Novel Madin Darby canine kidney cell clones exhibit unique phenotypes in response to morphogens.
Novel Madin Darby canine kidney cell clones exhibit unique phenotypes in response to morphogens.
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新型 Madin Darby 犬肾细胞克隆对形态发生素表现出独特的表型。
DOI：
10.1007/bf02722959
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Avner,ED
中科院分区：
文献类型：
--
作者：
Orellana,SA;Neff,CD;Sweeney,WE;Avner,ED
分离了新的马丁达比犬肾细胞克隆。这些细胞克隆分别对胶原凝胶培养中的小管或囊肿形成诱导剂（肝细胞生长因子或细胞内cAMP形成诱导剂）表现出不同的反应。凝胶培养中，克隆OR93.22。D6形成囊肿，并对肝细胞生长因子和前列腺素E1都有形态转化反应，除了其更高的经上皮电阻外，D6是最典型的一种先前描述的细胞类型。OR55.25。II20在培养中形成小管，对肝细胞生长因子无反应，形成前列腺素诱导的球形囊肿。OR55.28。V2在控制条件下形成致密的细胞球，在肝细胞生长因子的诱导下形成小管，对前列腺素无反应。OR55.29只形成囊肿，是唯一在单层培养中形成圆顶的克隆。肝细胞生长因子诱导小管形成，除OR55.25外。II20被中和抗体阻断。在确定的培养基中，不含肝细胞生长因子或前列腺素，OR55.25。II20形成自发小管。这一发现表明，管源性血清因子不负责观察到的表型。前列腺素浓度增加导致小管形成的抑制和囊肿形成的增加。这一观察结果表明，细胞内cAMP形成的诱导对这些细胞的小管形成起到负调控作用，并暗示膀胱形成可能是小管形成受损的“默认途径”。这些观察结果表明，肾小管形成的某些方面可能独立于肝细胞生长因子，在比较使用不同克隆的生物学研究时必须谨慎。
Novel Madin Darby Canine Kidney cell clones were isolated. These cell clones exhibit differential responsiveness to inducers of tubule or cyst formation in collagen gel culture: hepatocyte growth factor or inducers of intracellular cAMP formation, respectively. In gel culture, clone OR93.22.D6 forms cysts and responds with morphological transformation to both hepatocyte growth factor and prostaglandin E1, and is most typical of a previously described cell type except for its higher transepithelial electrical resistance. OR55.25.II20 forms tubules in culture, is unresponsive to hepatocyte growth factor, and forms prostaglandin-induced spherical cysts. OR55.28.V2 forms dense cell spheres under control conditions, is induced to form tubules by hepatocyte growth factor, and is unresponsive to prostaglandin. OR55.29 forms only cysts, and is the only clone to form domes in monolayer culture. Tubule formation induced by hepatocyte growth factor, in all clones except OR55.25.II20, is blocked by a neutralizing antibody. In defined medium, without hepatocyte growth factor or prostaglandin, OR55.25.II20 forms spontaneous tubules. This finding indicates that a tubulogenic serum factor is not responsible for the observed phenotype. Increasing prostaglandin concentrations lead to inhibition of tubule formation and increased cyst formation. This observation suggests that induction of intracellular cAMP formation negatively regulates tubule formation in these cells, and implies that cystogenesis may represent a “default pathway” for impaired tubulogenesis. These observations demonstrate that some facets of renal tubulogenesis may be independent of hepatocyte growth factor, and that care must be exercised when comparing biological studies utilizing different clones.