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17β-Estradiol (E2) is an important regulator of energy homeostasis and glucose metabolism, thus making it a potential target for preventing or treating metabolic disorders. However, the exact mechanism by which E2 affects high glucose-induced oxidative stress remains unclear. Therefore, the present study investigated the role of E2 in high glucose-induced mitochondrial reactive oxygen species (mtROS) production through estrogen receptor (ER)-mediated signaling in human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) in vitro. In addition, the effect of hUCB-MSC transplantation on mouse skin wound healing induced by E2 in ovariectomized (OVX) diabetic mice in vivo was also studied. High glucose (D-glucose, 25mM) increased mtROS production, resulting in increase of Beclin1 expression and the LC3-II/LC3-I ratio, leading to decreased cell viability. Conversely, E2 (10nM) treatment significantly decreased high glucose-induced mtROS levels and subsequently restored cell viability, suggesting that E2 serves as a strong antioxidant. High glucose downregulated Nrf2 levels in nucleus, subsequently culminating in Sirt3 downregulation and manganese superoxide dismutase (MnSOD) acetylation. However, we found that E2 induces nuclear Nrf2 expression via interaction with ERα. The increased nuclear translocation of Nrf2 triggered Sirt3 upregulation and MnSOD activation, both of which play important roles in decreasing mtROS levels. Thus, the therapeutic effect of hUCB-MSC transplantation on skin wound healing in OVX diabetic mice was enhanced by E2 treatment compared with the findings in OVX diabetic mice treated only with hUCB-MSCs. In addition, blood vessels with well-developed branches were observed in OVX diabetic mice that underwent hUCB-MSC transplantation and E2 treatment compared with the effects of ERα siRNA-transfected hUCB-MSC transplantation alone. In conclusion, our results imply that E2 protects cells against high glucose-induced mtROS production and autophagic cell death through increasing nuclear translocation of Nrf2, which was followed by Sirt3 upregulation and MnSOD activation in hUCB-MSCs.
This article was published in the following journal.
Name: Free radical biology & medicine
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Stem cells are a population of undifferentiated cells that originated from embryonic and fetal stages of development. Stem cells possess the potency to produce cells that ultimately form different tis...
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Bone-marrow-derived, non-hematopoietic cells that support HEMATOPOETIC STEM CELLS. They have also been isolated from other organs and tissues such as UMBILICAL CORD BLOOD, umbilical vein subendothelium, and WHARTON JELLY. These cells are considered to be a source of multipotent stem cells because they include subpopulations of mesenchymal stem cells.
Transfer of MESENCHYMAL STEM CELLS between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS).
Cells that can develop into distinct mesenchymal tissue such as BONE; TENDONS; MUSCLES; ADIPOSE TISSUE; CARTILAGE; NERVE TISSUE; and BLOOD and BLOOD VESSELS.
Colony-forming cells which give rise to NEOPLASMS. They have properties similar to normal stem cells, i.e., high proliferative and self-renewal capacities.
Specialized stem cells that are committed to give rise to cells that have a particular function; examples are MYOBLASTS; MYELOID PROGENITOR CELLS; and skin stem cells. (Stem Cells: A Primer [Internet]. Bethesda (MD): National Institutes of Health (US); 2000 May [cited 2002 Apr 5]. Available from: http://www.nih.gov/news/stemcell/primer.htm)
Track and monitor developments in stem cell research and commercial development. Follow the tabs above to read the latest global news, research, clinical trials on stem cells and follow companies active in the stem cell industry. BioPort...
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