来曲唑诱导的高雄激素小鼠输卵管中凋亡素和凋亡素受体蛋白的表达与定位

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Ayushmita Dutta, Borgohain Anima, Preethi Riba, Guruswami Gurusubramanian, Vikas Kumar Roy
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引用次数: 0

摘要

Apelin及其受体(APJ)在一些哺乳动物雌性的生殖器官中表达。有研究表明,在雄激素过多的情况下,输卵管的功能也会受到影响。然而,在雄激素过多的小鼠输卵管中并未发现凋亡素和 APJ 的表达。因此,本研究对来曲唑诱导的高雄激素小鼠输卵管中apelin和APJ的定位和表达进行了研究。组织形态学分析表明,高雄激素化小鼠的输卵管管腔缩小。我们的研究结果表明,在高雄激素化小鼠输卵管中,APJ的表达量升高,而凋亡素的丰度降低。这一结果表明,高雄激素化小鼠输卵管中的凋亡素信号转导功能受损。高雄激素化小鼠体内雄激素受体表达上调,而雌激素受体表达下调。在高雄激素化小鼠体内,HSP70的表达也下调,同时活性caspase 3和BAX的表达增加,BCL2的表达减少。此外,在高雄激素化小鼠的输卵管中,磷酸化-Ser473-Akt和磷酸化-Thr308-Akt也显示出不同的水平。这种Akt磷酸化的差异是否仅仅是由于输卵管中凋亡素信号传导受损所致,目前仍不清楚。此外,雄激素信号的增加和雌激素信号的抑制与细胞凋亡的增加同时发生。总之,雄激素过多的情况下,输卵管内的细胞凋亡也会影响配子的运输和受精过程。然而,要揭示凋亡在输卵管中的确切作用,还需要进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Expression and localization of apelin and apelin receptor protein in the oviduct of letrozole-induced hyperandrogenized mice

Apelin and its receptor (APJ) are expressed in the reproductive organs of some mammalian females. The function of oviduct has also been suggested to be compromised in the hyperandrogenism condition. However, expression of apelin and APJ has not been shown in the oviduct of hyperandrogenized mice. Thus, the present study has investigated the localization and expression of apelin and APJ in the letrozole-induced hyperandrogenized mice oviduct. Histomorphometric analysis showed decreased lumen of oviduct in the hyperandrogenized mice. Our results showed elevated expression of APJ and decreased abundance of apelin in the hyperandrogenized mice oviduct. This finding suggests impaired apelin signaling in the oviduct of hyperandrogenized mice. The expression of androgen receptor was upregulated while estrogen receptors were downregulated in the hyperandrogenized mice. The expression of HSP70 was also downregulated along with increased expression of active caspase 3 and BAX and decreased expression of BCL2 in hyperandrogenized mice. Furthermore, the phosphorylation of phospho-Ser473-Akt and phospho-Thr308-Akt also showed differential levels in the oviduct of hyperandrogenized mice. Whether this differential phosphorylation of Akt was solely due to impaired apelin signaling in the oviduct, remains unclear. Moreover, increased androgen signaling and suppressed estrogen signaling coincides with elevated apoptosis. In conclusion, hyperandrogenized conditions could also impair the gamete transport and fertilization process due to apoptosis in the oviduct. However, further study would be required to unravel the exact role of apelin signaling in the oviduct in relation to apoptosis.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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