AI Article Synopsis
- The study investigates how the loss of estrogen after menopause affects the function of human adipose-derived mesenchymal stem cells (hASCs) in women.
- It finds that post-menopausal hASCs have reduced responsiveness to estrogen and display higher oxidative stress, leading to impaired tissue repair abilities compared to pre-menopausal hASCs.
- By increasing the expression of an antioxidant enzyme called catalase in post-menopausal cells, the researchers demonstrate that they can restore estrogen receptor functionality and improve tissue repair outcomes in experimental models.
Article Abstract
Despite increasing interest in the reversal of age-related processes, there is a paucity of data regarding the effects of post-menopausal-associated estrogen loss on cellular function. We studied human adipose-derived mesenchymal stem cells (hASCs) isolated from women younger than 45 years old (pre-menopause, pre-hASC) or older than 55 years old (post-menopause, post-hASC). In this study, we provide proof of concept that the age-related ineffective functionality of ASCs can be reversed to improve their ability in promoting tissue repair. We found reduced estrogen receptor expression, decreased estrogen receptor activation, and reduced sensitivity to 17β-estradiol in post-hASCs. This correlated with decreased antioxidants (catalase and superoxide dismutase [SOD] expression) and increased oxidative stress compared with pre-hASCs. Increasing catalase expression in post-hASCs restored estrogen receptor (ER) expression and their functional capacity to promote tissue repair as shown in human skin ex vivo wound healing and in vivo mouse model of lung injury. Our results suggest that the consequences of 17β-estradiol decline on the function of hASCs may be reversible by changing the oxidative stress/antioxidant composition.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8821897 | PMC |
| http://dx.doi.org/10.1016/j.ymthe.2021.06.020 | DOI Listing |
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