Estrogen restricts the apoptosis of endometrial stromal cells by promoting TSLP secretion.

Estrogen restricts the apoptosis of endometrial stromal cells by promoting TSLP secretion.
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雌激素通过促进TSLP分泌来限制子宫内膜基质细胞的凋亡。

DOI:
10.3892/mmr.2018.9428
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发表时间:
2018-11
影响因子:
3.4
通讯作者:
Li MQ
Li MQ
中科院分区:
医学4区
文献类型:
--
作者:
Yang HL;Chang KK;Mei J;Zhou WJ;Liu LB;Yao L;Meng Y;Wang MY;Ha SY;Lai ZZ;Ye JF;Li DJ;Li MQ

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子宫内膜异位症(EMS)是一种女性生殖器依赖性疾病,其病因和发病机制的报道存在争议。由于增殖和脱落的动态周期,细胞凋亡在人类子宫内膜中特别重要。雌激素对子宫内膜间质细胞(ESC)具有抗凋亡作用,这似乎在EMS女性中加剧;然而,雌激素对ESC的抗凋亡作用的潜在机制仍不清楚。本研究旨在探讨雌激素是否通过胸腺基质淋巴细胞生成素(TSLP)调控胚胎干细胞凋亡及其相关机制。采用ELISA法检测雌激素处理的ESC培养液中TSLP的含量。流式细胞仪检测重组人TSLP、抗人TSLP中和抗体和雌激素对ESCs早期凋亡率和B细胞淋巴瘤(Bcl-2)表达的影响。在本研究中,据报道,在没有雌激素的情况下,ESC表现出基础TSLP分泌,如在以前的研究中所报道的,并且雌激素以剂量依赖性方式促进ESC的TSLP分泌。结果表明,雌激素抑制ESCs的凋亡与促进Bcl-2的表达有关,抑制TSLP可部分逆转这种抑制作用。因此,本研究的结果揭示了一种新的机制,雌激素依赖性的凋亡抑制ESCs与TSLP分泌和Bcl-2的调节。内源性和雌激素诱导的子宫内膜TSLP可能通过抑制细胞凋亡促进EMS的发生和发展。
Endometriosis (EMS) is a female hormone-dependent disease with controversial reports of its etiology and pathogenesis. Apoptosis is particularly important in the human endometrium due to the dynamic cycles of proliferation and shedding. Estrogen possessed antiapoptotic effects on endometrial stromal cells (ESCs), which appears to be exacerbated in women with EMS; however, the underlying mechanism of the antiapoptotic effects of estrogen on ESC remains unknown. The present study aimed to determine whether estrogen regulates the apoptosis of ESCs via thymic stromal lymphopoietin (TSLP) and the associated mechanism. An ELISA was conducted to detect TSLP content in the ESC culture medium treated with estrogen. Subsequently, the early apoptotic rate and expression of B-cell lymphoma (Bcl-2) of ESCs were analyzed by flow cytometry in the presence of recombinant human TSLP, anti-human TSLP neutralizing antibody or estrogen. In the present study, it was reported that ESCs exhibited basal TSLP secretion in the absence of estrogen as reported in previous studies, and that estrogen promoted TSLP secretion of ESCs in a dose-dependent manner. The results demonstrated that estrogen suppressed the apoptosis of ESCs associated with the promotion of Bcl-2 expression, which may be partly reversed by inhibiting TSLP. Therefore, the findings of the present study revealed a novel mechanism of estrogen-dependent apoptotic suppression of ESCs associated with TSLP secretion and Bcl-2 regulation. Endogenous and estrogen-induced endometrial TSLP may promote the initiation and development of EMS via the inhibition of apoptosis.
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发表时间: 2013-07-01
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