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PGE2信号通路对子宫内膜异位症发病机制的影响 被引量:6

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摘要 子宫内膜异位症(EMs)是育龄期妇女常见的一种多基因、多因素发病的良性疾病,但是目前具体发病机制尚不明确。最近研究表明PGE2与EMs的发病及相关并发症的发生密切相关。EMs具有雌激素依赖性,患者体内机体免疫细胞清除机制受到抑制,其体内PGE2水平升高,不但可以直接促进异位内膜细胞的存活和增殖,而且具有促进雌激素合成、抑制机体免疫细胞清除机制及促进生长因子产生的作用。因此,PGE2通过直接与间接途径对EMs中异位内膜的存活和增殖进行调节,对EMs的发病具有重要作用。但是目前还不能表明PGE2对EMs作用的确切病理机制,尚需进一步研究明确PGE2信号通路异常的分子机制。
出处 《生殖与避孕》 CAS CSCD 北大核心 2011年第8期544-548,共5页 Reproduction and Contraception
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参考文献28

  • 1Attar E, Tokunaga H, Imir G, et al. Prostaglandin E2 via steroidogenic factor-1 coordinately regulates transcription of steroidogenic genes necessary for estrogen synthesis in endometriosis. J Clin Endocrinol Metab, 2009, 94(2):623-31.
  • 2Chuang PC, Lin YJ, Wu MH, et al. Inhibition of CD36- dependent hagocytosis by prostaglandin E2 contributes to the development of endometriosis. Am J Pathol, 2010, 176 (2):850-60.
  • 3Gurates B, Bulun SE. Endometriosis: the ultimate hormonal disease. Sem in Reproduc Med. 2003, 21(2): 125-34.
  • 4Olivares C, Bilotas M, Buquet R, et al. Effects of a selective cyclooxygenase-2 inhibitor on endometrial epithelial cells from patients with endometriosis. Hum Reprod, 2008, 23 (12):2701-8.
  • 5Cha YI, DuBois RN. NSA1Ds and cancer prevention: targets downstream of COX-2. Annu Rev Med, 2007, 58:239-52.
  • 6Banu SK, Lee J, Starzinski-Powitz A, et al. Gene expression profiles and functional characterization of human immortalized endometriotic epithelial and stromal cells. Fertil Steril, 2008, 90(4):972-87.
  • 7Banu SK, Lee J, Speights VO Jr, et al. Selective inhibition of prostaglandin E2 receptors EP2 and EP4 induces apoptosis of human endometriotic cells through suppression of ERK1/2, AKT, NFnB, and β-catenin pathways and activation of Intrinsic apoptotic mechanisms. Mol Endocrinol, 2009, 23 (8): 1291-305.
  • 8Tsai S J, Wu MH, Lin CC, et al. Regulation of steroidogenic acute regulatory protein expression and progesterone production in endometriotic stromal cells. J Clin Endocrinol Metab, 2001, 86(12):5765-73.
  • 9Bulun SE, Cheng YH, Yin P, et al. Progesterone resistance in endometriosis: link to failure to metabolize estradiol. Mol Cell Endocrinol, 2006, 248(1-2) :94-103.
  • 10Bulun SE, Utsunomiya H, Lin Z, et al. Steroidogenic factor- 1 and endometriosis. Mol Cell Endocrinol, 2009, 300(1-2): 104-8.

二级参考文献19

  • 1郎景和.子宫内膜异位症研究的新里程[J].中华妇产科杂志,2005,40(1):3-4. 被引量:278
  • 2王文萍,林金芳.子宫内膜与腹膜粘附过程中相互作用的研究[J].现代妇产科进展,2006,15(3):199-202. 被引量:1
  • 3SaLes K J, Jabbour NJ. Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium[J]. Reproduction, 2003,126,559 - 567.
  • 4Brenner RM, Nayak NR, SLayden OD, et al. Premenstrual and menstrual changes in the macaque and human endometrium:relevance to endometriosis[J]. Ann N Y Acad Sc, 2002,955:60-74, discussion 86-8, 396-406.
  • 5Majima M, Hayashi I, Muramatsu M, et al. Cyclooxygenase-2 enhance basic growth factor induction of vascular endothelial growth factor in rat sponge implants[J]. Br J Pharmacol, 2000,130:641 - 649.
  • 6Hyder SM, Stancel GM, Chiappetta C, et al. Uterine expression of vascular endothelial growth factor is increased by estradiol and tamoxifen[J]. Cancer Res, 1996,56:3954-3960.
  • 7Greb RR, Heikinheimo O, Williams RF, et al. Vascular endothelial growth factor in primate endometrium is regulated by oestrogen-receptor and progesterone-receptor ligands in vivo[J].Hum Reprod, 1997,12.:1280 - 1292.
  • 8Orlicky DJ, lieberman R, Gerschenson LE. Prostaglandin F2 alpha and E1 regulation of proliferation in primary cultures of rabbit endometrial cells[J]. J Cell Physio, 1986, 127(1): 55-60.
  • 9Koukourakis MI, Giatromanolaki A, liberis V, et al. Hypexia inducible factor 1 alpha and 2 alpha expression is independent of anemia in patients with stage Ⅰ endometrial cancer[J]. Anticancer Res, 2002, 22(6C): 4137-4140.
  • 10Momi H, Matsuyama W, Inoue K, et al. Vascular endothelial growth factor and proinflammatory cytokines in pleural effusions[J]. Respir Med, 2002, 96(10): 817-822.

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