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ADSCs inhibit photoaging‐ and photocarcinogenesis‐related inflammatory responses and extracellular matrix degradation
Author(s) -
Gong Meihua,
Zhai Xu,
Yu Li,
Li Chunyang,
Ma Xu,
Shen Qi,
Han Yubo,
Yang Daping
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29354
Subject(s) - photoaging , extracellular matrix , chemistry , skin aging , microbiology and biotechnology , cancer research , stem cell , downregulation and upregulation , biochemistry , biology , medicine , dermatology , gene
Background Skin is a dynamic organ that maintains homeostasis and provides protection against environmental stimuli and pathogens. However, constant solar ultraviolet (UV) radiation can induce photoaging and photocarcinogenesis, thus reducing skin barrier function by altering skin at the cellular and structural levels. Adipose‐derived stem cells (ADSCs) ameliorate signs of skin photoaging, but their antiphotoaging mechanism remains elusive. In this study, we explored the mechanism by which ADSCs improve skin photoaging. Methods Female C57BL/6J mice were used as experimental subjects and were randomly divided into three groups. We used Western blot analysis, Real time‐polymerase chain reaction, and immunofluorescence to analyze the expression of photoaging‐ and photocarcinogenesis‐related inflammasomes, extracellular matrix components, and related factors. Results The results showed that ADSCs reduced the UVB irradiation‐mediated increase in MMP2, MMP13, phospho‐NF‐κB p65, Nlrp3, and VCAM‐1 mRNA expression. The TGF‐β2 expression trend was opposite that of the above genes. ADSCs ameliorated the downregulation of α6 integrin, CD34, and collagen I by UVB irradiation. Simultaneously, ADSCs reduced the overexpression of COX2 and TNF‐α induced by UVB irradiation. Conclusion These results demonstrated that ADSCs could restore skin barrier function at the cellular and structural levels, enhance hair follicle stem cell (HFSCs) activity by regulating TGF‐β2 and inhibit photoaging‐ and photocarcinogenesis‐related inflammatory responses and extracellular matrix degradation.