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

Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

You might also read

Related Articles

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

Sort by
Same author

Microvascular Rarefaction and Myocardial Fibrosis in Hypertrophic Obstructive Cardiomyopathy: A Histopathological Comparison of Pediatric and Adult Patients.

The heart surgery forum·2022
Same author

Automated In-Line Artificial Intelligence Measured Global Longitudinal Shortening and Mitral Annular Plane Systolic Excursion: Reproducibility and Prognostic Significance.

Journal of the American Heart Association·2022
Same author

Regulating the Imbalance of Gut Microbiota by <i>Smilax china</i> L. Polyphenols to Alleviate Dextran Sulfate Sodium-induced Inflammatory Bowel Diseases.

The American journal of Chinese medicine·2022
Same author

PD-L1 combined with HDAC9 is a useful prognostic predictor in hepatocellular carcinoma.

Translational cancer research·2022
Same author

2-(Naphthalene-2-thio)-5,8-dimethoxy-1,4-naphthoquinone induces apoptosis via ROS-mediated MAPK, AKT, and STAT3 signaling pathways in HepG2 human hepatocellular carcinoma cells.

Drug and chemical toxicology·2022
Same author

Modeling Androgen Deprivation Therapy-Induced Prostate Cancer Dormancy and Its Clinical Implications.

Molecular cancer research : MCR·2022

Related Experiment Videos

[p38 MAPK/cPLA2 pathway mediates interleukins release in inflammatory cell model].

Xiao-hui Wang1, Guang-tao Yan, Kai Zhang

  • 1Research Laboratory of Biochemistry, Basic Medical Institute, General Hospital of PLA, Beijing 100853, China.

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue = Chinese Critical Care Medicine = Zhongguo Weizhongbing Jijiuyixue
|January 9, 2007
PubMed
Summary

Lipopolysaccharide (LPS) triggers interleukin-1 beta (IL-1 beta) and IL-6 release in HeLa cells via the p38 MAPK/cPLA(2) pathway. This study identifies p38 MAPK and cPLA(2) as key mediators, excluding COX-2

Related Experiment Videos

Area of Science:

  • Cellular biology
  • Immunology
  • Molecular biology

Context:

  • Lipopolysaccharide (LPS) is a potent activator of inflammatory responses.
  • Interleukin-1 beta (IL-1 beta) and IL-6 are critical pro-inflammatory cytokines.
  • HeLa cells are a widely used model for studying cellular responses to stimuli.

Purpose:

  • To elucidate the mechanism of LPS-induced IL-1 beta and IL-6 release in HeLa cells.
  • To investigate the role of the p38 mitogen-activated protein kinase (MAPK) pathway.
  • To identify downstream signaling molecules involved in this inflammatory process.

Summary:

  • LPS challenge in HeLa cells activated the p38 MAPK pathway.
  • Inhibition of p38 MAPK and cytosolic phospholipase A(2) (cPLA(2)) significantly reduced IL-1 beta and IL-6 release.
  • COX-2 expression was negligible and its inhibition did not affect cytokine production, indicating it is not involved.

Impact:

  • Establishes the p38 MAPK/cPLA(2) signaling axis as central to LPS-induced IL-1 beta and IL-6 production in HeLa cells.
  • Provides mechanistic insight into cytokine regulation.
  • Offers potential targets for anti-inflammatory therapies.