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Merck
  • 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
要旨

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
モノクロナール抗β-アクチン マウス宿主抗体, clone AC-15, ascites fluid
Sigma-Aldrich
モノクロナール抗アクチン, α-平滑筋, clone 1A4, ascites fluid
Sigma-Aldrich
老化細胞組織化学染色キット, sufficient for 100 tests
Sigma-Aldrich
抗アクチンα-平滑筋-FITC抗体、マウスモノクローナル マウス宿主抗体, clone 1A4, purified from hybridoma cell culture
Sigma-Aldrich
抗p62/SQSTM1 ウサギ宿主抗体, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
抗ATG7 ウサギ宿主抗体, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
抗ATG5 (N-末端) ウサギ宿主抗体, affinity isolated antibody, PBS solution
Sigma-Aldrich
Anti-Acetyl (Lys 319) p53 Antibody, C-Terminal antibody produced in rabbit, affinity isolated antibody