Cell-cell communication between mouse mammary epithelial cells and 3T3-L1 preadipocytes: effect on triglyceride accumulation and cell proliferation.

V. Julianelli, L. Guerra, J. Calvo
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引用次数: 6

Abstract

Interaction between parenchyma and stroma is essential for organogenesis, morphogenesis, and differentiation. Mammary gland has being the chosen model for developmental biologist because the most striking changes in morphology and function take place after birth. We have demonstrated a regulation of triglyceride accumulation by protein factors synthesized by normal mouse mammary gland epithelial cells (NMMG), acting on a cell line, 3T3-L1, long used as a model for adipogenesis. In this paper, we demonstrate that this inhibitory effect seems to be shared by other cells of epithelial origin but not by other cell types. We found a regulation of cell proliferation when NMMG cells are cultured in the presence of conditioned media from Swiss 3T3 or 3T3-L1 cells. We found a possible point of regulation for the mammary factor on a key enzyme of the lipid metabolic pathway, the glycerol-3-phosphate dehydrogenase. The inhibitory factor seems to have an effect on this enzyme's activity and reduces it. The results presented herein contribute to the understanding of cell-cell communication in a model of a normal mammary gland.
小鼠乳腺上皮细胞与3T3-L1前脂肪细胞之间的细胞-细胞通讯:对甘油三酯积累和细胞增殖的影响。
薄壁组织和间质之间的相互作用对器官发生、形态发生和分化至关重要。乳腺一直是发育生物学家选择的模型,因为最显著的形态学和功能变化发生在出生后。我们已经证明了正常小鼠乳腺上皮细胞(NMMG)合成的蛋白质因子对甘油三酯积累的调节,作用于细胞系3T3-L1,长期以来被用作脂肪形成的模型。在本文中,我们证明了这种抑制作用似乎在其他上皮细胞中共享,而不是在其他细胞类型中共享。我们发现,当NMMG细胞在瑞士3T3或3T3- l1细胞的条件培养基中培养时,细胞增殖有调节作用。我们发现乳腺因子可能调控脂质代谢途径的一个关键酶,甘油-3-磷酸脱氢酶。抑制因子似乎对这种酶的活性有影响并使其降低。本文提出的结果有助于理解正常乳腺模型中的细胞-细胞通讯。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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