Anti-ITGA5 monoclonal antibody, clone IN bmqib 6 [Biotin]

Mesenchymal stromal cells (MSCs) are a promising source for tissue engineering of soft connective tissues. However, the differentiation capacity of MSCs varies among individual cell lines. Here, we show marker genes to predict the adipogenic potential of MSCs. To clarify the correlation between gene expression patterns before adipogenic induction and the differentiation level of MSCs after differentiation, we compared mRNA levels of 95 genes and glycerol-3-phosphate dehydrogenase (GPDH) activities in 15 MSC lines (five jaw and 10 ilium MSCs) from 15 donors. Expression profiles of 22 genes before differentiation significantly correlated with GPDH activities after differentiation. Expression levels of 11 out of the 22 genes in highly potent ilium MSCs were at least three times higher compared with jaw MSCs, which have limited differentiation potential. Furthermore, three-dimensional scatter plot for mRNA expression of ITGA5, CDKN2D, and CD74 could completely distinguish highly potent MSCs from poorly potent MSCs for adipogenesis. The treatment of MSC cultures with the anti-ITGA5 antibody reduced adipogenic differentiation of MSCs. Collectively, these results suggest that the three genes play a role in adipogenesis before induction and can serve as predictors to select potent MSCs for adipogenic differentiation.

OBJECTIVE: Previous studies have shown that microRNA-328-3p (miR-328-3p) is involved in tumorigenesis of many human cancers. However, the specific function of miR-328-3p remains unclear in bladder cancer (BC). Therefore, this research was designed to investigate the role of miR-328-3p in BC. PATIENTS AND METHODS: Expressions of miR-328-3p and integrin alpha 5 (ITGA5) were measured by quantitative Real-time polymerase chain reaction (qRT-PCR). MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assays were used to explore the function of miR-328-3p in BC. The expression of the corresponding genes was observed via Western blot and immunocytochemical assays. The dual luciferase assay was applied to verify the relationship between miR-328-3p and ITGA5. Tumor growth was measured via xenograft tumor formation assay. RESULTS: Downregulation of miR-328-3p was identified in BC tissues, which predicted poor prognosis in BC patients. Moreover, miR-328-3p suppressed cell proliferation, migration and invasion in BC through targeting ITGA5. Furthermore, miR-328-3p inhibited epithelial-mesenchymal transition (EMT) and inactivated PI3K/AKT pathway in BC. Besides that, miR-328-3p was found to inhibit tumor growth of BC. CONCLUSIONS: MiR-328-3p inhibited tumorigenesis of BC through targeting ITGA5 and inactivating the PI3K/AKT pathway.