Effect of Regulating PPARγ by mTOR Signaling on Adipogenesis of Bone Marrow Mesenchymal Stem Cells from Aplastic Anemia / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To study the effect and mechanism of mTOR signaling on adipogenesis of bone marrow mesenchymal stem cells(BM-MSCs) from aplastic anemia (AA) patients through regulation of PPARγ.</p><p><b>METHODS</b>BM-MSCs were isolated from 24 newly diagnosed AA patients and 24 healthy controls. The surface antigen expression of BM-MSCs was identified by flow cytometry. The capacity of adipogenic differentiation of BM-MSCs was determined by lipid droplets based on Oil Red O staining and by the expression of FABP4 based on Western blot. Protein levels of mTOR signaling and PPARγ were tested by immunofluorescence and Western blot.</p><p><b>RESULTS</b>AA BM-MSCs displayed an enhanced capacity of differentiating into adipocytes, compared with control BM-MSCs. It was found that mTOR was activated in AA BM-MSCs. Moreover, the expression levels of p-mTOR and PPAR-γ in AA BM-MSCs showed a parallel differentiation-dependent increase during adipogenic differentiation, which were significantly higher than that of control BM-MSCs at the same time point of adipogenic differentiation. mTOR inhibitor rapamycin did not only inhibit the adipogenic differentiation of BM-MSCs from AA pateints at the early-middle stage, but also partly reversed the adipogenic differention of BM-MSCs from AA pateints at the late stage by PPARγ regulation.</p><p><b>CONCLUSION</b>mTOR signaling may play a critical role in the adipogenic differentiation of BM-MSCs from AA patients by positively regulating PPARγ expression.</p>

Advances in research of the mechanism of "covert disorder" in diabetic skin / 中华烧伤杂志

The diabetic ulceration is not uncommon, and becomes refractory, as the skin in a diabetic patient is relatively thin as well as hypoesthetic and less sensitive to temperature. As there are already preexisting histological and cellular derangement in the skin, healing of the skin injury is difficult, thus resulting in an intractable ulceration. When diabetes is not controlled, the skin contents of sugar and advanced glycation end product accumulate, invoking cellular deformation and accumulation of matrix metalloproteinases (MMP), resulting in an imbalance between MMP and its inhibitors, malfunction of growth factors, and inflammatory reaction. These processes lead to obvious skin thinning, denaturation of connective tissues, thickening of vascular basal membrane, and neuropathy, etc. These pathological alterations could be recognized as "covert disorder" of skin in diabetic patients and may be underlying disorders in producing indolent diabetic ulcers.