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  • Defective autophagy in vascular smooth muscle cells accelerates senescence and promotes neointima formation and atherogenesis.

Defective autophagy in vascular smooth muscle cells accelerates senescence and promotes neointima formation and atherogenesis.

Autophagy (2015-09-24)
Mandy Oj Grootaert, Paula A da Costa Martins, Nicole Bitsch, Isabel Pintelon, Guido Ry De Meyer, Wim Martinet, Dorien M Schrijvers
RESUMO

Autophagy is triggered in vascular smooth muscle cells (VSMCs) of diseased arterial vessels. However, the role of VSMC autophagy in cardiovascular disease is poorly understood. Therefore, we investigated the effect of defective autophagy on VSMC survival and phenotype and its significance in the development of postinjury neointima formation and atherosclerosis. Tissue-specific deletion of the essential autophagy gene Atg7 in murine VSMCs (atg7

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Sigma-Aldrich
Antiβ-actina monoclonal, clone AC-15, ascites fluid
Sigma-Aldrich
Anti-actina monoclonal, α-músculo liso, clone 1A4, ascites fluid
Sigma-Aldrich
Senescence Cells Histochemical Staining Kit, sufficient for 100 tests
Sigma-Aldrich
Anti-actina monoclonal, α-músculo liso, clone 1A4, purified from hybridoma cell culture
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Anti-p62/SQSTM1 antibody produced in rabbit, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-ATG7 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-ATG5 (N-terminal) antibody produced in rabbit, affinity isolated antibody, PBS solution
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Anti-Acetyl (Lys 319) p53 Antibody, C-Terminal antibody produced in rabbit, affinity isolated antibody