Long Non-Coding RNA Malat1 Regulates Angiogenesis in Hindlimb Ischemia

MALAT1
DOI: 10.3390/ijms19061723 Publication Date: 2018-06-11T15:01:01Z
ABSTRACT
Angiogenesis is a complex process that depends on the delicate regulation of gene expression. Dysregulation transcription during angiogenesis often leads to various human diseases. Emerging evidence has recently begun show long non-coding RNAs (lncRNAs) may mediate in both physiological and pathological conditions; concurrently, underlying molecular mechanisms are largely unexplored. Previously, our lab identified metastasis associates lung adenocarcinoma transcript 1 (Malat1) as an oxygen-glucose deprivation (OGD)-responsive endothelial lncRNA. Here we reported genetic deficiency Malat1 reduced blood vessel formation local flow perfusion mouse hind limbs at one four weeks after hindlimb ischemia. vascular growth factor receptor 2 (VEGFR2) levels were found be increased cultured primary skeletal muscle microvascular cells (SMMECs) 16 h OGD followed by 24 reperfusion gastrocnemius underwent ischemia 28 days reperfusion. Moreover, silencing locked nucleic acid (LNA)-GapmeRs significantly tube formation, cell migration, proliferation SMMEC cultures. Mechanistically, RNA subcellular isolation RNA-immunoprecipitation experiments demonstrate directly targets VEGFR2 facilitate angiogenesis. The results suggest regulates cell-autonomous through direct VEGFR2.
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