miR-133a-3p regulates the proliferation and apoptosis of intestinal epithelial cells by modulating the expression of TAGLN2

xlomafota13 shared this article with you from Inoreader miR-133a-3p regulates the proliferation and apoptosis of intestinal epithelial cells by modulating the expression of TAGLN2 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Aug;22(2):824. doi: 10.3892/etm.2021.10256. Epub 2021 Jun 2. ABSTRACT Sepsis is one of the most common diseases in patients in intensive care units. Intestinal barrier dysfunction serves a critical role in the pathogenesis and progression of sepsis. Therefore, preservation of the intestinal epithelial barrier function is an area of ongoing research in the treatment of sepsis. The present study investigated the effects of miR-133a-3p on the proliferation and apoptosis of intestinal epithelial cells and the possible mechanism underlying its actions. miR-133a-3p was used to upregulate the intestinal epithelial FHs 74 Int cell line and cell proliferation and apoptosis were investigated. A luciferase reporter assay was used to determine whether the 3'-UTR of TAGLN2 mRNA was a binding target of miR-133a-3p. FHs 74 Int cells were transfected with TAGLN2 shRNA and the effects of TAGLN2 on the proliferation and apoptosis of i ntestinal epithelial cells were investigated. It was found that miR-133a-3p inhibited the proliferation and promoted the apoptosis of intestinal epithelial cells. A luciferase reporter assay confirmed that miR-133a-3p targeted TAGLN2 directly. In addition, low expression of TAGLN2 inhibited the proliferation and promoted the apoptosis of intestinal epithelial cells. The results of the present study suggested that the miR-133a-3p inhibition of proliferation and promotion of apoptosis occurred via the inhibition of TAGLN2. These results suggested that miR-133a-3p may be a promising therapeutic target for the diagnosis and treatment of gut-origin sepsis. PMID:34149870 | PMC:PMC8200801 | DOI:10.3892/etm.2021.10256 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.