Long Noncoding RNA SOX2-OT Aggravates Doxorubicin-Induced Apoptosis of Cardiomyocyte by Targeting miR-942-5p/DP5.

Background: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis.

Epigallocatechin-3-gallate regulates mitofusin 2 expression through the peroxisome proliferator-activated receptor-γ coactivator-1α and estrogen-related receptor-α pathway.

Our previous study showed that epigallocatechin-3-gallate (EGCG) inhibition of human aortic smooth muscle cell (HASMC) proliferation might be mediated via upregulation of mitofusin 2 (Mfn-2). Studies on the mechanism of Mfn-2 inhibition of cell proliferation have mainly focused on downstream signaling. However, it is still not clear how upstream signaling molecules regulate Mfn-2.

Toll‑like receptor 4 is expressed and functional in late endothelial progenitor cells.

It has been previously demonstrated that lipopolysaccharides (LPS) inhibit the viability, migration, adhesion and in vitro angiogenesis of late endothelial progenitor cells (EPCs). However, the mechanisms underlying this LPS‑induced impairment of late EPC functional activity are unknown. The aim of the present study was to investigate whether Toll‑like receptor 4 (TLR4) is expressed and functional on late EPCs, using late EPCs of 3‑5 passages.

Epigallocatechin-3-gallate inhibits proliferation of human aortic smooth muscle cells via up-regulating expression of mitofusin 2.

Previous studies have shown that epigallocatechin-3-gallate (EGCG) inhibits the proliferation of vascular smooth muscle cells (VSMCs) via the extracellular-signal-regulated kinase (ERK1/2) and mitogen activated protein kinases (MAPKs) pathway. Mitofusin 2 (Mfn-2) also suppresses VSMC proliferation through Ras-Raf-ERK/MAPK, suggesting a possible link between EGCG, Mfn-2 and ERK/MAPK. However, the effect of EGCG on Mfn-2 remains unknown.

Lipopolysaccharide impaired the functional activity of endothelial colony-forming cells.

Background: Recent studies have shown that endothelial progenitor cells (EPCs) contribute to lung repair after lipopolysaccharide (LPS)-induced lung injury and infusion of LPS decreased early EPCs in human peripheral blood. However, the effects of LPS on endothelial colony-forming cells (ECFCs) remain to be determined.

Objective: To investigate possible effects of LPS on the functional activity of ECFCs.