Long‐chain noncoding RNA GAS5 mediates oxidative stress in cardiac microvascular endothelial cells injury

Abstract

This study is performed to figure out the role of long‐chain noncoding RNA growth‐arrest specific transcript 5 (GAS5) in homocysteine (HCY)‐induced cardiac microvascular endothelial cells (CMECs) injury. CMECs were cultured and the model of CMECs injury was established by coincubation with HCY. To construct stable overexpression of GAS5 cells, the expression of GAS5, microRNA‐33a‐5p (miR‐33a‐5p) and ATP‐binding cassette transporter A1 (ABCA1), and biological characteristics of cells were determined. The messenger RNA (mRNA) level and secretion of vascular endothelial growth factor (VEGF), activity of reactive oxygen species (ROS) and superoxide dismutase (SOD), and the content of malondialdehyde (MDA) were measured. The binding site between GAS5 and miR‐33a‐5p and between miR‐33a‐5p and ABCA1 was verified. CMECs were successfully cultured. Reduction of GAS5 expression and ABCA1 expression together with increased expression of miR‐33a‐5p was found in CMECs induced by HCY. After overexpression of GAS5, there showed increased proliferative activity, decreased cell apoptosis rate and apoptosis index, enhanced cell migration ability, increased number of lumen formation, increased mRNA expression of VEGF in cells and the secretion in the supernatant, decreased activity of ROS and SOD in cells, and decreased content of ROS in cells. miR‐33a‐5p could promote the enrichment of GAS5 and ABCA1 was the direct target gene of miR‐33a‐5p. Our study suggests that the low expression of GAS5 was observed in HCY‐induced CMECs injury, and the upregulation of GAS5 could attenuate HCY‐induced CMECs injury by mediating oxidative stress, and its mechanism is related to the upregulation of ABCA1 expression by competitively binding with miR‐33a‐5p.

Tcf3‐activated lncRNA Gas5 regulates newborn mouse cardiomyocyte apoptosis in diabetic cardiomyopathy

“…11 And lncRNA GAS5 can regulate the oxidative stress in the heart. 12 In our study, we implemented high-glucose treatment to NRC and NMC and tested the expression of lncRNA GAS5 in NRC and NMC by qRT-PCR assay. And we found that lncRNA GAS5 expression was increased with the time of high-glucose treatment increasing.…”

“…11 And lncRNA GAS5 can regulate oxidative stress in the heart. 12 Here we detected the expression of lncRNA Gas5 in NRC and NMC when treated with 30 mmol/L high glucose via qRT-PCR assay ( Figure 1A). We found the expression of lncRNA GAS5 was upregulated with the hours of 30 mmol/L high-glucose treatment.…”

“…11 And lncRNA GAS5 can regulate oxidative stress in the heart. 12 However, the function of lncRNA GAS5 in diabetic cardiomyopathy is still not clear. Thus, in this study, we are going to fully investigate the progression of the lncRNA GAS5 in diabetic cardiomyopathy.…”

Impact of homocysteine levels on clinical outcome in patients with acute ischemic stroke receiving intravenous thrombolysis therapy

“…Besides, the increased risk of cardiovascular disease could also be partially attributed to Hhcy ( Borowczyk et al, 2019 ). Its possible underlying mechanism is that elevated serum homocysteine (Hcy) may lead to endothelial dysfunction ( Esse et al, 2019 ; Wu et al, 2019 ; Yan et al, 2019 ), neurotoxicity ( Moretti & Caruso, 2019 ) and up-regulation of thrombosis formation factors ( Diao et al, 2019 ; Jin et al, 2018 ). However, the likelihood of applying Hcy to prognosticate AIS patients’ clinical outcomes after rtPA therapy hasn’t been thoroughly investigated.…”

MiR-33a-5p targets NOMO1 to modulate human cardiomyocyte progenitor cells proliferation and differentiation and apoptosis

“…And miR-33a-5p has been proved to inhibit the growth and migration of colorectal cancer by targeting MTHFD2 [13]. MiR-33a-5p also plays a role in cardiovascular diseases, according to Liwei Diao et al [14] increased expression of miR-33a-5p was found in cardiac microvascular endothelial cell injury. Another study [15] found that inhibition of miR-33a could inhibit cardiac fibrosis.…”