Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

4.4K
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...
4.4K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.2K
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...
2.2K
Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

348
Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
348
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

7.4K
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...
7.4K
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

8.9K
The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
8.9K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

2.7K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Re-evaluating the role of TRPV6 deficiency in human and mouse pancreatitis.

American journal of physiology. Gastrointestinal and liver physiology·2026
Same author

Small molecule-mediated activation of Notch signal transduction.

Cell death & disease·2026
Same author

SARS-CoV-2 (E)-protein induces rapid TLR2-mediated T cell activation in mouse lungs revealed by intravital lung microscopy.

The European respiratory journal·2026
Same author

IRG1/itaconate rewires macrophage and lung tumor metabolism through G6PD inhibition.

Cell metabolism·2026
Same author

Extracorporeal Photopheresis: Secreted Factors That Promote Immunomodulation.

Transplantation direct·2026
Same author

Enhanced fatty acid availability rewires fibroblasts metabolism and decreases collagen deposition in lung fibrosis.

Cellular and molecular life sciences : CMLS·2026

Related Experiment Video

Updated: Aug 30, 2025

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.0K

Notch1 Induces Defective Epithelial Surfactant Processing and Pulmonary Fibrosis.

Roxana Wasnick1, Martina Korfei1, Katarzyna Piskulak1

  • 1University of Giessen and Marburg Lung Center (UGMLC), member of the German Center for Lung Research (DZL), 35392 Giessen, Germany.

American Journal of Respiratory and Critical Care Medicine
|September 1, 2022
PubMed
Summary
This summary is machine-generated.

Notch signaling drives lung fibrosis in idiopathic pulmonary fibrosis (IPF) by impairing alveolar epithelial cell (AEC2) differentiation and promoting proliferation. Inhibiting Notch signaling improves AEC2 function and reverses fibrosis.

Keywords:
diffuse parenchymal lung diseaseepithelial regenerationidiopathic pulmonary fibrosisinterstitial lung diseaselung surfactant

More Related Videos

Studying Wnt Signaling During Patterning of Conducting Airways
13:00

Studying Wnt Signaling During Patterning of Conducting Airways

Published on: October 16, 2016

7.4K
Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

256

Related Experiment Videos

Last Updated: Aug 30, 2025

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.0K
Studying Wnt Signaling During Patterning of Conducting Airways
13:00

Studying Wnt Signaling During Patterning of Conducting Airways

Published on: October 16, 2016

7.4K
Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

256

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Fibrosis Research

Background:

  • Type II alveolar epithelial cells (AEC2s) are crucial for lung regeneration but are chronically injured in idiopathic pulmonary fibrosis (IPF).
  • Understanding the mechanisms regulating AEC2 fate in IPF is vital for developing effective therapies.

Purpose of the Study:

  • To investigate the role of Notch signaling in AEC2 proliferation, differentiation, and the development of lung fibrosis in IPF.
  • To determine if Notch signaling impacts surfactant processing machinery and contributes to fibrotic changes.

Main Methods:

  • Utilized a combination of in vitro (cell lines, primary cells), ex vivo (lung slices), and in vivo (animal models) approaches.
  • Employed techniques including microarray analysis, kinome profiling, flow cytometry, immunofluorescence, western blotting, and qPCR.
  • Assessed epithelial differentiation, proliferation, surfactant processing, and matrix deposition.

Main Results:

  • IPF AEC2s exhibit surfactant protein processing defects due to Napsin A loss, leading to alveolar collapse and endoplasmic reticulum stress.
  • Notch1 signaling is activated early in IPF, inhibiting AEC2 differentiation, increasing proliferation, and promoting lung fibrosis, potentially via JAK/STAT pathways.
  • Pharmacological inhibition of Napsin A induced AEC2 injury and lung fibrosis in vivo.
  • Inhibition of Notch signaling in IPF lung slices improved AEC2 function and reversed fibrosis.

Conclusions:

  • Notch1 signaling is a key regulator of AEC2 fate in IPF.
  • Notch1 activation contributes to alveolar epithelial proliferation, Napsin A loss, impaired surfactant processing, and fibroproliferation in IPF.
  • Targeting Notch signaling presents a potential therapeutic strategy for IPF.