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Published on: June 10, 2016
Leptin augments myofibroblastic conversion and fibrogenic activity of human peritoneal mesothelial cells: a
An-Hang Yang1, Seng-Wong Huang, Jin-Yang Chen
1Division of Ultrastructural and Molecular Pathology, Department of Pathology, Taipei Veterans General Hospital, Taipei 112, Taiwan. ahyang@vghtpe.gov.tw
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-beta1-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-beta1-dependent, suggesting that leptin promoted peritoneal fibrogenesis through synergistic activation of the TGF-beta1 signaling system. Leptin and TGF-beta1 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-beta1 activated cytokine in peritoneal bioenvironment associated with TGF-beta1 activated pathogenic processes.
Insights
Leptin enhances the fibrotic effects of TGF-beta1 on human peritoneal mesothelial cells (HPMCs). This suggests leptin acts as a profibrogenic cytokine in peritoneal injury, promoting fibrogenesis.
Area of Science:
- Cell Biology
- Molecular Biology
- Pathology
Background:
- Mesothelial cells undergo myofibroblastic conversion after serosal membrane injury, contributing to pathological changes.
- Understanding the molecular mechanisms driving this conversion is crucial for addressing peritoneal pathologies.
Purpose of the Study:
- To investigate the role of leptin in modulating the behavior of human peritoneal mesothelial cells (HPMCs).
- To elucidate the signaling pathways involved in leptin-mediated effects on HPMCs, particularly in the context of TGF-beta1 stimulation.
Main Methods:
- Isolation and culture of human peritoneal mesothelial cells (HPMCs).
- Assessment of gene expression using RT-PCR.
- Determination of signal transduction activation via western blot and densitometry.
- Observation of morphological changes using phase-contrast and electron microscopy.
Main Results:
- Leptin significantly enhanced TGF-beta1-induced myofibroblastic growth of HPMCs in vitro.
- Leptin augmented the expression of alpha-smooth muscle actin, fibronectin, and type I collagen mRNA in a TGF-beta1-dependent manner.
- Leptin and TGF-beta1 synergistically activated signaling components including MAPK, STAT3, and Smad pathways.
Conclusions:
- Leptin promotes peritoneal fibrogenesis by synergistically activating the TGF-beta1 signaling system.
- Leptin may function as a profibrogenic cytokine in the peritoneal environment, particularly in pathological conditions involving TGF-beta1 activation.
