T-cadherin、VE-cadherin蛋白与子宫腺肌病及子宫内膜异位症关系的研究
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摘要
目的:
     观察子宫腺肌病(adenomyosis, AM)及子宫内膜异位症(endometriosis, EM)中T-钙粘蛋白(T-cad)、血管内皮钙粘蛋白(VE-cad)表达,并探讨T-cad和VE-cad与子宫腺肌病及子宫内膜异位症发病的关系。
     方法:
     采用免疫组织化学方法(SP二步法)检测子宫腺肌病组异位内膜及在位内膜、卵巢子宫内膜异位囊肿组异位内膜及在位内膜、子宫腺肌病合并卵巢子宫内膜异位囊肿组腺肌病异位内膜、卵巢异位内膜、在位内膜及正常子宫内膜组中T-cad与VE-cad的表达水平,分析各组内膜的表达差异并行相关性分析。
     结果:
     1.在腺肌病组中,T-cad在异位内膜的高表达率为6.67%,低于在位内膜的11.11%(P<0.05);二者均低于正常子宫内膜组的37.78%(P<0.05)。在卵巢子宫内膜异位囊肿组中,T-cad在异位内膜的高表达率为24.44%,高于在位内膜的4.44%(P<0.05);二者均低于正常子宫内膜组的37.78%(P<0.05)。在合并组中,T-cad在腺肌病异位内膜的高表达率为2.22%,低于卵巢异位内膜的6.67%(P<0.05);二者均低于该组在位内膜的11.11%(P<0.05);T-cad在合并组在位内膜的高表达率低于正常子宫内膜组的37.78%(P<0.05)。腺肌病组、卵巢子宫内膜异位囊肿组及合并组的在位内膜之间T-cad高表达率无明显统计学差别(P>0.05),但均低于正常子宫内膜组(P<0.05)。
     2.在腺肌病组中,VE-cad在异位内膜的高表达率为71.11%,高于在位内膜的26.67%及正常子宫内膜组的17.78%(P<0.05);而在位内膜与正常子宫内膜组之间无明显统计学差别(P>0.05)。在卵巢子宫内膜异位囊肿组中,VE-cad在异位内膜的高表达率为64.44%,高于在位内膜的28.89%及正常子宫内膜组的17.78%(P<0.05);而在位内膜与正常子宫内膜组之间无明显统计学差别(P>0.05)。在合并组中,VE-cad在卵巢异位内膜的高表达率为68.89%,高于腺肌病异位内膜的42.22%(P<0.05),二者均高于该组在位内膜的33.33%(P<0.05);而VE-cad在该组在位内膜的高表达率与正常子宫内膜组无明显差别(P>0.05)。四组的在位内膜VE-cad高表达率均无明显统计学差别(P>0.05)。
     3. T-cad在卵巢子宫内膜异位囊肿组异位内膜及合并组卵巢异位内膜中表达为Ⅲ-Ⅳ期表达较Ⅰ-Ⅱ期表达显著降低,呈负相关(P0.05)。
     4. T-cad与VE-cad在各组子宫内膜上表达无显著相关性(P>0.05)。
     结论:
     1.T-钙粘蛋白在子宫内膜异位性疾病在位内膜上表达明显低于正常子宫内膜,提示其在位内膜与正常内膜相比已经发生改变,具有了一定的迁徙能力。
     2.血管内皮钙粘蛋白在子宫内膜异位性疾病异位内膜上的高表达可能与异位内膜的新生血管机制相关。
     3.T-钙粘蛋白在三组的在位内膜表达无明显差异,提示子宫腺肌病和子宫内膜异位症虽发病机制不一样,但其侵袭、迁移的过程可能是相同的。
     4.T-钙粘蛋白与血管内皮钙粘蛋白无相关性,提示两者在疾病发展过程中所起作用可能是一个先后的关系。
Objective:
     To observe the expressions of T-cadherin (T-cad) and VE-cadherin (VE-cad) proteins in adenomyosis (AM) and endometriosis (EM), and investigate the relationship between the two proteins.
     Methods:
     The expression level of T-cad and VE-cad in the ectopic and eutopic endometrium of AM group, the ectopic and eutopic endometrium of EM group, the ovary ectopic, myometrium ectopic and eutopic endometrium of EM-AM-combined group and the control group was detected via immunohistochemistry method (SP two-step), and analysis the differential expression of the two proteins in all kinds of endometrium and do the correlation studies.
     Results:
     1. The T-cad expression in the ectopic endometrium of the AM group is significantly down-regulated compared to the eutopic endometrium of the same group (6.67%compared to11.11%, P<0.05); and both are down-regulated compared to the control group (6.67%and11.11%compared to37.78%, P<0.05). The T-cad expression in the ectopic endometrium of the EM group is up-regulated compared to the eutopic endometrium of the same group (24.44%compared to4.44%, P<0.05); and both are down-regulated compared to the control group (24.44%and4.44%compared to37.78%, P0.05), but lower than the control group.
     2. The VE-cad expression in the ectopic endometrium of the AM group is up-regulated compared to the eutopic endometrium of the same group and the control group (71.11%compared to26.67%and17.78%, P<0.05); and the latter one the VE-cad expression has no statistical difference compared to the control group (26.67%compared to17.78%, P>0.05). The VE-cad expression in the ectopic endometrium of the EM group is up-regulated compared to the eutopic endometrium of the same group and the control group (64.44%compared to28.89%and17.78%, P<0.05); and the latter one the VE-cad expression has no statistical difference compared to the control group (28.89%compared to17.78%, P>0.05). The T-cad expression in the ovary ectopic endometrium of the combined group is up-regulated compared to the myometrium ectopic endometrium of the same group (68.89%compared to42.22%, P<0.05), both are up-regulated compared to the the eutopic endometrium of the same group (68.89%and42.22%compared to33.33%, P<0.05), and the eutopic endometrium of the combined group has no statistical difference compared to the control group (33.33%compared to17.78%, P<0.05). The VE-cad expression in the control group and eutopic endometrium of AM group, EM group, combined group have no statistical difference (P>0.05).
     3. The expression level of T-cad in the ectopic endometrium of EM group and the ovary ectopic endometrium of combined group has significant correlation with the r-AFS stages (P<0.05). There is no significant correlation between the expression level of VE-cad and r-AFS stages in all groups (P>0.05).
     4. There is no significant correlation between the expression level of T-cad and VE-cad in all groups (P>0.05).
     Conclusion:
     1. Compared with the control group, the expression level of T-cadherin is lower in both AM and EM eutopic endometrium, indicated the eutopic endometrium of AM and EM have already had pathological changes, and got some kind of invasive ability.
     2. The high expression of VE-cadherin in the ectopic endometrium of AM and EM may be involved in the mechanism of the angiogenesis in the AM and EM ectopic endometrium.
     3. The expression level of T-cadherin in the eutopic endometrium of the three groups had no statistical difference, indicates though the mechanism of AM and EM are different, the process of the immigration and invasion may be the same.
     4. In this research, T-cadherin and VE-cadherin have foud no significant correlation in this research, and they may palyed significant roles together through a sequencing way in the mechanism of AM and EM.
引文
[1]Guo SW. Recurrence of endometriosis and its control [J]. Hum Reprod Update,2009,15(4):441-461.
    [2]Resink TJ, Philippova M, Joshi MB, et al. Cadherins in cardiovascular disease[J]. Swiss Med Wkly,2009; 139(9-10):122-134.
    [3]Vestal DJ, Ranscht B. Glycosyl phosphatidylinositol-anchored T-cadherin mediates calcium-dependent, homophilic cell adhesion[J]. J Cell Biol,1992,119(2): 451-461.
    [4]Brock MV, Hooker CM, Ota-Machida E, et al. DNA Methylation Markers and Early Recurrence in Stage I Lung Cancer[J]. N Engl J Med,2008,13; 358(11): 1118-1128.
    [5]Pfaff D, Philippova M, Kyriakakis E, et al. Paradoxical effects of T-cadherin on squamous cell carcinoma:up- and down-regulation increase xenograft growth by distinct mechanisms [J]. J Pathol,2011,225:512-524.
    [6]Pfaff D, Philippova M, Buechner SA, et al. T-cadherin loss induces an invasive phenotype in human keratinocytes and squamous cell carcinoma (SCC) cells in vitro and is associated with malignant transformation of cutaneous SCC in vivo [J]. Br J Dermatol,2010,163(2):353-363.
    [7]Lin YL, Sun G, Liu XQ, et al. Clinical Significance of T-Cadherin Tissue Expression in Patients with Bladder Transitional Cell Carcinoma[J]. Urol Int,2011,86: 340-345]
    [8]Labelle M, Schnittler HJ, Aust DE, et al. Vascular endothelial cadherin promotes breast cancer progression via transforming growth factor beta signaling[J]. Cancer Res,2008,68(5):1388-1397.
    [9]Zhang LZ, Mei J, Qian ZK, et al. The Role of VE-adherin in Osteosarcoma Cells[J]. Pathol Oncol Res,2010,16(1):111-117.
    [10]Loges S, Clausen H, Reichelt U, et al. Determination of microvessel density by quantitative real-time PCR in esophageal cancer: correlation with histologic methods, angiogenic growth factor expression, and lymph node metastasis [J]. Clin Cancer Res,2007,13(1):76-80.
    [11]叶常青.形态计量学在病理学中应用的回顾与展望[J].中华病理学杂志,1990,19(4):241.
    [12]张伟,孙丽娟,林钊宇,et al.微小RNA-15b及其靶蛋白BMI1的表达与 舌鳞癌患者化疗耐药、预后的关系[J].中国口腔颌面外科杂志,2012,10(6):454-460.
    [13]Liu H, Lang JH. Is abnormal eutopic endometrium the cause of endometriosis? The role of eutopic endometrium in pathogenesis of endometriosis[J]. Med Sci Monit,2011,17(4):RA92-99.
    [14]Berx G and van Roy F. Involvement of Members of the Cadherin Superfamily in Cancer[J]. Cold Spring Harb Perspect Biol,2009, 1(6):a003129.
    [15]Jennbacken K, Tesan T, Wang W, et al. N-cadherin increases after androgen deprivation and is associated with metastasis in prostate cancer[J]. Endocr Relat Cancer,2010,17(2):469-479.
    [16]Kreizenbeck GM, Berger AJ, Subtil A, et al. Prognostic significance of cadherin-based adhesion molecules in cutaneous malignant melanoma[J]. Cancer Epidemiol Biomark Prev,2008,17:949-958.
    [17]Mahler-Araujo B, Savage K, Parry S, et al. Reduction of E-cadherin expression is associated with non-lobular breast carcinomas of basal-like and triple negative phenotype[J]. J Clin Pathol,2008,61(5):615-620.
    [18]Hulit J, Suyama K, Chung S, et al. N-cadherin signaling potentiates mammary tumor metastasis via enhanced extracellular signal-regulated kinase activation[J]. Cancer Res,2007,67(7):3106-3116.
    [19]Zhai B, Yan HX, Liu SQ, et al. Reduced expression of E-cadherin/catenin complex in hepatocellular carcinomas[J]. World J Gastroenterol,2008,14(37): 5665-5673.
    [20]Lin Q, Li M, Shen ZY, et al. Prognostic impact of vascular endothelial growth factor-A and E-cadherin expression in completely resected pathologic stage I non-small cell lung cancer[J]. Jpn J Clin Oncol,2010,40(7):670-676.
    [21]Park JH, Lee BI, Song ES, et al. Hypermethylation of E-cadherin in endometrial carcinoma[J]. J Gynecol Oncol,2008,19(4):241-245.
    [22]Sawada K, Mitra AK, Radjabi AR, et al. Loss of E-cadherin promotes ovarian cancer metastasis via alpha 5-integrin, which is a therapeutic target. Cancer Res,2008,68(7):2329-2339.
    [23]Hu J, Shao S, Song Y, et al. Hepatocyte growth factor induces invasion and migration of ovarian cancer cells by decreasing the expression of E-cadherin, beta-catenin, and caveolin-1[J]. Anat Rec (Hoboken),2010,293(7):1134-1139.
    [24]康佳丽,管春香,黄晓晖,et al. E-cadherin, CD44变异体6在子宫腺肌 病发病机制的研究[J].中华妇幼临床医学杂志,2006,2(6):315-317.
    [25]张月梅,潘燕,刘子龙.E-钙粘蛋白在子宫腺肌病组织中的表达[J].医学分子生物学杂志,2004,1(6):338-340.
    [26]金海燕,王欢,周龙书.子宫内膜异位症E-钙粘素的异常表达及意义[J].现代药物与临床,2010,25(3):226-228.
    [27]Ranscht B, Bronner-Fraser M. T-cadherin expression alternates with migrating neural crest cells in the trunk of the avian embryo[J]. Development,1991, 111(1):15-22.
    [28]Angst B D, Marcozzi C, Magee A L. The T-cadherin superfamily:diversity in from and function[J]. J Cell Sci,2001,114:629-641.
    [29]Hug C, Wang J, Ahmad NS, et al. T-cadherin is a receptor for hexameric and high-molecular-weight forms of Acrp30/adiponectin[J]. Proc Natl Acad Sci USA, 2004,101(28):10308-10313.
    [30]Suzuki S, Sano K, Tahihara H. Diversity of the cadherin family:evidence for eight new cadherins in nervous tissue[J]. Cell Regul,1991,2(4):261-270.
    [31]Lampugnani MG, Resnati M, Raiteri M, et al. A novel endothelial-specific membrane protein is a marker of cell-cell contacts[J]. J Cell Biol,1992,118: 1511-1522.
    [32]Taddei A, Giampietro C, Conti A, et al. Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5[J]. Nat Cell Biol,2008,10(8):923-934.
    [33]Vestweber D. VE-cadherin:the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation[J]. Arterioscler Thromb Vase Biol,2008,28(2):223-232.
    [34]Gottschalk C, Malberg K, Arndt M, et al. Matrix metalloproteinases and TACE play a role in the pathogenesis of endomertriosis[J]. Adv Exp Med Biol,2000, 477:483-486.
    [35]Matsuda M, Sasabe H, Adachi Y et al. Increased invasion activity of endometrial stromal cells and elevated expression of matrix metalloproteinase messenger RNA in the uterine tissue of mice with experimentally induced adenomyosis[J]. Am J Obstet Gynecol,2001,185(6):1374-1380.
    [36]胡亚敏,郑红兵.VEGF-C和ICAM-1在子宫腺肌病中的表达及意义[J].华中科技大学学报,2009,38(2):217-219.
    [37]Kyriakakis E, Maslova K, Philippova M, et al. T-Cadherin Is an Auxiliary Negative Regulator of EGFR Pathway Activity in Cutaneous Squamous Cell Carcinoma:Impact on Cell Motility[J]. J Invest Dermatol,2012,132(9),2275-2285.
    [38]郜景和.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.
    [39]Philippova M, Joshi MB, Kyriakakis E, et al. A guide and guard:the many faces of T-cadherin[J].ll Signal,2009,21(7):1035-1044.
    [40]Nisolle M, Casanas-Roux F, Marbaix E, et al. Transplantation of cultured explants of human endometrrum into nude mice[J]. Hum Reprod,2000,15(3): 572-577.
    [41]马颖,何援利.人子宫内膜异位症裸鼠模型的血管生成[J].中国组织工程研究与临床康复,2010,14(46):8612-8615.
    [42]Ota H, Igarashi S, Tanaka T. Morphometric evaluation of stromal vascularization in the endometrium in adenomyosis[J]. Hum Reprod,1998,13(3): 715.
    [43]Li T, Li YG, Pu DM. Matrix metalloproteinase-2 and-9 expression correlated with angiogenesis in human adenomyosis[J]. Gynecol Obstet Invest,2006,62(4): 229-235.
    [44]Tokyol C, Aktepe F, Dilek FH, et al. Expression of cyclooxygenase-2 and matrix metalloproteinase-2 in adenomyosis and endometrial polyps and its correlation with angiogenesis[J]. Int J Gynecol Pathol,2009,28(2):148-156.
    [45]Goteri G, Lucarini G, Montik N, et al. Expression of vascular endothelial growth factor (VEGF), hypoxia inducible factor-1 alpha (HIF-1alpha), and microvessel density in endometrial tissue in women with adenomyosis[J]. Int J Gynecol Pathol,2009,28(2):157-163.
    [46]Jingting C, Yangde Z, Yi Z, et al. Expression of heparanase and angiopoietin-2 in patients with endometriosis[J]. Eur J Obstet Gynecol Reprod Biol, 2008,136(2):199-209.
    [47]范俊,栾少红,孙宝治,et al. GnRHa对子宫内膜异位症血管生成素-2的影响[J].中国优生与遗传杂志,2013,21(2):63-64.
    [48]Liu R, Cao Z, Tu J, et al. A novel function of lycorine hydrochloride in the inhibition of metastatic melanoma C8161 cell-dominant vasculogenic mimicry[J]. Pigment Cell Melanoma Res,2012,25(5):630-638.
    [49]Muramatsu F, Kidoya H, Naito H, et al. MicroRNA-125b inhibits tube formation of blood vessels through translational suppression of VE-cadherin[J]. Oncogene,2013,32(4):414-421.
    [1]Bergeron C, Amant F, Ferenczy A. Pathology and physiopathology of adenomyosis[J]. Best Pract Res Clin Obstet Gynaecol,2006,20(4):511-521.
    [2]Frankl O. Adenomyosis uteri[J]. Am J Obstet Gynecol,1925,10:680-684.
    [3]Bird CC, McElin TW, Manalo-Eslrella P. The elusive adenomyosis of the uterus[J]. Am J Obstet Gynecol,1972,112(5):583-593.
    [4]Frontino G, Bianchi S, Ciappina N, et al. The unicornuate uterus with an occult adenomyotic rudimentary horn[J]. J Minim Invasive Gynecol,2009, 16(5):622-625.
    [5]Bulun SE. Endometriosis[J]. N Engl J Med,2009; 360:268-279.
    [6]Matalliotakis IM, Katsikis IK, Panidis DK. Adenomyosis:what is the impact on fertility?[J]. Curr Opin Obstet Gynecol,2005,17(3):261-264.
    [7]Weiss G, Maseelall P, Schott LL, et al. Adenomyosis a variant not a disease? Evidence from hysterectomized menopausal women in the SWAN study[J]. Fertil Steril,2009,91(1):201-206.
    [8]Levgur M. Diagnosis of adenomyosis[J]. J Reprod Med,2007,52(3): 177-193.
    [9]Cullen TS. Adenomyoma of the Uterus[J]. JAMA,1908, L(2):107-115.
    [10]Curtis KM, Hillis SD, Marchbanks PA, et al. Disruption of the Endometrial-myometrial border during pregnancy as a risk factor for Adenomyosis [J]. Am J Obstet Gynecol,2002,187:543-544.
    [11]Ben-Aissia N, Berriri H, Gara E. Adenomyosis:analysis of 35 Cases[J]. Tunis Med,2001,79:447-451.
    [12]Panganamamula UR, Harmanli OH, Isik-Akbay EF, et al. Is prior uterine surgery a risk factor for adenomyosis[J]. Obstet Gynecol,2004,104(1):1034-1038.
    [13]Leyendecker G, Wildt L, Mall G. The pathophysiology of endometriosis and adenomyosis:tissue injury and repair[J]. Arch Gynecol Obstet,2009,280:529-538.
    [14]Liu H, Lang JH. Is abnormal eutopic endometrium the cause of endometriosis? The role of eutopic endometrium in pathogenesis of endometriosis[J]. Med Sci Monit,2011,17(4):RA92-99.
    [15]Mori T, Ohta Y, Nagasawa H. Ultrastructural changes in uterine myometrium of mice with experimentally induced adenomyosis[J]. Experientia,1984, 40:1385-1387.
    [16]Uduwela AS, Perera MAK, Li A, et al. Endometrial-myometrial interface: relationship to adenomyosis and changes in pregnancy [J]. Obstet Gynecol Surv,2000, 55(2):390-400.
    [17]Lacassagne A. Modification progressive de l'uterus de la souris sous l'action prolongee de l'oestrone[J]. CR Sean Soc Biol,120:1156-1158.
    [18]Takahashi K, Nagata H, Kitao M. Clinical usefulness of determination of estradiol level in the menstrual blood for patients with endometriosis[J]. Nippon Sanka Fujinka Gakkai Zasshi,1989(41):1849-1850.
    [19]Kitawaki J. Adenomyosis:the pathophysiology of an oestrogen-dependent disease[J]. Best Pract Res Clin Obstet Gynaecol,2006,20(4):493-502.
    [20]Yamamoto T, Noguchi T, Tamura T, et al. Evidence for estrogen synthesis in adenomyotic tissues[J]. Am J Obstet Gynecol,1993(169):734-738.
    [21]Kitawaki J, Noguchi T, Amatsu T, et al. Expression of aromatase cytochrome P450 protein and messenger ribonucleic acid in human endometriotic and adenomyotic tissues but not in normal endometrium [J]. Biol Reprod,1997(57): 514-519.
    [22]Kitawaki J, Kusuki I, Koshiba H, et al. Detection of aromatase cytochrome P450 in endometrial biopsy specimens as a diagnostic test for endometriosis [J]. Fertil Steril,1999,72(6):1100-1106.
    [23]Bulun SE, Imir G, Utsunomiya H, et al. Aromatase in endometriosis and uterine leiomyomata[J]. J Steroid Biochem Mol Biol,2005,95(1-5):57-62.
    [24]Leyendecker G, Kunz G, Noe M, et al. Endometriosis:a dysfunction and disease of the archimetra[J]. Hum Reprod Update,1998,4(5):752-762.
    [25]Maia H Jr, Casoy J, Correia T, et al. Effect of the menstrual cycle and oral contraceptives on aromatase and cyclooxygenase-2 expression in adenomyosis[J]. Gynecol Endocrinol,2006,22(10):547-551.
    [26]Wolfler MM, Nagele F, Kolbus A, et al. A predictive model for endometriosis[J]. Hum Reprod,2005,20(6):1702-1708.
    [27]Ishihara H, Kitawaki J, Kado N, et al. Gonadotropin-releasing hormone agonist and danazol normalize aromatase cytochrome P450 expression in eutopic endometrium from women with endometriosis, adenomyosis, or leiomyomas[J]. Fertil Steril,2003,79 Suppl 1:735-742.
    [28]Kimura F, Takahashi K, Takebayashi K, et al. Concomitant treatment of severe uterine adenomyosis in a premenopausal woman with an aromatase inhibitor and a gonadotropin-releasing hormone agonist[J]. Fertil Steril,2007,87(6): 1468.e9-12.
    [29]Baskin GB, Smith SM, et al. Endometrial Hyperplasia, Polyps, and Adenomyosis Associated with Unopposed Estrogen in Rhesus Monkeys(Macaca mulatta)[J]. Vet Pathol,2002,39:572-575.
    [30]Mehasseb MK, Panchal R, Taylor AH, et al. Estrogen and progesterone receptor isoform distribution through the menstrual cycle in uteri with and without adenomyosis[J]. Fertil Steril,2011,95(7):2228-2235.
    [31]Mehasseb MK, Habiba MA. Adenomyosis uteri:an update[J]. The Obstet Gynecol,2009(11):41-47.
    [32]Oehler MK, Greschik H, Fischer DC, et al. Functional characterization of somatic point mutation of the human estrogen receptor alpha(hERalpha) in edenomyosis uteri [J]. Mol Hum Reprod,2004,10(12):853-860.
    [33]Lavery S, Gillmer M. Malignant transformation of residual endometriosis in women on unopposed oestrogen hormone replacement therapy[J]. BJOG,2001, 108(10):1106-1107.
    [34]康佳丽,管春香,黄晓晖,et al. E-cadherin, CD(44)变异体6在子宫腺肌病发病机制的研究[J].中华妇幼临床医学杂志,2006,2(6):315-317.
    [35]张月梅,潘燕,刘子龙.E-钙粘蛋白在子宫腺肌病组织中的表达[J].医学分子生物学杂志,2004,1(6):338-340.
    [36]胡亚敏,郑红兵VEGF-C和ICAM-1在子宫腺肌病中的表达及意义[J].华中科技大学学报,2009,38(2):217-219.
    [37]Matsuda M, Sasabe H, Adachi Y et al. Increased invasion activity of endometrial stromal cells and elevated expression of matrix metalloproteinase messenger RNA in the uterine tissue of mice with experimentally induced adenomyosis[J]. Am J Obstet Gynecol,2001,185(6):1374-1380.
    [38]Tokyol C, Aktepe F, Dilek FH, et al. Expression of cyclooxygenase-2 and matrix metalloproteinase-2 in adenomyosis and endometrial polyps and its correlation with angiogenesis[J]. Int J Gynecol Pathol,2009,28(2):148-156.
    [39]Ikenaka Y, Yoshiji H, Kuriyama S, et al. Tissue inhibitor of metalloproteinases-1(TIMP-1) inhibits tumor growth and angiogenesis in the TIMP-1 transgenic mouse model[J]. Int J Cancer,2003,105(3):340-346.
    [40]Pang IH, Hellberg PE, Fleenor DL, et al. Expression of matrix metalloproteinases and their inhibitors in human trabecular meshwork cells [J]. Invest Ophthalmol Vis Sci,2003,44(8):3485-3493.
    [41]Gottschaik C, Malberg K, Arndt M, et al. Matrix metalloproteinases and TACE play a role in the pathogenesis of endomertriosis[J]. Adv Exp Med Biol,2000, 477:483-486.
    [42]闫丽萍,惠京.子宫腺肌病患者内膜组织中PTTG的表达及与MMP-2和TIMP-1的关系[J].实用妇产科杂志,2009,25(3):174-177.
    [43]艾志刚,管洁.MMP-9及TIMP-1在子宫腺肌病中的表达及临床意义[J].现代妇产科进展,2011,20(5):388-391.
    [44]Ota H, Igarashi S, Hatazawa J, et al. Is adenomyosis an immune disease?[J] Hum Reprod Update,1998,4(4):360-367.
    [45]Ota H, Igarashi S. Expression of major histocompatibility complex class II antigen in endometriotic tissue in patients with endometriosis and adenomyosis [J]. Fertil Steril,1993,60:834-838.
    [46]Koumantakis EE, Panayiotides JG, Goumenou AG, et al. Different HLA-DR expression in endometriotic and adenomyotic lesions:correlation with transvaginal ultrasonography findings[J]. Arch Gynecol Obstet,2010,281:851-856.
    [47]Ishii K, Takakuwa K, Mitsui T, et al. Studies on the human leukocyte antigen-DR in patients with endometriosis:genotyping of HLA-DRB1 alleles[J]. Hum Reprod,2002,17(3):560-563.
    [48]Urosevic M, Kurrer MO, Kamarashev J, et al. Human leukocyte antigen G up-regulation in lung cancer associates with high-grade histology, human leukocyte antigen class I loss and interleukin-10 production[J]. Am J Pathol,2001,159: 817-824.
    [49]Lefebvre S, Antoine M, Uzan S, et al. Specific activation of the non-classical class I histocompatibility HLA-G antigen and expression of the ILT2 inhibitory receptor in human breast cancer[J]. J Pathol,2002,196:266-274.
    [50]Carosella ED, Moreau P, Le Maoult J, et al. HLA-G molecules:from maternal tolerance to tissue acceptance [J]. Adv Immunol,2003,81:199-252.
    [51]Wang F, Wen ZQ, Li H, et al. Human leukocyte antigen-G is expressed by the eutopic and ectopic endometrium of adenomyosis[J]. Fertil Steril,2008,90(5): 1599-1604.
    [52]Tremellen KP, Russell P. The distribution of immune cells and macrophages in the endometrium of women with recurrent reproductive failure. II:adenomyosis and macrophages[J]. J Reprod Immunol,2012,93:58-63.
    [53]Wicherek L. Alterations in RCAS1 serum concentration levels during menstrual cycle in patients with uterine leiomyoma and lack of analogical changes in adenomyosis[J]. Gynecol Obstet Invest,2009,67:195-201.
    [54]Huang HY, Yu HT, Chan SH, et al. Eutopic endometrial interleukin-18 system mRNA and protein expression at the level of endometrial-myometrial interface in adenomyosis patients[J]. Fertil Steril,2010,94(1):33-39.
    [55]Ota H. Evaluation of hysteroscopy in the diagnosis of adenomyosis[J]. Jpn J Fertil Steril,1992,37(1):49-55.
    [56]Ota H, Igarashi S, Tanaka T. Morphometric evaluation of stromal vascularization in the endometrium in adenomyosis[J]. Hum Reprod,1998,13(3): 715-719.
    [57]韩燕华,周应芳,郑淑蓉.子宫腺肌病患者子宫各部位血管形态的研究[J].中国实用妇科与产科杂志,2002,18:605-607.
    [58]Smith SK. Vascular endothelial growth factor and the endometrium [J]. Hum Reprod,1996, 11(Suppl 2):55-61.
    [59]Fujii EY, Nakayama M, Nakagawa A. Concentrations of receptor for advanced glycation end products, VEGF and CML in plasma follicular fluid, and peritoneal fluid in women with and without endometriosis[J]. Reprod Sci,2008, 15(10):1066-1074.
    [60]Lin XJ, Lai MD, Lei HY, et al. Neutroprils and macrophages promote angiogenesis in the early stage of endometriosis in amouse model[J]. Endoerinology, 2006,147(3):1278-1286.
    [61]Propst AM, Quade BJ, Gargiulo AR, et al. Adenomyosis demonstrates increased expression of the basic fibroblast growth factor receptor/ligand system compared with autologous endometrium [J]. Menopause,2001,8(5):368-371.
    [62]Hofmann UB, Westphal JR, Vanmuijen GN, et al. Matrix metalloproteinases in human melanoma[J]. J Invest Dermatol,2000,115(3):337-344.
    [63]Li T, Li YG, Pu DM. Matrix metalloproteinase-2 and-9 expression correlated with angiogenesis in human adenomyosis[J]. Gynecol Obstet Invest,2006,62(4): 229-235.
    [64]Resink TJ, Philippova M, Joshi MB, et al. Cadherins in cardiovascular disease[J]. Swiss Med Wkly,2009; 139(9-10):122-134.
    [65]Taddei A, Giampietro C, Conti A, et al. Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5[J]. Nat Cell Biol,2008,10(8):923-934.
    [66]Vestweber D. VE-cadherin:the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation[J]. Arterioscler Thromb Vasc Biol,2008,28(2):223-232.
    [67]Dejana E, Orsenigo F, Lampugnani MG The role of adherens junctions and VE-cadherin in the control of vascular permeability [J]. J Cell Sci,2008,121(Pt 13): 2115-2122.
    [68]Zhou Y, Fisher SJ, Janatpour M, et al. Human cytotrophoblasts adopt a vascular phenotype as they differentiate. A strategy for successful endovascular invasion?[J] J Clin Invest,1997,99(9):2139-2151.
    [69]Kerr JFR, Wyllie AH, Currie AR. Apoptosis:a basic biological phenomenon with wide-ranging implications in tissue kinetics[J]. Br J Cancer,1972(26):239-257.
    [70]Hopwood D, Levison DA. Atrophy and apoptosis in the cyclical human endometrium[J]. J Pathol,1976,119(3):159-166.
    [71]Khan KN, Masuzaki H, Fujishita A, et al. Immunoexpression of hepatocyte growth factor and c-Met receptor in the eutopic endometrium predicts the activity of ectopic endometrium[J]. Fertil Steril,2003,79(1):173-181.
    [72]Beierle EA, Dai W, Iyengar R, et al. Differential expression of Bcl-2 and Bax may enhance neuroblastoma survival[J]. J Pediatr Surg,2003,38:486-491.
    [73]Meresman GF, Vighi S, Buquet RA, et al. Apoptosis and expression of Bcl-2 and Bax in eutopic endometrium from women with endometriosis[J]. Fertil Steril, 2000,74(4):760-766.
    [74]Coumenou A, Panayiotides I, Matalliotakis I, et al. Bcl-2 and Bax expression on in human endometriotic and adenomyotic tissues[J]. Eur J Obstet Gynecol Reprod Biol,2001,99(2):256-260.
    [75]Marusawa H, Marusawa S, Welsh K, et al. HBXIP function as a cofactor of survivin in apoptosis suppression[J]. EMBO J,2003,22(11):2729-2740.
    [76]Chawla-Sarkar M, Bae SI, Reu FJ, et al. Downregulation of Bcl-2, FLIP or IAPs (XIAP and survivin) by siRNAs sensitizes resistant melanoma cells to Apo2L/TRAIL-induced apoptosis[J]. Cell Death Differ,2004,11(8):915-923.
    [77]Tarkowski R, Kotarski J, Polak G, et al. Expression of the survivin gene in the scar endometriosis and in normal human endometrium[J]. Ginekol Pol,2001, 72(12A):1539-1542.
    [78]Ueda M, Yamashita Y, Takehara M, et al. Survivin gene expression in endometriosis [J]. J Clin Endocrinol Metab,2002,87(7):34-52.
    [79]薛晴,周应芳,刘运明,et al.子宫内膜细胞增生相关核抗原ki-67和CA125在子宫腺肌病组织中的表达[J].实用妇产科杂志,2003,19(5):290-292.
    [80]Yang JH, Wu MY, Den CD, et al. Altered apoptosis and proliferation in endometrial stromal cells of women with adenomyosis[J]. Hum Reprod,2007,22(4): 945-952.
    [81]Mai KT, Yazadi HM, Perkins DG, et al. Pathogeneitc role of stromal cells in endometriosis and adenomyosis[J]. Histopathology,1997,30:430-432.
    [82]Sahin AA, Silva EG, Landon G, et al. Endometrial tissue in myometrial vessels not associated with menstruation[J]. Int J Gynecol Pathol,1989,8:139-146.
    [83]Meenakshi M, McCluggage WG. Vascular involvement in adenomyosis: report of a large series of a common phenomenon with observations on the pathogenesis of adenomyosis [J]. Int J Gynecol Pathol,2010,29:117-121.
    [84]Greenburg G, Hay ED. Epithelia suspended in collagen gels can lose polarity and express characteristics of migrating mesenchymal cells[J]. J Cell Biol, 1982,95:333-339.
    [85]Savagner P. The epithelial-mesenchymal transition (EMT) phenomenon [J]. Ann Oncol,2010,21 Suppl 7:vii89-92.
    [86]Thiery JP, Acloque H, Huang RY, et al. Epithelial-mesenchymal transitions in development and disease[J]. Cell,2009,139(5):871-890.
    [87]Matsuzaki S, Darcha C. Epithelial to mesenchymal transition-like and mesenchymal to epithelial transition-like processes might be involved in the pathogenesis of pelvic endometriosis[J]. Hum Reprod,2012,27(3):712-721.
    [88]Chen YJ, Li HY, Huang CH, et al. Oestrogen-induced epithelial-mesenchymal transition of endometrial epithelial cells contributes to the development of adenomyosis [J]. J Pathol,2010,222:261-270.
    [89]Emge LA. The elusive adenomyosis of the uterus. Its historical past and its present state of recognition[J]. Am J Obstet Gynecol,1962,83:1541-1563.
    [90]Arnold LL, Ascher SM, Simon JA. Familial adenomyosis:a case report[J]. Fertil Steril,1994,61(6):1165-1167.
    [91]Arnold LL, Meck JM, Simon JA. Adenomyosis:evidence for genetic cause[J]. Am J Med Genet,1995,55(4):505-506.
    [92]Kennedy S, Mardon H, Barlow D. Familial endometriosis[J].J Assist Reprod Genet,1995,12(1):32-34.
    [93]Pandis N, Karaiskos C, Bardi G, et al. Chromosome analysis of uterine adenomyosis. Detection of the leiomyoma-associated del(7q) in three cases[J]. Cancer Genet Cytogenet,1995,80(2):118-120.
    [94]Goumenou AG, Arvanitis DA, Matalliotakis IM, et al. Loss of heterozygosity in adenomyosis on hMSH2, hMLHI, P16Ink4 and GALT loci[J]. Int J Mol Med,2000,6(6):667-671.
    [95]Gargett CE. Uterine stem cells:What is the evidence?[J] Hum Reprod Update,2007,13(1):87-101.
    [96]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.

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