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Related Concept Videos

Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
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...

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Related Experiment Video

Updated: Jun 30, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
08:56

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

Published on: February 10, 2015

Hedgehog signaling in biliary fibrosis.

Linda E Greenbaum1

  • 1Division of Gastroenterology, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. greenbal@mail.med.upenn.edu

The Journal of Clinical Investigation
|September 20, 2008
PubMed
Summary

Biliary diseases involve cholangiocyte (bile duct cell) dysfunction and fibrosis. This study reveals paracrine hedgehog signaling between myofibroblasts and cholangiocytes is crucial for biliary repair and fibrogenesis.

Area of Science:

  • Hepatology and Gastroenterology
  • Cell Biology
  • Molecular Medicine

Background:

  • Cholangiopathies, diseases of the biliary tree, contribute significantly to morbidity and mortality.
  • In advanced stages, cholangiocyte proliferation failure leads to bile duct loss, fibrosis, cirrhosis, and liver failure.
  • Epithelial-mesenchymal transition (EMT) is hypothesized to drive cholangiocyte proliferation and fibrogenesis in biliary diseases.

Discussion:

  • This study investigated the role of paracrine hedgehog signaling in myofibroblast-cholangiocyte interactions.
  • Evidence supports increased mesenchymal marker expression in cholangiocytes within this context.
  • The findings highlight the interplay between cell types in biliary disease pathology.

Key Insights:

  • Paracrine hedgehog signaling is critical in the communication between myofibroblasts and cholangiocytes.

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A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia

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Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
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Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

Related Experiment Videos

Last Updated: Jun 30, 2026

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
08:56

Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis

Published on: February 10, 2015

A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia
09:12

A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia

Published on: February 3, 2023

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

  • Cholangiocytes exhibit increased expression of mesenchymal markers, suggesting EMT involvement.
  • This interaction influences both cholangiocyte repair mechanisms and fibrotic processes.

    • Outlook:

    • Further research is needed to elucidate the precise contribution of hedgehog signaling in cholangiocyte repair.
    • Understanding hedgehog signaling's role in fibrogenesis is essential for developing targeted therapies.
    • These findings pave the way for novel therapeutic strategies for biliary diseases.