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NDT Advance Access originally published online on December 1, 2006
Nephrology Dialysis Transplantation 2007 22(3):756-762; doi:10.1093/ndt/gfl715
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Leptin augments myofibroblastic conversion and fibrogenic activity of human peritoneal mesothelial cells: A functional implication for peritoneal fibrosis

An-Hang Yang1,4, Seng-Wong Huang5, Jin-Yang Chen2,6, Jan-Kou Lin3,5 and Chun-Yi Chen1

1Division of Ultrastructural and Molecular Pathology, Department of Pathology, 2Division of Nephrology, Department of Medicine and 3Division of Colorectal surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, 4Department of Pathology, 5Department of Surgery and 6Department of Medicine, National Yang Ming University, Taipei, Taiwan

Correspondence and offprint requests to: Dr An-Hang Yang, Division of Ultrastructural and Molecular Pathology, Department of Pathology, Taipei Veterans General Hospital, Taipei 112, Taiwan. Email: ahyang{at}vghtpe.gov.tw



  Abstract

Background. Myofibroblastic conversion of mesothelial cells is proposed to play an important role in pathological changes following serosal membrane injury.

Methods. Human peritoneal mesothelial cells (HPMCs) were isolated and maintained in culture. The gene expression was assessed by RT–PCR. Activation of signal transduction was determined by western blot and densitometry. Morphological changes were observed by phase-contrast and electron microscopy.

Results. In vitro study showed that TGF-ß1-induced myofibroblastic growth of HPMCs was significantly enhanced in the presence of leptin. Augmented expression of {alpha}-smooth muscle actin, fibronectin and type I collagen mRNA in HPMCs induced by leptin were TGF-ß1-dependent, suggesting that leptin promoted peritoneal fibrogenesis through synergistic activation of the TGF-ß1 signaling system. Leptin and TGF-ß1 synergistically augmented activation of signalling components of mitogen-activated protein kinase (MAPK), STAT3 and Smad but did not modulate the expression of LEPR-B.

Conclusion. Leptin may act as a profibrogenic TGF-ß1 activated cytokine in peritoneal bioenvironment associated with TGF-ß1 activated pathogenic processes.

Keywords: dialysis; fibrosis; leptin; mesothelial cell; myofibroblast; TGF-ß1

Received for publication: 22. 7.06
Accepted in revised form: 3.11.06


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