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Tytuł pozycji:

Transient protection from heat-stress induced apoptotic stimulation by metastasis-associated protein 1 in pachytene spermatocytes.

Tytuł :
Transient protection from heat-stress induced apoptotic stimulation by metastasis-associated protein 1 in pachytene spermatocytes.
Autorzy :
Li, Wei
Wu, Zhi-qun
Zhao, Jie
Guo, Sheng-jie
Li, Zhen
Feng, Xiao
Ma, Li
Zhang, Jin-shan
Liu, Xin-ping
Zhang, Yuan-qiang
Pokaż więcej
Temat :
Signaling in Cellular Processes
Cellular Types
Signaling Cascades
Research Article
Biology
Molecular Cell Biology
Cell Death
Signal Transduction
Reproductive System
Reproductive Physiology
Apoptotic Signaling Cascade
Medicine
Infertility
Anatomy and Physiology
Urology
Science
Apoptotic Signaling
Germ Cells
Źródło :
PLoS ONE, Vol 6, Iss 10, p e26013 (2011)
Wydawca :
Public Library of Science (PLoS), 2011.
Rok publikacji :
2011
Oryginalny identyfikator :
pmc: PMC3192157
pmid: 22022494
Język :
English
ISSN :
1932-6203
DOI :
10.1371/journal.pone.0026013
Background Deregulated thermal factors have been frequently implicated in the pathogenesis of male infertility, but the molecular basis through which certain responses are directed remain largely unknown. We previously reported that overexpression of exogenous Metastasis-associated protein 1 (MTA1) protects spermatogenic tumor cells GC-2spd (ts) against heat-induced apoptosis. To further dissect the underlying mechanism, we addressed here the fine coordination between MTA1 and p53 in pachytene spermatocytes upon hyperthermal stimulation. Methodology/Principal Findings High level of MTA1 expression sustained for 1.5 h in primary spermatocytes after heat stress before a notable decrease was detected conversely correlated to the gradual increase of acetylation status of p53 and of p21 level. Knockdown of the endogenous MTA1 in GC-2spd (ts) elevated the acetylation of p53 by diminishing the recruitment of HDAC2 and thereafter led to a dramatic increase of apoptosis after heat treatment. Consistent with this, in vivo interference of MTA1 expression in the testes of C57BL/6 mice also urged an impairment of the differentiation of spermatocytes and a disruption of Sertoli cell function due to the elevated apoptotic rate after heat stress. Finally, attenuated expression of MTA1 of pachytene spermatocytes was observed in arrested testes (at the round spermatid level) of human varicocele patients. Conclusions These data underscore a transient protective effect of this histone modifier in primary spermatocytes against heat-stress, which may operate as a negative coregulator of p53 in maintenance of apoptotic balance during early phase after hyperthermal stress.

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