This study highlights key mechanistic pathways through which vitamin D decreases fibrosis, and provides a rationale for studies to test vitamin D supplementation as a preventive and/or early treatment strategy for keloid and related fibrotic disorders.
Cav-1 appears to participate in the pathogenesis of tissue fibrosis in keloid. Restoration of cav-1 function by treatment with a cell-permeable peptide corresponding to the cav-1 scaffolding domain may be a novel therapeutic approach in keloid.
The present study aimed to investigate the biological function and underlying molecular mechanisms of miR-31 in osteoarthritis (OA). Reverse transcription-quantitative polymerase chain reaction was used to detect miR-31 expression, and it was found that miR-31 was downregulated in the cartilage tissues of OA patients.
was used to predict the gene targets of miR-31, and dual luciferase reporter assays were used to verify that C-X-C motif chemokine ligand 12 (CXCL12) was a direct target of miR-31. The human chondrocyte cell line CHON-001 was used to perform MTT and cell migration assays. Western blotting was used to measure the protein expression of CXCL12, type I collagen and aggrecan. The results suggested that CXCL12 was a target of miR-31, and the expression of CXCL12 was negatively regulated by miR-31 in CHON-001 cells. miR-31 increased CHON-001 cell viability and migration, as well as the expression of type I collagen and aggrecan. Furthermore, the overexpression of CXCL12 eliminated the effects of miR-31 mimics on CHON-001 cells. In conclusion, the data indicated that miR-31 promoted chondrocyte viability and migration by directly targeting CXCL12, which provided evidence for CXCL12 as a potential target in OA therapy.
Osteoporosis is a systemic bone metabolic disease that is highly prevalent in the elderly population, particularly in postmenopausal women, which results in enhanced bone fragility and an increased susceptibility to fractures. However, the underlying molecular pathogenesis mechanisms still remain to be further elucidated. In this study, in a rat ovariectomy- (OVX-) induced postmenopausal osteoporosis model, aberrant expression of a microRNA miR-142-5p and vascular cell adhesion molecule 1 (VCAM-1) was found by RNA sequencing analysis and qRT-PCR. Using a dual-luciferase reporter assay, we found that miR-142-5p can bind to and decrease expression of VCAM-1 mRNA. Such reduction was prohibited when the miR-142-5p binding site in VCAM-1 3′UTR was deleted, and Western blotting analyses validated the fact that miR-142-5p inhibited the expression of VCAM-1 protein. Bone marrow-derived mesenchymal stem cells (BMMSCs) transfected with miR-142-5p showed a significantly decreased migration ability in a Transwell migration assay. Collectively, these data indicated the important role of miR-142-5p in osteoporosis development involving targeting VCAM-1 and inhibiting BMMSC migration.
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