Hou LeWei

Objective:To explore the relationship of α-smooth muscle actin(α-SMA) in human's thoracic aorta dissection(TAD).Methods:Tissue samples of dissected thoracic aorta(DA) and normal thoracic aorta(NA) were evaluated.Western Blotting and immunohistochemical studies were performed to detected α-SMA expression in tissues.Results:α-SMA expression was apparently downregulated in DA group,while proliferated phenotype was predominated among vascular smooth muscle cells.Conclusion:Expression of α-SMA was mainly downregulated in VSMC of vascular media wall.Phenotype change of VSMC was occurred sent so that elasticity of the media was lack and dissection of vascular was performed.Therefore,α-SMA might play a key role in the development of human's thoracic aorta dissection,which is need to be further explored.

FHL family contains four and a half LIM domain.Five members have been found in vivo.They are FHL1,FHL2,FHL3, FHL4and FHL5/ACT.The expression of FHL family members is tissue-specific.The FHL family members interact with other proteins by their LIM domain,and play important roles in growth and diferentiation of myocyte,tumorigenesis and development and transcription regulation.

Objective:To investigate the intracellular copper zinc superoxide dismutase (SOD-1) expression in human thoracic aortic dissection (hTAD) and its possible roles in TAD.Methods:Western blot was performed to detect the expression of SOD-1 in dissected thoracic aortas and normal controls.Immunohistochemistry was used to validate its expression and localization. Results: Western blot and immunohistochemistry showed that the SOD-1 expression decreased in TAD compared with normaI controls (P 0.05).Immunohistochemistry showed further that SOD-1 mainly Iocalized in the cytoplasm of smooth muscle cells (SMCs) in the media, disappeared in the edges of the region where the media was divulsed.Conclusion:The SOD-1 expression decreased in TAD, which could attribute to some mechanisms such as participating the lipid peroxidation and Inflammatory reaction induced by oxidative stress, in addition,the degradation of extracellular matrix(ECM).