Restoring multidrug resistance-associated protein 3 attenuates cell proliferation in the polycystic kidney

Eun Sun Chang, Eun Young Park, Yu Mi Woo, Duk Hee Kang, Young Hwan Hwang, Curie Ahn, Jong Hoon Park

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4 Scopus citations


Autosomal dominant polycystic kidney disease (ADPKD) is characterized by abnormal proliferation of renal tubular epithelial cells, resulting in the loss of renal function. Despite identification of the genes responsible for ADPKD, few effective drugs are currently available for the disease. Thus finding additional effective drug targets is necessary. The functions of multidrug- resistance-associated protein 3 (MRP3) have been reported only in the field of drug resistance, and the renal functions of MRP3 are mostly unknown. In this study, we found that MRP3 was significantly downregulated in kidneys of human patients with ADPKD and polycystic kidney disease (PKD) mouse models. Our results suggest that downregulated MRP3 stimulated renal epithelial cell proliferation through the B-Raf/MEK/ERK signaling pathway. In contrast, we found that restoring MRP3 reduced cell proliferation and cystogenesis in vitro. These results suggest that the renal function of MRP3 is related to renal cell proliferation and cyst formation and that restoring MRP3 may be an effective therapeutic approach for PKD.

Original languageEnglish
Pages (from-to)F1004-F1011
JournalAmerican Journal of Physiology - Renal Physiology
Issue number9
StatePublished - 1 May 2015

Bibliographical note

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© 2015 the American Physiological Society


  • Cell proliferation
  • Cystogenesis
  • Multidrug resistance-associated protein 3 (MRP3)
  • Polycystic kidney


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