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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
ZUSAMMENFASSUNG

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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Monoklonales Anti-β-Aktin in Maus hergestellte Antikörper, clone AC-15, ascites fluid
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Monoklonaler Anti-Aktin-Antikörper , α-Glattmuskel, clone 1A4, ascites fluid
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Histochemisches Färbungskit für Seneszenzzellen, sufficient for 100 tests
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Monoklonaler Anti-Aktin α-Glattmuskel-FITC-Antikörper der Maus in Maus hergestellte Antikörper, clone 1A4, purified from hybridoma cell culture
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Anti-p62/SQSTM1 in Kaninchen hergestellte Antikörper, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution
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Anti-ATG7 in Kaninchen hergestellte Antikörper, affinity isolated antibody, buffered aqueous solution
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Anti-ATG5 (N-terminal) in Kaninchen hergestellte Antikörper, affinity isolated antibody, PBS solution
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Anti-Acetyl (Lys 319) p53 Antibody, C-Terminal antibody produced in rabbit, affinity isolated antibody