PPT1 regulation of HSP90α depalmitoylation participates in the pathogenesis of hyperandrogenism.
PPT1 regulation of HSP90α depalmitoylation participates in the pathogenesis of hyperandrogenism.
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PPT 1调节HSP 90 α去棕榈酰化参与高雄激素血症的发病机制
DOI：
10.1016/j.isci.2023.106131
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发表时间：
2023-03-17
期刊：
影响因子：
5.8
通讯作者：
Yao, Bing
中科院分区：
文献类型：
--
作者：
Xue, Tongmin;Zhao, Shanmeizi;Zhang, Hong;Tang, Ting;Zheng, Lu;Jing, Jun;Ge, Xie;Ma, Rujun;Ma, Jinzhao;Ren, Xiaoyan;Jueraitetibaike, Kadiliya;Guo, Zhigang;Chen, Li;Yao, Bing
Ovarian granulosa cells (GCs) in the follicle are the important mediator of steroidogenesis and foster oocyte maturation. Evidences suggested that the function of GCs could be regulated by S-palmitoylation. However, the role of S-palmitoylation of GCs in ovarian hyperandrogenism remains elusive. Here, we demonstrated that the protein from GCs in ovarian hyperandrogenism phenotype mouse group exhibits lower palmitoylation level compared with that in the control group. Using S-palmitoylation-enriched quantitative proteomics, we identified heat shock protein isoform α (HSP90α) with lower S-palmitoylation levels in ovarian hyperandrogenism phenotype group. Mechanistically, S-palmitoylation of HSP90α modulates the conversion of androgen to estrogens via the androgen receptor (AR) signalling pathway, and its level is regulated by PPT1. Targeting AR signaling by using dipyridamole attenuated ovarian hyperandrogenism symptoms. Our data help elucidate ovarian hyperandrogenism from perspective of protein modification and provide new evidence showing that HSP90α S-palmitoylation modification might be a potential pharmacological target for ovarian hyperandrogenism treatment. HSP90α S-palmitoylation participates in the pathogenesis of hyperandrogenemia HSP90α-palmitoylation modulates the conversion of androgen to estrogens HSP90α depalmitoylation could be regulated by PPT1 Dipyridamole attenuated ovarian hyperandrogenism in a DHEA-induced model Health sciences; Molecular biology; Proteomics
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影响因子：
--
作者：
Lyly, Annina;von Schantz, Carina;Kyttala, Aija
通讯作者：
Kyttala, Aija
CD36 通过动态棕榈酰化调节的内吞作用促进脂肪酸摄取
影响因子：
16.6
作者：
Hao JW;Wang J;Guo H;Zhao YY;Sun HH;Li YF;Lai XY;Zhao N;Wang X;Xie C;Hong L;Huang X;Wang HR;Li CB;Liang B;Chen S;Zhao TJ
通讯作者：
Zhao TJ
影响因子：
4
作者：
Krzemien-Ojak, Lucja;Goral, Agnieszka;Fabczak, Hanna
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Fabczak, Hanna
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影响因子：
5.5
作者：
Min Z;Long X;Zhao H;Zhen X;Li R;Li M;Fan Y;Yu Y;Zhao Y;Qiao J
通讯作者：
Qiao J
影响因子：
4.8
作者：
Davies, TH;Ning, YM;Sánchez, ER
通讯作者：
Sánchez, ER