Adipokine-producing fatty tissues, composed of preadipocytes, adipocytes, and mesenchymal stem cells, surround the kidney. To study the interaction between renal tubular cells and adipose tissue, we cocultured adipose tissue fragments and MDCK cells. MDCK cells in the coculture showed a taller columnar shape with improved organization of their microvilli and basal lamina than that seen in MDCK cell monoculture. The adipose tissue-induced change in morphology was replicated when we added leptin to MDCK cells cultured alone. Adiponectin abolished the leptin effect. Adipose tissue fragments inhibited MDCK cell division and also the formation of single-stranded DNA, an indicator of apoptosis. The fragments promoted the expression of polarity-associated proteins, including the tight junction molecules, ZO-1, atypical protein kinase C, and Cdc42. Further, the fragments also accelerated the expression of pendrin, the chloride/iodide transporter in the MDCK cells. In turn, MDCK cells decreased the number of preadipocytes and CD44/CD105 mesenchymal stem cells in the fragments, and promoted adiponectin production from the fragments. Thus, our study shows that adipose tissue fragments promote the hypertrophy, polarization, and differentiation of MDCK cells by attenuating their growth and apoptosis through opposing endocrine or paracrine effects of leptin and adiponectin. Further, MDCK cells inhibit the regeneration of preadipocytes and mesenchymal stem cells in adipose tissue.
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