Article ID Journal Published Year Pages File Type
10815407 Cellular Signalling 2012 8 Pages PDF
Abstract
► MSCs from SLE patients showed characteristics of senescence. ► p16INK4A was increased in the MSCs from both untreated and treated SLE patients. ► Knockdown of p16INK4A reverse the senescent features of MSCs. ► p16INK4A promote MSCs senescence via suppression ERK1/2 signal pathway activation.
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Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Biochemistry
Preview
Upregulation of p16INK4A promotes cellular senescence of bone marrow-derived mesenchymal stem cells from systemic lupus erythematosus patients
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