MSCs rescue impaired wound healing in a murine LAD1 model by adaptive responses to low TGF-β1 levels.
作者： Dongsheng Jiang , Karmveer Singh , Jana Muschhammer , Susanne Schatz , Anca Sindrilaru
关键词: Myofibroblast 、 CD18 、 Chemistry 、 Transforming growth factor 、 Transplantation 、 Mesenchymal stem cell 、 Adipose tissue 、 Receptor 、 Gene silencing 、 Cell biology
摘要: Mutations in the CD18 gene encoding common β-chain of β2 integrins result impaired wound healing humans and mice suffering from leukocyte adhesion deficiency syndrome type 1 (LAD1). Transplantation adipose tissue-derived mesenchymal stem cells (MSCs) restores normal CD18-/- wounds by restoring decreased TGF-β1 concentrations. released MSCs leads to enhanced myofibroblast differentiation, contraction, vessel formation. We uncover that are equipped with a sensing mechanism for concentrations at sites. Low as occurring induce release MSCs, whereas high suppress production. This regulation depends on TGF-β receptor is relayed microRNA-21 (miR-21), which subsequently suppresses translation Smad7, negative regulator signaling. Inactivation receptor, or overexpression silencing miR-21 abrogates sensing, thus prevents adaptive MSC responses required tissue repair.
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