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Objective: To investigate the effect and potential mechanism of silencing TCAB1 on the proliferation of human aortic smooth muscle cells(HASMC). Methods: Three si RNA sequences(siTCAB1-331, si TCAB1-619, si TCAB-749) targetingTCAB1 and one negative sequence(NC) were designed, synthesized and then transfected into HASMC with Lipofectamine-TM2000. HASMC were divided three groups: interference group, blank control group, negative control group. Cell transfection was observed under fluorescence microscope. The m RNA and protein expression levels of TCAB1 were detected by RT-q PCR and Western blotting, the best target was selected from the three interfering targets. The effective si RNA(si TCAB1-749) was further transfected into HASMC with LipofectamineTM2000. The changes of cell cycle and CyclinD1 expression of HASMC cells were assessed using flow cytometry,RT-qPCR and Western blotting, respectively. The proliferation of HASMC was assessed using MTS assay after transfecting si TCAB1-749 at 24 h, 48 h,72 h. Results: RT-qPCR and Western blot indicated that the si TCAB1-749 was the best target in the three interfering targets. MTS revealed that the number of cell growth in si TCAB1-749 group was significantly lower than BC group and NCgroup at 24 h, 48 h, 72 h(P<0.05); the percentages of S phases in the cell cycle of si TCAB1-749 group was decreased and G1 phases was increased at 48 h(P < 0.05). In addition, the expression of cyclinD1 was decreased in si TCAB1-749 group(P<0.05). Conclusion:Silencing TCAB1 can inhibit the proliferation of HAVSMC, and its mechanism may be related to the inhibition of Cell cycle protein D1. [ABSTRACT FROM AUTHOR]

The O-GlcNAcylation as the post-translational modification(PTM) of protein, involves in important life activities such as gene transcription, signal transduction, cell differentiation. Chondrocytes and osteoblasts are two important cells in the skeletal system, and their differentiation is important for bone formation. Recent studies show that the O-GlcNAcylation affects the differentiation of chondrocytes and osteoblasts by regulating the activity of key molecules in multiple signaling pathways. In order to further elucidate the molecular regulation mechanism of O-GlcNAcylation in Chondrocytes and osteoblasts differentiation, and hopefully provide new intervention targets and new therapy strategy for clinical treatment of osteoarthritis and osteoporosis in future, we mainly overview the currunt study of how the O-GlcNAcylation regulates the differentiation of Chondrocytes and osteoblasts. [ABSTRACT FROM AUTHOR]