ABSTRACT
Smad3 is a major transporter in the transforming growth factor β (TGF-β) signaling pathway.It is in charge of the transfer of TGF-β signal from the surface of the cell membrane into the nucleus.The TGF-β signal can be bound to the target gene in the nucleus and regulate its expression.Abnormalities in Smad3 expression level and functional status will lead to abnormal signal transduction,involving cell growth,proliferation,development,differentiation,migration,apoptosis and other basic life activities.This review focused on the differential expression of Smad3 in hepatocellular carcinoma (HCC)and the adjacent tissue.The character of Smad3 in HCC is outlined in three parts:Smad3 upstream signaling source,Smad3 self-assembly maturation and Smad3 downstream effects,which may provide a summary and reference for the follow-up study on Smad3.
ABSTRACT
AIM: To investigate the effects of TGF-?_1 and signal protein Smad3 on rat cardiac myocyte hypertrophy.METHODS: The total protein was analyzed by flow cytometry and the ANF mRNA expression was measured by RT-PCR to judge the hypertrophy of cultured neonatal cardiac myocytes.Smad3 mRNA expression in cardiac myocytes was measured by RT-PCR,and the protein expression of Smad3 was analyzed by Western blotting.RESULTS: TGF-?_1 significantly increased the total protein in cardiac myocytes and promoted ANF mRNA expression,compared with control group.In cultured neonatal myocytes,AS-ODN of Smad3 inhibited myocyte hypertrophy induced by TGF-?_1.Smad3 mRNA and protein expression increased at 15 min after incubated with TGF-?_1,reached the peak at 1 h,and declined at 4 h.CONCLUSION: TGF-?_1 and signal protein Smad3 may participate in the progress of rat cardiac myocyte hypertrophy.