Related Experiment Video

Updated: Jul 16, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion
07:39

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion

Published on: June 29, 2012

Pro-fibrogenic potential of PDGF-D in liver fibrosis

Erawan Borkham-Kamphorst1, Claudia R C van Roeyen, Tammo Ostendorf

  • 1Institute of Clinical Chemistry and Pathobiochemistry, and Division of Nephrology, RWTH-University Hospital Aachen, D-52074 Aachen, Germany.

Journal of Hepatology
|April 3, 2007
PubMed
Abstract

Insights

Platelet-derived growth factor D (PDGF-D) is upregulated in liver fibrosis and activates hepatic stellate cells (HSC) and myofibroblasts (MFB), promoting matrix remodeling.

Area of Science:

  • Hepatology
  • Cell Biology
  • Molecular Biology

Background:

  • Liver fibrosis is a complex process involving the activation of hepatic stellate cells (HSC) and myofibroblasts (MFB).
  • Platelet-derived growth factors (PDGFs) are implicated in fibrogenesis, but the specific role of PDGF-D remains to be fully elucidated.

Purpose of the Study:

  • To investigate the expression and biological function of PDGF-D in a rat model of bile duct ligation (BDL)-induced liver fibrosis.
  • To assess the role of PDGF-D in HSC and MFB activation and signaling pathways.

Main Methods:

  • Quantitative assessment of PDGF and PDGF receptor mRNA and protein levels in normal and fibrotic rat livers.
  • Immunohistochemistry to determine PDGF-D localization.
  • Analysis of PDGF-D-mediated signaling in cultured HSC and MFB, including receptor phosphorylation and downstream kinase activation.

Main Results:

  • PDGF-D mRNA and protein levels were significantly upregulated in fibrotic livers following BDL.
  • PDGF-D localized to fibrotic septa and potently activated PDGFRbeta signaling in HSC/MFB, comparable to PDGF-B.
  • PDGF-D demonstrated significant mitogenic and fibrogenic effects on cultured HSC and MFB.

Conclusions:

  • PDGF-D plays a significant role in the pathogenesis of liver fibrosis.
  • PDGF-D promotes HSC activation and extracellular matrix remodeling, suggesting it as a potential therapeutic target.

Related Concept Videos

Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Liver Regeneration01:24

Liver Regeneration

The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are large...
Introduction to Fibroblasts01:09

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...