Heat Shock Protein Family A Member 1A Attenuates Apoptosis and Oxidative Stress via ERK/JNK Pathway in Hyperplastic Prostate DOI Creative Commons
Huan Liu, Yongying Zhou, Zhen Wang

и другие.

MedComm, Год журнала: 2025, Номер 6(3)

Опубликована: Март 1, 2025

Benign prostatic hyperplasia (BPH) is a prevalent disorder in aging males. It investigated whether heat shock protein family A member 1A (HSPA1A), cytoprotective chaperone induced under stress, has been implicated the development of BPH. RNA-sequencing and single-cell sequencing analyses revealed significant upregulation HSPA1A BPH compared to controls. In vitro experiments elucidated that was localized epithelium stroma, with upregulated expression tissues. Moreover, silencing augmented apoptosis reactive oxygen species (ROS) accumulation, inhibiting proliferation via ERK/JNK activation, while overexpression reversed these effects BPH-1 WPMY-1 cells. Additionally, ERK1/2 suppression U0126 rescued silencing. vivo, testosterone-induced (T-BPH) rat models treated antagonist KNK437 exhibited atrophy molecular changes consistent reduced activity. Finally, we conducted tissue microarray (TMA) analysis 139 specimens from Zhongnan Hospital Wuhan University, which positive correlation between clinical parameters, including prostate volume (PV), tPSA, fPSA, IPSS. conclusion, our findings suggested attenuated oxidative stress through signaling pathway, contributing pathogenesis.

Язык: Английский

Heat Shock Protein Family A Member 1A Attenuates Apoptosis and Oxidative Stress via ERK/JNK Pathway in Hyperplastic Prostate DOI Creative Commons
Huan Liu, Yongying Zhou, Zhen Wang

и другие.

MedComm, Год журнала: 2025, Номер 6(3)

Опубликована: Март 1, 2025

Benign prostatic hyperplasia (BPH) is a prevalent disorder in aging males. It investigated whether heat shock protein family A member 1A (HSPA1A), cytoprotective chaperone induced under stress, has been implicated the development of BPH. RNA-sequencing and single-cell sequencing analyses revealed significant upregulation HSPA1A BPH compared to controls. In vitro experiments elucidated that was localized epithelium stroma, with upregulated expression tissues. Moreover, silencing augmented apoptosis reactive oxygen species (ROS) accumulation, inhibiting proliferation via ERK/JNK activation, while overexpression reversed these effects BPH-1 WPMY-1 cells. Additionally, ERK1/2 suppression U0126 rescued silencing. vivo, testosterone-induced (T-BPH) rat models treated antagonist KNK437 exhibited atrophy molecular changes consistent reduced activity. Finally, we conducted tissue microarray (TMA) analysis 139 specimens from Zhongnan Hospital Wuhan University, which positive correlation between clinical parameters, including prostate volume (PV), tPSA, fPSA, IPSS. conclusion, our findings suggested attenuated oxidative stress through signaling pathway, contributing pathogenesis.

Язык: Английский

Процитировано

1