Diabetes Mellitus-Induced Erectile Dysfunction

MALAT1[LncRNA]

miR-206[miRNA]

VEGFA[mRNA]

endothelial cells

Homo sapiens (human)

Cell Cycle. 2020 Nov;19(22):3018-3028. doi: 10.1080/15384101.2020.1829799. Epub 2020 Oct 29.

LncRNA MALAT1 facilitates BM-MSCs differentiation into endothelial cells via targeting miR-206/VEGFA axis.

Luciferase reporter assay;RNA pull-down;

Bone marrow-derived mesenchymal stem cells (BM-MSCs) implantation shows a repair effect on erectile function in diabetes mellitus-induced erectile dysfunction (DMED) due to its differentiative capacity into endothelial cells (ECs) that contributes to endothelial repair. This study was designed to explore the functional role and mechanism of long noncoding RNA (lncRNA)-metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in BM-MSCs-mediated DMED repairing. The DMED rat model was established and the erectile function was evaluated by calculating the intracavernous pressure (ICP)/mean arterial pressure (MAP) ratio in the DMED models with or without BM-MSCs implantation. The differentiation of BM-MSCs toward ECs was assessed by measuring the expression of EC-specific genes. RNA pull-down and luciferase reporter assay were performed to explore the interaction between miR-206 and MALAT1 or VEGFA. BM-MSCs implantation improved the erectile function of DMED rats and increased MALAT1 expression. MALAT1 was time-dependently upregulated during the VEGF-induced BM-MSCs differentiation into ECs. Mechanistically, MALAT1 acted as a sponge of miR-206 to upregulate VEGFA expression, thereby promoting the differentiation of BM-MSCs into ECs. Moreover, MALAT1 silencing in vivo impaired the repairing effect of BM-MSCs on erectile dysfunction. Collectively, MALAT1 facilitates BM-MSCs differentiation into ECs via regulating miR-206/VEGFA axis.