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

Product Number

Brand

Product Description

A0856

Sigma-Aldrich

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

A5441

Sigma-Aldrich

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

A2547

Sigma-Aldrich

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

A2856

Sigma-Aldrich

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

P0067

Sigma-Aldrich

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

SAB4503014

Sigma-Aldrich

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

CS0030

Sigma-Aldrich

Senescence Cells Histochemical Staining Kit, sufficient for 100 tests

F3777

Sigma-Aldrich

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