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Involvement of CaM-CaMKII-ERK in bisphenol A-induced Sertoli cell apoptosis.

Abstract：

:Bisphenol A (BPA), one of the most prevalent chemicals for daily use, has been reported as a xenoestrogen to induce reproductive toxicity, but its mechanism is poorly understood. In the present study, we aimed to explore whether CaM-CaMKII-ERK1/2 signaling pathway was involved in BPA-induced Sertoli cells injury via the mitochondrial apoptotic pathway. TM4 cells were cultured with 0, 0.02, 0.2, 2.0, 20μM BPA, and cell viability, mitochondrial function and CaM-CaMKII-ERK1/2 signal pathway were examined. With the MTT assay, BPA was found to suppress cell viability in a dose- and time-dependent manner. Moreover, mitochondrial mass loss, membrane potential decrease, cytochrome c release, Bcl-2 family members down-regulation and caspases-3 up-regulation were obviously observed when the TM4 cells were exposed to BPA. Additionally, the expression of calmodulin (CaM) and phosphorylation of calcium/calmodulin dependent kinase II (CaMKII) significantly increased, and pretreatment with 10μM antagonist of CaM (W-7) or CaMKII (KN62) prevented cell damage through mitochondrial apoptotic pathway. In parallel, ERK1/2 pathway was proved to participate in BPA-induced cell damage, since W-7 and KN62 partially suppressed ERK1/2 activation, and PD98059, the ERK1/2 antagonist, significantly attenuated BPA-induced cell damage. These data, taken together, indicated that CaM-CaMKII-ERK axis might transmit apoptotic signals to the mitochondria during BPA-induced cell apoptosis. By exploring the mechanisms of the Ca(2+) homeostasis and the corresponding proteins, our study provides new insight into BPA-induced reproductive toxicity.

journal_name

Toxicology

journal_title

Toxicology

authors

Qian W,Zhu J,Mao C,Liu J,Wang Y,Wang Q,Liu Y,Gao R,Xiao H,Wang J

doi

10.1016/j.tox.2014.06.001

subject

Has Abstract

pub_date

2014-10-03 00:00:00

pages

27-34

eissn

0300-483X

issn

1879-3185

pii

S0300-483X(14)00113-9

journal_volume

324

pub_type

杂志文章

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