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

X-Inactivation01:58

X-Inactivation

42.7K
The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
42.7K
What is Cell Signaling?02:03

What is Cell Signaling?

131.1K
Despite the protective membrane that separates a cell from the environment, cells need the ability to detect and respond to environmental changes. Additionally, cells often need to communicate with one another. Unicellular and multicellular organisms use a variety of cell signaling mechanisms to communicate to respond to the environment.
131.1K
Paracrine Signaling01:21

Paracrine Signaling

59.7K
Paracrine signaling allows cells to communicate with their immediate neighbors via secretion of signaling molecules. Such a signal can only trigger a response in nearby target cells because the signal molecules degrade quickly or are inactivated if not taken up. Prominent examples of paracrine signaling include nitric oxide signaling in blood vessels, synaptic signaling of neurons, the blood clotting system, tissue repair/wound healing, and local allergic skin reactions. Nitric oxide as a...
59.7K
Positive Regulator Molecules01:45

Positive Regulator Molecules

136.5K
To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
136.5K
What is the Immune System?01:38

What is the Immune System?

132.4K
Overview
132.4K
Humoral Immune Responses01:36

Humoral Immune Responses

84.1K
Overview
84.1K

You might also read

Related Articles

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

Sort by
Same author

Caregiver decision-making on pediatric research participation in congenital heart disease in western China: a qualitative study.

Frontiers in public health·2026
Same author

Fully quantitative CMR rest perfusion reveals myocardial perfusion abnormality in Kawasaki disease: Association with left ventricular Remodeling.

International journal of cardiology·2026
Same author

Pediatric Cardiac Function Staging and Management Recommendations.

Pediatric discovery·2026
Same author

Long-term lessons from MATCH01 macrophage therapy in cirrhosis.

Cell stem cell·2026
Same author

Predictors of Heart Failure in Pediatric Patients with End-Stage Kidney Disease Secondary to Nephrotic Syndrome.

Medicina (Kaunas, Lithuania)·2026
Same author

"Double-hit" precipitates fulminant cardiac dysfunction in a child with homozygous CAP2 variant: a case report.

Frontiers in cardiovascular medicine·2026

Related Experiment Video

Updated: Feb 13, 2026

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
06:03

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

1.9K

Inactivation Rap2a in Endothelial Cell Prevents Pulmonary Fibrosis by Regulating Immune Microenvironment Through

Xiaolan Zheng1, Peng Yue1, Kaiyu Zhou1

  • 1Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|February 11, 2026
PubMed
Summary
This summary is machine-generated.

Idiopathic pulmonary fibrosis (IPF) involves lung scarring and inflammation. Researchers found that Rap2a protein in endothelial cells drives this process, suggesting it as a potential therapeutic target for lung fibrosis.

Keywords:
CellNexRap2aendothelial cellsimmune microenvironmentpulmonary fibrosis

More Related Videos

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

1.1K
Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis
07:11

Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis

Published on: May 23, 2025

961

Related Experiment Videos

Last Updated: Feb 13, 2026

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
06:03

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

1.9K
Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

1.1K
Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis
07:11

Establishment and Validation of a Rat Model of Pulmonary Arterial Hypertension Associated with Pulmonary Fibrosis

Published on: May 23, 2025

961

Area of Science:

  • Pulmonary Medicine
  • Cellular Biology
  • Immunology

Background:

  • Idiopathic pulmonary fibrosis (IPF) features progressive lung scarring, endothelial dysfunction, and immune cell infiltration.
  • Intracellular signaling pathways linking inflammation to endothelial-immune interactions in IPF are not fully understood.
  • The role of Ras-related protein Rap2a (RAP2A) in pulmonary endothelial cells during fibrotic lung injury is unexplored.

Purpose of the Study:

  • To investigate the role of RAP2A in pulmonary endothelial cells during experimental lung fibrosis.
  • To elucidate the mechanisms by which RAP2A influences endothelial activation and immune cell interactions in fibrosis.
  • To assess the therapeutic potential of targeting RAP2A in fibrotic lung disease.

Main Methods:

  • Utilized a bleomycin-induced mouse model of lung fibrosis.
  • Examined RAP2A expression in pulmonary endothelial cells.
  • Employed endothelium-enriched knockdown of Rap2a using AAV9-Cdh5-shRNA.
  • Performed in vitro assays to assess endothelial activation and adhesiveness.

Main Results:

  • RAP2A expression was significantly upregulated in pulmonary endothelial cells and correlated with IPF severity.
  • Knockdown of Rap2a reduced inflammatory cell adhesion, fibrotic remodeling, and improved lung function.
  • RAP2A enhanced MAP4K4-dependent signaling and VCAM1 expression, promoting leukocyte-endothelial interactions.
  • RAP2A deficiency impaired TNF-α-induced endothelial adhesiveness without affecting basal integrity.

Conclusions:

  • Endothelial RAP2A acts as a key regulator of inflammatory endothelial activation in experimental lung fibrosis.
  • Targeting RAP2A-mediated signaling may offer a novel therapeutic strategy for IPF.
  • Modulating endothelial-immune crosstalk via RAP2A could be beneficial in treating fibrotic lung injury.