Key result
Lentiviral-mediated silencing of MCEMP1 enhanced angiogenesis and suppressed neuronal apoptosis in rats with cerebral ischemic stroke.
Why the study?
Cerebral ischemic stroke causes high morbidity and mortality, and MCEMP1 functions in ischemic stroke, but its specific role in angiogenesis, neuronal proliferation, and apoptosis remains to be explored.
Does lentiviral-mediated silencing of MCEMP1 improve angiogenesis and reduce neuronal apoptosis in rats with cerebral ischemic stroke?
Does lentiviral-mediated silencing of MCEMP1 improve angiogenesis and reduce neuronal apoptosis in rats with cerebral ischemic stroke?
Silencing MCEMP1 enhances angiogenesis and suppresses neuronal apoptosis in a rat model of cerebral ischemic stroke, highlighting a potential therapeutic target.
Answers are grounded in this paper and cite their sources.
May support MCEMP1 silencing for angiogenesis in rodent stroke models; leaves open translation to human therapy.
Cerebral ischemic stroke is a devastating neurological disease with high rates of morbidity, disability, and mortality. Lentiviral-mediated mast cell-expressed membrane protein 1 (MCEMP1) has been shown to function in ischemic stroke. Hence, this study aims to explore the function of MCEMP1 specifically in angiogenesis, neuronal proliferation, and apoptosis in rats with cerebral ischemic stroke. Initially, stroke-related genes were obtained through microarray-based gene expression analysis, followed by the construction of a lentiviral vector for MCEMP1 shRNA and establishment of the middle cerebral artery occlusion model. After rats were transfected with MCEMP1 shRNA lentivirus, microvessel density (MVD), expression of MCEMP1, caspase-3, and vascular endothelial growth factor (VEGF), and neuronal proliferation and apoptosis were measured to explore the role of MCEMP1 in cerebral ischemic stroke. MCEMP1 was found to be highly expressed in rats with cerebral ischemic stroke. Silencing of MCEMP1 led to upregulation of VEGF, while downregulation of caspase-3, and resulted in the promotion of MVD in rats with ischemic stroke. Moreover, MCEMP1 silencing could increase Ki67 positive cells and reduce terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling positive cells in the marginal zone of cortical infarction in rats. Our study provides evidence that silenced MCEMP1 could enhance angiogenesis and suppress neuronal apoptosis in rats with cerebral ischemic stroke, highlighting that MCEMP1 silencing could serve as a therapeutic target for cerebral ischemic stroke treatment.
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Jian et al. (2019) studied Cerebral ischemic stroke. Lentiviral-mediated MCEMP1 shRNA was evaluated on Angiogenesis, neuronal proliferation, and apoptosis. Lentiviral-mediated silencing of MCEMP1 enhanced angiogenesis and suppressed neuronal apoptosis in rats with cerebral ischemic stroke.
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