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首页> 外文期刊>Journal of Cellular Physiology >Functional role of matrix metalloproteinases (MMPs) in mammary epithelial cell development.
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Functional role of matrix metalloproteinases (MMPs) in mammary epithelial cell development.

机译：基质金属蛋白酶的功能作用(基质金属蛋白酶)在乳腺上皮细胞的发展。

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摘要

The extracellular matrix (ECM) is an important regulator of mammary epithelial cell (MEC) function and is remodeled by matrix metalloproteinases (MMPs). To investigate the significance and regulation of MMP activity in normal MEC, we utilized a primary culture model in which rat MEC were grown three dimensionally within a reconstituted basement membrane (RBM) in defined serum-free medium. Zymograms of culture medium demonstrated that five major gelatinases of 97, 80, 74, 69, and 65 kDa were secreted by MEC and were distinct from gelatinases of RBM origin. Based on molecular weight, p-aminophenylmercuric acid activation, immunoblotting with MMP-specific antibodies, inhibition by EDTA, a peptide containing the prodomain sequence of MMP (TMRKPRCGNPDVAN) and two synthetic MMP inhibitors (BB-94 and CGS 27023A), these were classified as inactive and active forms of MMP-9 and MMP-2. The maximal MMP activities occurred when MEC were in a rapid proliferation and branching phase and declined after they underwent functional differentiation. Known regulators of MEC growth and differentiation were evaluated for their ability to modulate gelatinase activity in primary culture. Secretion of one or both MMPs was inhibited by EGF, TGFalpha, prolactin, and hydrocortisone and stimulated by progesterone. Furthermore, the functional significance of MMPs was demonstrated since three MMP inhibitors blocked branching morphogenesis elicited by the absence of hydrocortisone. Additionally, two synthetic MMP inhibitors not only inhibited epithelial cell growth but also inhibited normal alveolar development of the MEC. Finally, these drugs were found to enhance MMP secretion from MEC, although the activity of the secreted MMPs was inhibited as long as the drug was present. Copyright 2001 Wiley-Liss, Inc.
机译：细胞外基质(ECM)是一个重要的监管机构的乳腺上皮细胞(MEC)功能和改建的矩阵金属蛋白酶()。意义和监管的MMP的活动正常MEC,我们使用一个主要的文化模式老鼠MEC在三维生长在重组基底膜(元)定义的无血清培养基。中表明,五大明胶酶97、80、74、69和65 kDa分泌MEC有别于明胶酶的遏制来源。p-aminophenylmercuric酸活化,免疫印迹和MMP-specific抗体,包含的EDTA的抑制肽prodomain MMP的序列(TMRKPRCGNPDVAN)和两个合成MMP抑制剂(bb - 94和研究生院理事会27023 a),这些都是归类为不活跃活动形式的MMP-9和MMP-2。活动发生在MEC迅速核扩散和分支阶段和拒绝后进行功能分化。已知MEC增长和监管者分化进行评估的能力在主要调节白明胶酶的活动文化。催乳素抑制EGF, TGFalpha,氢化可的松,孕激素刺激。此外,基质金属蛋白酶的功能意义是证明因为三个MMP抑制剂分支形态发生阻塞引起的缺乏氢化可的松。不仅合成MMP抑制剂抑制上皮细胞生长,也抑制了正常肺泡MEC的发展。药物被发现提高MMP的分泌物MEC,尽管分泌基质金属蛋白酶的活动抑制药物只要是礼物。版权2001 Wiley-Liss公司。

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