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TGF-β Mediates Aortic Smooth Muscle Cell Senescence in Marfan Syndrome

TGF-β Mediates Aortic Smooth Muscle Cell Senescence in Marfan Syndrome

Wei You, Yimei Hong, Haiwei He, Xiaoran Huang, Wuyuan Tao, Xiaoting Liang, Yuelin Zhang, Xin Li

Aging (Albany NY). 2019 May 30;11(11):3574-3584.

PMID: 31147528

Abstract:

Formation of aortic aneurysms as a consequence of augmented transforming growth factor β (TGF-β) signaling and vascular smooth muscle cell (VSMC) dysfunction is a potentially lethal complication of Marfan syndrome (MFS). Here, we examined VSMC senescence in patients with MFS and explored the potential mechanisms that link VSMC senescence and TGF-β. Tissue was harvested from the ascending aorta of control donors and MFS patients, and VSMCs were isolated. Senescence-associated β-galactosidase (SA-β-gal) activity and expression of senescence-related proteins (p53, p21) were significantly higher in aneurysmal tissue from MFS patients than in healthy aortic tissue from control donors. Compared to control-VSMCs, MFS-VSMCs were larger with higher levels of both SA-β-gal activity and mitochondrial reactive oxygen species (ROS). In addition, TGF-β1 levels were much higher in MFS- than control-VSMCs. TGF-β1 induced VSMC senescence through excessive ROS generation. This effect was suppressed by Mito-tempo, a mitochondria-targeted antioxidant, or SC-514, a NF-κB inhibitor. This suggests TGF-β1 induces VSMC senescence through ROS-mediated activation of NF-κB signaling. It thus appears that a TGF-β1/ROS/NF-κB axis may mediate VSMC senescence and aneurysm formation in MFS patients. This finding could serve as the basis for a novel strategy for treating aortic aneurysm in MFS.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP354812172	SC-514		354812-17-2	Price

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