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Prostasin与相关疾病关系的研究进展

Progress in association between prostasin and relative diseases

中文摘要英文摘要

Prostasin,又称通道激活蛋白酶-1,是1994年在人类精液中首次被发现的一种具有胰蛋白酶活性的丝氨酸蛋白酶。其广泛存在于人前列腺、卵巢、乳腺、肺、胎盘及其他组织中,能够以膜结合蛋白和分泌型蛋白两种形式存在。Prostasin参与了机体某些重要的生理功能,如调节上皮钠离子通道,维持钠盐平衡、细胞外渗透压及血压稳定;抑制肿瘤细胞、胎盘绒毛外滋养细胞侵袭;维持胎盘正常发育及分化等。此外,我们的前期研究结果证实prostasin的异常表达水平与子痫前期的病情程度及重要临床指标密切相关。同时,进一步研究证实胎盘 prostasin表达水平与基质金属蛋白酶MMP2(matrix metalloproteinases 2,MMP2)、MMP9表达也具有相关性,其可能通过抑制滋养细胞分泌MMP2及MMP9,进而抑制滋养细胞的侵袭、迁移能力,参与子痫前期"胎盘浅着床"的病理生理过程。因此,prostasin在心血管疾病、肿瘤及妊娠相关疾病等的发病机制中可能发挥了重要作用。 ?????

Prostasin, also called channel activation protease-1, was initially discovered in human semen in 1994. Prostasin is a glycosylphosphatidyl inositol-anchored active serine protease, displaying trypsin-like enzymatic activities. Moreover, it can also be in the form of secretory protein. It is widely distributed in the prostate, ovaries, mammary glands, lungs, placenta, and other tissues. Prostasin has been shown to participate in regulating the epithelial sodium channel, mataining the sodium balance and the stability of extracellular osmotic pressure and blood pressure, supressing the invasion of cancer cells and extravillous trophoblast cells, as well as ensuring the placental development and function. Our previous studies have demonstrated that prostasin is closely related to the severity of preeclampsia and some clinical parameters of severe preeclampsia. Our studies further suggests that prostasin is correlated with the expression of matrix metalloproteinases 2 (MMP2) and MMP9. Prostasin may inhibit the invasion and migration ability of trophoblasts in preeclampsia by decreasing the secretion of MMP2 and MMP9, which contributes to the inadequate trophoblastic invasion. Therefore, prostasin may play important roles in the pathogenesis of cardiovascular diseases, cancer and pregnancy associated diseases.

代莉、龚云辉、杨艳、周容

基础医学妇产科学肿瘤学

妇产科学Prostasin研究进展

Obstetrics and Gynecologyprostasinprogress

代莉,龚云辉,杨艳,周容.Prostasin与相关疾病关系的研究进展[EB/OL].(2014-11-15)[2025-08-25].http://www.paper.edu.cn/releasepaper/content/201411-246.点此复制

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