| 000 | 03078cam a2200373 4500500 | ||
|---|---|---|---|
| 005 | 20250121154736.0 | ||
| 041 | _afre | ||
| 042 | _adc | ||
| 100 | 1 | 0 |
_aCao, Ke _eauthor |
| 700 | 1 | 0 |
_a Chen, Guangjie _eauthor |
| 700 | 1 | 0 |
_a Chen, WenChieh _eauthor |
| 700 | 1 | 0 |
_a Hou, Xiaoxiao _eauthor |
| 700 | 1 | 0 |
_a Hu, Tingting _eauthor |
| 700 | 1 | 0 |
_a Lu, Lingyi _eauthor |
| 700 | 1 | 0 |
_a Wang, Lanqi _eauthor |
| 700 | 1 | 0 |
_a Pan, Zhanyan _eauthor |
| 700 | 1 | 0 |
_a Wu, Qiong _eauthor |
| 700 | 1 | 0 |
_a Li, Xin _eauthor |
| 700 | 1 | 0 |
_a Wei, Ziyu _eauthor |
| 700 | 1 | 0 |
_a Ma, Ying _eauthor |
| 700 | 1 | 0 |
_a Zouboulis, Christos C. _eauthor |
| 700 | 1 | 0 |
_a Ju, Qiang _eauthor |
| 245 | 0 | 0 | _aFormalin-killed Propionibacterium acnes activates the aryl hydrocarbon receptor and modifies differentiation of SZ95 sebocytes in vitro |
| 260 | _c2021. | ||
| 500 | _a43 | ||
| 520 | _aBackground: Acne vulgaris is a common pilosebaceous disease associated with Propionibacterium acnes ( P. acnes). Resolution of comedones may occur in association with shrunken sebaceous glands (SGs) containing de-differentiated cells, however the role of P. acnes is unclear. Objectives: To investigate the effects of P. acnes on aryl hydrocarbon receptor (AhR) activation, lipogenesis and differentiation in cultured immortalized human SZ95 sebocytes. Materials & Methods: Cultured sebocytes were incubated with formalin-killed (f-) P. acnes (f- P. acnes) at different ratios of multiplicity of infection. The mRNA levels of the AhR downstream cytochrome P450 (CYP) genes were measured by quantitative RT-PCR, nuclear translocation of AhR by western blot and immunofluorescence, lipogenesis and keratinization by gene set enrichment analysis (GSEA), lipid related analysis by Oil red O staining and Nile red staining, and sebaceous differentiation-related gene expression by western blot. Results: f- P. acnes upregulated CYPs mRNA levels and induced translocation of AhR protein from the cytoplasm into the nucleus. GSEA revealed downregulation of lipogenesis and upregulation of keratinization. f- P. acnes inhibited linoleic acid-induced neutral lipid synthesis and expression of sebocyte markers, keratin 7 and mucin1/EMA, but increased expression of keratinocyte markers, keratin 10 and involucrin, which were abolished by AhR gene silencing. Inhibition of lipogenesis-related genes, such as sterol response element-binding protein, was also observed. Conclusion: f- P. acnes inhibits lipogenesis and induces terminal differentiation of sebocytes, into keratinocyte-like cells, via activation of the AhR pathway in vitro, suggesting that follicular P. acnes is not only acnegenic but also promotes acne remission through feedback regulation of sebum production. | ||
| 690 | _alipogenesis | ||
| 690 | _aacne vulgaris | ||
| 690 | _aAhR | ||
| 690 | _aP. acnes | ||
| 690 | _aSZ95 sebocytes | ||
| 786 | 0 | _nEuropean Journal of Dermatology | 31 | 1 | 2021-01-01 | p. 32-40 | 1167-1122 | |
| 856 | 4 | 1 | _uhttps://shs.cairn.info/revue-european-journal-of-dermatology-2021-1-page-32?lang=en&redirect-ssocas=7080 |
| 999 |
_c603191 _d603191 |
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