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Related Concept Videos

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...
NF-kB-dependent Signaling Pathway02:26

NF-kB-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...
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,...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...

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Related Experiment Video

Updated: Jun 24, 2026

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

Biomechanical thresholds regulate inflammation through the NF-kappaB pathway: experiments and modeling.

Jin Nam1, Baltazar D Aguda, Bjoern Rath

  • 1Biomechanics and Tissue Engineering Laboratory, College of Dentistry, The Ohio State University, Columbus, OH, USA.

Plos One
|April 17, 2009
PubMed
Summary

Mechanical forces on cartilage can either protect or damage it. This study reveals critical thresholds in dynamic compressive strain that regulate inflammation, identifying specific levels that promote healing versus destruction.

Related Experiment Videos

Last Updated: Jun 24, 2026

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

Area of Science:

  • Biomedical Engineering
  • Mechanobiology
  • Cellular Signaling

Background:

  • Cartilage integrity relies on dynamic compressive forces during normal activity.
  • Non-physiologic forces can trigger inflammation and cartilage destruction.
  • Understanding chondrocytic responses to mechanical load is crucial for joint health.

Purpose of the Study:

  • To investigate the magnitude-dependent regulation of chondrocytic responses by compressive forces.
  • To elucidate the role of the nuclear factor-kappa B (NF-kappaB) signaling pathway in mediating these responses.
  • To develop a mathematical model predicting the thresholds of mechanical stimulation.

Main Methods:

  • Chondrocytic cells in 3-D scaffolds were subjected to dynamic compressive strain (DCS).
  • Pro-inflammatory gene expression, specifically nitric oxide synthase (NOS2), was measured.
  • NF-kappaB signaling pathway activation was assessed via IkappaB-alpha phosphorylation and degradation, and NF-kappaB p65 translocation.
  • A mathematical model was developed to analyze the system's dynamics.

Main Results:

  • A threshold in DCS magnitude was identified, regulating NOS2 expression.
  • Low-magnitude DCS inhibited interleukin-1beta (IL-1beta)-induced NOS2 expression by attenuating the NF-kappaB pathway.
  • Higher-magnitude DCS induced NOS2 expression.
  • The mathematical model predicted two critical thresholds for DCS effects.

Conclusions:

  • Biomechanical signals, at critical thresholds, can suppress or induce inflammation via NF-kappaB pathway modulation.
  • These thresholds are linked to the bistable behavior of signaling networks with positive feedback.
  • Findings provide a foundation for distinguishing beneficial from detrimental physical activity levels for joint health.