 0.0%. The most prevalent chronic changes were myocyte hypertrophy (median=69.0%, IQR 46.8-92.1%) and fibrosis (median=35.0%, IQR 35.0-90.5%). SARS-CoV-2 was detected in the myocardium with median prevalence of 60.8% (IQR 40.4-95.6%).Our systematic review confirmed the high prevalence of acute and chronic cardiac pathologies in COVID-19, SARS-CoV-2 cardiac tropism, and the low prevalence of myocarditis in COVID-19 disease.
Qeios
2022 Sep 21
Fessel, J;
| DOI: 10.32388/cf8mip
Mental disability is a serious and often disabling symptom of Long Covid, for which currently there is no recommendable pharmacotherapy for those patients whose response to psychotherapy is suboptimal. Treatment could be formulated by using drugs that address the brain cell-types that have been demonstrated as dominantly affected in Long Covid. Those cell-types are astrocytes, oligodendrocytes, endothelial cells/pericytes, and microglia. Lithium and fluoxetine each address all of those four cell-types. They should be administered in combination for both depth of benefit and reduction of dosages. Low dosage of each is likely to be well-tolerated and to cause neither adverse events (AE) nor serious adverse events (SAE).
Viruses
2022 Jun 03
Lamoureux, L;Sajesh, B;Slota, JA;Medina, SJ;Mayor, M;Frost, KL;Warner, B;Manguiat, K;Wood, H;Kobasa, D;Booth, SA;
PMID: 35746689 | DOI: 10.3390/v14061218
The numerous neurological syndromes associated with COVID-19 implicate an effect of viral pathogenesis on neuronal function, yet reports of direct SARS-CoV-2 infection in the brain are conflicting. We used a well-established organotypic brain slice culture to determine the permissivity of hamster brain tissues to SARS-CoV-2 infection. We found levels of live virus waned after inoculation and observed no evidence of cell-to-cell spread, indicating that SARS-CoV-2 infection was non-productive. Nonetheless, we identified a small number of infected cells with glial phenotypes; however, no evidence of viral infection or replication was observed in neurons. Our data corroborate several clinical studies that have assessed patients with COVID-19 and their association with neurological involvement.
Science Translational Medicine
2022 Jun 07
Frere, J;Serafini, R;Pryce, K;Zazhytska, M;Oishi, K;Golynker, I;Panis, M;Zimering, J;Horiuchi, S;Hoagland, D;Møller, R;Ruiz, A;Kodra, A;Overdevest, J;Canoll, P;Borczuk, A;Chandar, V;Bram, Y;Schwartz, R;Lomvardas, S;Zachariou, V;tenOever, B;
| DOI: 10.1126/scitranslmed.abq3059
The host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can result in prolonged pathologies collectively referred to as post-acute sequalae of COVID-19 (PASC) or long COVID. To better understand the mechanism underlying long COVID biology, we compared the short- and long-term systemic responses in the golden hamster following either SARS-CoV-2 or influenza A virus (IAV) infection. Results demonstrated that SARS-CoV-2 exceeded IAV in its capacity to cause permanent injury to the lung and kidney and uniquely impacted the olfactory bulb (OB) and epithelium (OE). Despite a lack of detectable infectious virus, the OB and OE demonstrated myeloid and T cell activation, proinflammatory cytokine production, and an interferon response that correlated with behavioral changes extending a month post viral clearance. These sustained transcriptional changes could also be corroborated from tissue isolated from individuals who recovered from COVID-19. These data highlight a molecular mechanism for persistent COVID-19 symptomology and provide a small animal model to explore future therapeutics.
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| 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 | |
| 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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