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

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

PROVIDER: PRJNA780551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16951715_1.fastq.gz	Fastqsanger.gz
	SRR16951715_2.fastq.gz	Fastqsanger.gz
	SRR16951716_1.fastq.gz	Fastqsanger.gz
	SRR16951716_2.fastq.gz	Fastqsanger.gz
	SRR16951717_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

Project description: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 I

Project description: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 III

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

Project description:ncRNA SNHG12 regulates angiogenesis in ischemic limbs

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

Project description:ncRNA SNHG12 regulates angiogenesis in ischemic limbs

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Chronic intermittent hypoxia inhibits the revascularization of the ischemic retina and aggravates neurodegeneration and neovascularization

Project description:Neovascular retinopathies and edema are sign threatening complications of ischemic retinopathies, such as retinopathy of prematurity (ROP) and diabetic retinopathy (DR). Sleep apnea that leads to chronic intermittent hypoxia (CIH) is an independent risk factor for severe disease, but the underlying mechanisms are unknown. Here we show that experimental CIH during the ischemic phase of oxygen induced retinopathy in mice severely reduces beneficial revascularitzation of the ischemic retina, and increases neuronal loss and pathological neovascularization. Mechanistically we demonstrate that CIH reduces both colony stimulation factor 1 (CSF-1) expression and the ischemia-induced increase of retinal microglial cells that promotes the revascularization of the ischemic retina in the absence of CIH. Local CSF1R inhibition during ischemic retinopathy reduced the number of microglial cells, inhibited revascularization, and exacerbated pathological neovascularization, recapitulating several effects of CIH. Our findings provide a novel mechanism by which sleep apnea and CIH aggravate ischemic retinopathies, underscoring the importance of treating apnea in ROP and DR to help prevent sight threatening severe disease.

2025-03-19 | GSE268420 | GEO

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

Chronic intermittent hypoxia inhibits the revascularization of the ischemic retina and aggravates neurodegeneration and neovascularization

Project description:Chronic intermittent hypoxia inhibits the revascularization of the ischemic retina and aggravates neurodegeneration and neovascularization

| PRJNA1117071 | ENA

Downregulation of SENP1 impairs nuclear condensation of MEF2C and deteriorates ischemic cardiomyopathy

Project description:Downregulation of SENP1 impairs nuclear condensation of MEF2C and deteriorates ischemic cardiomyopathy

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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

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