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

PMID26391655

ABSTRACT

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

MATERIALS

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Brand

Product Description

P0067

Sigma-Aldrich

Anti-p62/SQSTM1 antibody produced in rabbit, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution

A0856

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Anti-ATG5 (N-terminal) antibody produced in rabbit, affinity isolated antibody, PBS solution

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Anti-ATG7 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution

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Monoclonal Anti-β-Actin antibody produced in mouse, clone AC-15, ascites fluid

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Monoclonal Anti-Actin, α-Smooth Muscle, clone 1A4, ascites fluid

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Senescence Cells Histochemical Staining Kit, sufficient for 100 tests

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Anti-Acetyl (Lys 319) p53 Antibody, C-Terminal antibody produced in rabbit, affinity isolated antibody

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Anti-Actin, α-Smooth Muscle - FITC antibody, Mouse monoclonal, clone 1A4, purified from hybridoma cell culture