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RNA-sequencing of CCN2 knockout and wild type mice following 4 hours after IRI

ABSTRACT: In order to identify major regulatory events in the immediate phase of renal IRI associated with CCN2, we performed full transcriptome RNA-sequencing on a cDNA library constructed from RNA extracted from samples of kidney cortex.

ORGANISM(S): Mus musculus

PROVIDER: GSE186316 | GEO | 2021/10/28

REPOSITORIES: GEO

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RNA-sequencing of CCN2 knockout and wild type mice following 4 hours after IRI

Project description:RNA-sequencing of CCN2 knockout and wild type mice following 4 hours after IRI

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Effect of knockout of ALKBH5 on gene expression and m6A modifications during IRI in mice

Project description:To identify the direct m6A demethylation targets of ALKBH5 at the onset of renal IRI, we performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) using RNA isolated from IRI mouse kidney of WT and KO mice 24h after I/R (WT n=3 vs. KO n=3)

2023-02-05 | GSE224289 | GEO

Transcriptomic changes associated with CCN2/CTGF deficiency in the mouse embryonic retina

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CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development

Project description:Vascular smooth muscle cell (VSMC) phenotypic switching is widely recognized as a key mechanism responsible for the pathogenesis of several aortic diseases such as aortic aneurysm. Cellular communication network factor 2 (CCN2), often upregulated in human pathologies and animal disease models, exerts a myriad of context-dependent biological functions. However, current understanding of the role of SMC-CCN2 in SMC phenotypic switching and its function in the pathology of abdominal aortic aneurysm (AAA) is lacking. Here we report the effect of SMC-restricted CCN2 deficiency of hypercholesterolemic mice on gene expression in infrarenal aorta with or without angiotensin II (Ang II)-infusion.

2023-03-02 | GSE221399 | GEO

CCN2-MAPK-Id-1 Loop Feedback Amplification is involved in Maintaining Stemness in Oxaliplatin-resistant Hepatocellular Carcinoma

Project description:Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide. Most patients are at an advanced stage at diagnosis, and are not eligible for curative therapy. Chemotherapy is an alternative treatment for advanced HCCs, but resistance is found in many patients. Understanding the underlying mechanisms in chemo-resistance is critical to further improve the efficacy of HCC treatment. In this study, we found that increased expression of Id-1 and CCN2 were closely related to oxaliplatin resistance in HCC. Upregulation of CCN2 and Id-1 was independently associated with shorter survival and increased recurrence in HCC patients, and significantly enhanced oxaliplatin resistance and promoted lung metastasis in vivo, whereas knock-down of their expression significantly reversed the chemo-resistance and inhibited HCC cell stemness. cDNA microarrays and PCR revealed that Id-1 and MAPK pathway were the downstream signaling of CCN2, and Id-1 could upregulate CCN2 in a positive feedback manner. Moreover, CCN2 significantly enhanced oxaliplatin resistance by activating the MAPK signaling pathway and upregulating Id-1 expression. Meanwhile, MAPK/Id-1 signaling was demonstrated as one of the most important autocrine signaling pathways regulated by CCN2 in oxaliplatin-resistant models, and combination with sorafenib could improve the efficacy of oxaliplatin in HCC. Conclusions: These findings suggest that CCN2-MAPK-Id-1 loop feedback amplification is involved in oxaliplatin-resistant HCC, and the combination of oxaliplatin with inhibitor of CCN2 or MAPK signaling could provide a promising approach to ameliorating HCC progression and oxaliplatin resistance.

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Microarray-based clustering analysis of miRNAs altered in IRI-AKI mouse kidney

Project description:The aim of this study was to identify miRNAs that regulate AKI and develop their applications as diagnostic biomarkers and therapeutic agents. First, kidney tissues from two different AKI mouse models, namely, AKI induced by the administration of lipopolysaccharide (LPS) causing sepsis (LPS-AKI mice) and AKI induced by renal ischemia–reperfusion injury (IRI-AKI mice), were exhaustively screened for their changes of miRNA expression compared with that of control mice by microarray analysis.

2021-05-14 | GSE172039 | GEO

Gene expression change in Keap1 knockdown (KD) mice in kidneys of ischemia-reperfusion injury (IRI)

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Project description:N-glycanase 1(NGLY1) catalyzes the removal of N-linked glycans from newly synthesized or misfolded protein to exert protein quality control function via the process of endoplasmic reticulum-associated degradation (ERAD). NGLY1 deficiency (OMIM 615273) is a newly diagnosed rare genetic disorder with ~60 patients worldwide to date. The affected individuals present a broad spectrum of clinical features, including developmental delay, seizures, muscle weakness, liver failure, and the reduced secretion of sweats and tears. Recent studies explored several possible molecular mechanisms of NGLY1 deficiency including in vivo proteostasis, mitochondrial homeostasis, innate immunity, water and ion transport, with the goal of linking these findings to the pathophysiology of the disease. This study focuses on the dysregulation of ERAD in NGLY1 deficiency. We demonstrate the abnormal accumulation of ERAD substrates in NGLY1 deficient cells. Comprehensive global quantitative proteomics discovered elevated levels of novel endogenous proteins in NGLY1 defective human and mouse cells. Further biological validation assays confirmed the altered abundance of several key candidates’ that were observed in the isobarically labeled proteomic experiments. CCN2 was selected for further analysis due to its high fold change in different cell models of NGLY1 deficiency. Functional assays show elevated CCN2 and over-stimulated TGF-β signaling in NGLY1 deficient cells. Given the important role of CCN2 and TGF-β pathway in mediating systemic fibrosis, we propose a potential link of increased CCN2 and TGF-β signaling to microscopic liver fibrosis in NGLY1 patients.

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2009-01-20 | E-GEOD-14373 | biostudies-arrayexpress

Real-time quantitative PCR analysis of Rag1-/- knockout and Rag1-/- Tbx21-/- double knockout mouse liver in a diet- and ischemia-reperfusion injury (IRI)-specific manner.

Project description:Differential gene expression of mouse cytokines and chemokines in Rag1 knockout (Rag1-/- or Rag1-KO) and Rag1-/- Tbx21-/- double knockout (Rag1-Tbet-DKO) was tested in fatty liver ischemic-reperfusion injury (IRI). C57BL/6 mice harboring Rag1-/- or Rag1-/- Tbx21-/- deletions were fed with a normal chow diet (ND, 4.09 kcal/gram,13.4% kJ/fat) or a high-fat diet (HFD, 5.10 kcal/gram, 60% kJ/fat). To induce liver ischemic-reperfusion injury in mice, an atraumatic micro clip was placed across the hepatic hilus, which interrupted the blood supply to the left and median lobes of the liver for 45-minutes of partial warm ischemia time. After 24 hours of liver IRI, the affected left lobe of the liver was harvested and stored in Allprotect Tissue Reagent (Qiagen). We used Qiagen RT² Profiler™ PCR Array for mouse cytokines & chemokines to distinguish immunologically related and diet-specific gene signatures specific to liver IRI in Rag1-KO and Rag1-Tbet-DKO mice.

2022-06-07 | GSE205510 | GEO

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