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Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway III

ABSTRACT: Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway III

PROVIDER: PRJNA780549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16951734_1.fastq.gz	Fastqsanger.gz
	SRR16951734_2.fastq.gz	Fastqsanger.gz
	SRR16951735_1.fastq.gz	Fastqsanger.gz
	SRR16951735_2.fastq.gz	Fastqsanger.gz
	SRR16951736_1.fastq.gz	Fastqsanger.gz

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Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway III

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Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway II

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Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway I

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Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway I

Project description:Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway I

| PRJNA780553 | ENA

Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway II

Project description:Deficiency of lncRNA SNHG12 impairs neovascularization in ischemic limbs by altering an endothelial cell cycle pathway II

| PRJNA780551 | ENA

Deficiency of lncRNA SNHG12 impairs ischemic limb neovascularization by altering an endothelial cell cycle pathway.

Project description:SNHG12, a long noncoding RNA (lncRNA) dysregulated in atherosclerosis, is known to be a key regulator of vascular senescence in endothelial cells (ECs). However, its role in angiogenesis and peripheral artery disease has not been elucidated. Hind-limb ischemia studies using femoral artery ligation (FAL) in mice showed that SNHG12 expression falls readily in the acute phase of the response to limb ischemia in gastrocnemius muscle and recovers to normal when blood flow recovery is restored to ischemic muscle, indicating that it likely plays a role in the angiogenic response to ischemia. Gain- and loss-of-function studies demonstrated that SNHG12 regulated angiogenesis - SNHG12 deficiency reduced cell proliferation, migration, and endothelial sprouting, whereas overexpression promoted these angiogenic functions. We identified SNHG12 binding partners by proteomics that may contribute to its role in angiogenesis, including IGF-2 mRNA-binding protein 3 (IGF2BP3, also known as IMP3). RNA-Seq profiling of SNHG12-deficient ECs showed effects on angiogenesis pathways and identified a strong effect on cell cycle regulation, which may be modulated by IMP3. Knockdown of SNHG12 in mice undergoing FAL using injected gapmeRs) decreased angiogenesis, an effect that was more pronounced in a model of insulin-resistant db/db mice. RNA-Seq profiling of the EC and non-EC compartments in these mice revealed a likely role of SNHG12 knockdown on Wnt, Notch, and angiopoietin signaling pathways. Together, these findings indicate that SNHG12 plays an important role in the angiogenic EC response to ischemia.

| S-EPMC8765056 | biostudies-literature

Endothelial CXCL12 regulates neovascularization during tissue repair and tumor progression

Project description:Tissue repair and tumor progression are linked by their reliance on the response to ischemia. Coordinated interplay between resident and circulating cells, governed by a myriad of factors, is critical for new blood vessel formation and tissue survival in both. The vascular endothelium exhibits paracrine activity and provides an interface for the recruitment of circulating cells, which in turn influence the neovascularization and extra-vascular tissue growth. CXC chemokine ligand 12 (CXCL12; stromal cell-derived factor 1 [SDF-1]) has been implicated in tumor biology and neovascularization, but its specific role and mechanism of action remain poorly understood. We have previously demonstrated that CXCL12 expression is hypoxia responsive and occurs in vascular endothelium. Here we use a conditional CXCL12 knockout mouse to show that endothelial-specific deletion of CXCL12 (eKO) reduces the survival of ischemic tissue, which alters both tissue repair and tumor progression. The loss of vascular endothelial CXCL12 disrupts endothelial – fibroblast crosstalk necessary for stromal growth and vascularization. Using single-cell gene expression analysis in combination with a parabiosis model, eKO is found to impair the recruitment of a specific population of non-inflammatory circulating cells defined by genes regulating cell survival and neovascularization. These findings indicate an essential role of endothelial CXCL12 expression during the adult neovascular response in tissue injury and tumor progression, paving the way for future therapeutic interventions.

2020-03-07 | GSE146529 | GEO

miRNAs expression profile in bone marrow-derived PACs during ischemia-induced neovascularization in cardiovascular risk factors conditions

Project description:Using NGS, we report the impact of cardiovascular risk factors (CRF) including hypercholesteolemia, aging and smoking compare to healthy control mice, on the differential-expression profile of miRNAs in proangiogenic cells (PACs) isolated during ischemia-induced neovascularization in a mouse model of hindlimb ischemia. Data of total miRNA expression are presented as normalized copy number: read per millions of read (RPM). Hindlimb ischemia was surgicaly induced by feromal artery ablation and the animal was sacrified 2 day after ischemic surgery for PACs isolation. After 4 days of culture, PACs RNAs were extracted to perform NGS.

2020-06-03 | GSE151609 | GEO

Short Hairpin RNA Silencing of PHD-2 Improves Neovascularization and Functional Outcomes in Diabetic Wounds and Ischemic Limbs.

Project description:The transcription factor hypoxia-inducible factor 1-alpha (HIF-1?) is responsible for the downstream expression of over 60 genes that regulate cell survival and metabolism in hypoxic conditions as well as those that enhance angiogenesis to alleviate hypoxia. However, under normoxic conditions, HIF-1? is hydroxylated by prolyl hydroxylase 2, and subsequently degraded, with a biological half-life of less than five minutes. Here we investigated the therapeutic potential of inhibiting HIF-1? degradation through short hairpin RNA silencing of PHD-2 in the setting of diabetic wounds and limb ischemia. Treatment of diabetic mouse fibroblasts with shPHD-2 in vitro resulted in decreased levels of PHD-2 transcript demonstrated by qRT-PCR, higher levels of HIF-1? as measured by western blot, and higher expression of the downstream angiogenic genes SDF-1 and VEGF?, as measured by qRT-PCR. In vivo, shPHD-2 accelerated healing of full thickness excisional wounds in diabetic mice compared to shScr control, (14.33 ± 0.45 days vs. 19 ± 0.33 days) and was associated with an increased vascular density. Delivery of shPHD-2 also resulted in improved perfusion of ischemic hind limbs compared to shScr, prevention of distal digit tip necrosis, and increased survival of muscle tissue. Knockdown of PHD-2 through shRNA treatment has the potential to stimulate angiogenesis through overexpression of HIF-1? and upregulation of pro-angiogenic genes downstream of HIF-1?, and may represent a viable, non-viral approach to gene therapy for ischemia related applications.

| S-EPMC4788284 | biostudies-literature

Transcription profiling of human non ischemic cardiomyopathy (NICM)- (n=12) NYHA III-IV CHF patients

Project description:Inflammatory mediators play a role in the pathogenesis/progression of chronic heart failure (CHF). The aim of the present study was to identify diagnostic/prognostic markers and gene expression profiles of CHF vs control. Experiment Overall Design: Gene expression profiling was performed in three patients' groups: 1) Ischemic cardiomyopathy (ICM)- (n=12) and 2) Non ischemic cardiomyopathy (NICM)- (n=12) NYHA III-IV CHF patients ; 3) Age- and gender matched controls (n=12) by Affymetrix microarrays. Data were then subjected to informatic analysis.

2008-06-17 | E-GEOD-9128 | biostudies-arrayexpress

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