Komar C M, Matousek M, Mitsube K, Mikuni M, Brännström M, Curry T E
Department of Obstetrics and Gynecology, Chandler Medical Center, University of Kentucky, 800 Rose Street, Room MS 331, Lexington, KY 40536-0298, USA.
Reproduction. 2001 Feb;121(2):259-65. doi: 10.1530/rep.0.1210259.
The matrix metalloproteinases (MMPs) play critical roles in the ovulatory process. Their expression and activity, together with those of the endogenous tissue inhibitors of metalloproteinases (TIMPs), are stimulated by LH. The LH surge initiates a cascade of events resulting in ovulation and formation of the corpus luteum via activation of protein kinases A and C, as well as tyrosine kinases. In vitro perfused rat ovaries were untreated, or treated with LH (0.2 microg ml(-1)) plus 0.2 mmol 3-isobutyl-1-methylxanthine l(-1) with 0, 10 or 100 micromol genistein l(-1) (an inhibitor of tyrosine kinases) to assess whether tyrosine kinases are mediators of the LH-stimulated increase in ovarian expression of the MMPs and TIMPs. After 10 h of perfusion, ovaries were collected and frozen until RNA isolation. Northern and RNase protection analyses were used to measure mRNA encoding collagenase 3, gelatinases A and B, and TIMPs-1, -2 and -3. Treatment with LH plus 3-isobutyl-1-methylxanthine resulted in a two- and fivefold increase in mRNA encoding collagenase 3 and TIMP-1, respectively (P < 0.05). Treatment with 100 micromol genistein l(-1) blocked the LH-stimulated increase in collagenase 3 (0.012 +/- 0.002 versus 0.028 +/- 0.005 relative units for 100 micromol genistein l(-1) versus LH; P < 0.05), whereas neither dose of genistein affected LH-induced TIMP-1 expression. LH alone or with genistein did not alter the expression of mRNA encoding TIMP-2 and TIMP-3, or mRNA encoding gelatinases A and B. These data indicate that tyrosine kinases play a role in the LH-induced tissue remodelling required for ovulation by mediating the LH-stimulated expression of collagenase 3.
基质金属蛋白酶(MMPs)在排卵过程中发挥着关键作用。其表达和活性,与内源性金属蛋白酶组织抑制剂(TIMPs)的表达和活性一起,受到促黄体生成素(LH)的刺激。LH峰通过激活蛋白激酶A、蛋白激酶C以及酪氨酸激酶,引发一系列导致排卵和黄体形成的事件。体外灌注大鼠卵巢未作处理,或用LH(0.2微克/毫升(-1))加0.2毫摩尔3 - 异丁基 - 1 - 甲基黄嘌呤(-1)与0、10或100微摩尔染料木黄酮(-1)(一种酪氨酸激酶抑制剂)进行处理,以评估酪氨酸激酶是否是LH刺激卵巢MMPs和TIMPs表达增加的介导因子。灌注10小时后,收集卵巢并冷冻直至进行RNA分离。采用Northern印迹和核糖核酸酶保护分析来测量编码胶原酶3、明胶酶A和B以及TIMP - 1、-2和-3的mRNA。用LH加3 - 异丁基 - 1 - 甲基黄嘌呤处理分别导致编码胶原酶3和TIMP - 1的mRNA增加两倍和五倍(P < 0.05)。用100微摩尔染料木黄酮(-1)处理可阻断LH刺激的胶原酶3增加(100微摩尔染料木黄酮(-1)组与LH组相对单位分别为0.012±0.002对0.028±0.005;P < 0.05),而两种剂量的染料木黄酮均不影响LH诱导的TIMP - 1表达。单独使用LH或与染料木黄酮一起使用均未改变编码TIMP - 2和TIMP - 3的mRNA表达,也未改变编码明胶酶A和B的mRNA表达。这些数据表明,酪氨酸激酶通过介导LH刺激的胶原酶3表达,在LH诱导的排卵所需的组织重塑中发挥作用。