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

ABSTRACT: ncRNA SNHG12 regulates angiogenesis in ischemic limbs

ORGANISM(S): Homo sapiens

PROVIDER: GSE188877 | GEO | 2022/01/26

REPOSITORIES: GEO

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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 III

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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

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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 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.

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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.

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Circadian Dysfunction in Skeletal Muscle Impairs Limb Perfusion and Muscle Regeneration in Peripheral Artery Disease

Project description:Peripheral arterial disease (PAD), caused by atherosclerosis, leads to limb ischemia, muscle damage, and impaired mobility in the lower extremities. Recent studies suggest that circadian rhythm disruptions can hinder vascular repair during ischemia, but the specific tissues involved and the impact on muscle health remain unclear. This study investigates the role of the skeletal muscle circadian clock in muscle adaptation to ischemic stress using a surgical mouse model of hindlimb ischemia. We used mice with specific genetic loss of the circadian clock activator, BMAL1, in adult skeletal muscle tissues (Bmal1muscle). Bmal1muscle mice and controls underwent femoral artery ligation surgery to induce hindlimb ischemia. Laser doppler imaging was used to assess limb perfusion at various time points after the surgery. Muscle tissues were analyzed with RNA sequencing and histological examination to investigate PAD-related muscle pathologies. Additionally, we studied the role of BMAL1 in muscle fiber adaptation to hypoxia using RNA and ATAC sequencing analyses in primary myotube culture model. Disrupted expression of circadian rhythm-related genes was observed in existing RNA-seq datasets from PAD patient-derived endothelial cells and ischemic limb skeletal muscles. Genetic loss of Bmal1 specifically in adult mouse skeletal muscle tissues delayed reperfusion recovery following induction of hindlimb ischemia. Histological examination of muscle tissues showed reduced regenerated myofiber number and a decreased proportion of type IIB fast-twitch myofibers in Bmal1musc mouse muscles in the ischemic limbs, but not in their contralateral non-ischemic limbs. Transcriptomic analysis revealed abrogated metabolic, angiogenic, and myogenic pathways relevant to hypoxia-adaptation in Bmal1musc mouse muscles. These changes were corroborated in Bmal1-deficient cultured primary myotubes cultured under hypoxic conditions.

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Sequencing of iMDK-treated regenerating limbs

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