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Related Concept Videos

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Activation of Integrins01:15

Activation of Integrins

Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.
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,...

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Related Experiment Video

Updated: May 23, 2026

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis
07:52

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Published on: December 21, 2014

Allosteric modulation of beta1 integrin function induces lung tissue repair.

Rehab Aljamal-Naylor1, Linda Wilson, Susan McIntyre

  • 1Avipero Ltd., 5th Floor, 125 Princes Street, Edinburgh EH2 4AD, UK.

Advances in Pharmacological Sciences
|April 17, 2012
PubMed
Summary

Altered cell-matrix interactions in lung injury cause mechanical missensing, leading to cell death. A novel antibody targeting β1 integrin remodels the matrix, enhancing cell survival and reversing lung tissue injury.

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Published on: June 10, 2016

Area of Science:

  • Cellular mechanobiology
  • Biomaterials science
  • Integrative biology

Background:

  • Cellular mechanical sensing relies on cytoskeleton, adhesion receptors, and extracellular matrix (ECM).
  • Lung injury disrupts ECM-integrin interactions, causing signaling alterations and mechanical missensing.
  • This missensing increases cellular stiffness, injury, and death.

Purpose of the Study:

  • To investigate the role of ECM-integrin interactions in lung injury.
  • To identify therapeutic targets for restoring mechanical homeostasis.
  • To evaluate a novel monoclonal antibody against β1 integrin.

Main Methods:

  • Analysis of ECM-integrin interactions in lung injury models.
  • Characterization of a monoclonal antibody against β1 integrin.
  • Assessment of antibody effects on cell survival and matrix remodeling.
  • Testing the antibody in an animal model of degenerative lung disease.

Main Results:

  • Lung injury alters ECM-integrin interactions, leading to mechanical missensing and cell death.
  • A monoclonal antibody targeting β1 integrin was identified.
  • This antibody acts as an allosteric dual agonist/antagonist, inducing matrix remodeling and enhancing cell survival.
  • The antibody reversed functional and structural lung tissue injury in vivo.

Conclusions:

  • Restoring mechanical sensing through targeted interventions is crucial for treating lung injury.
  • The identified β1 integrin antibody shows therapeutic potential for degenerative lung diseases.
  • Targeting integrin-ECM dynamics offers a novel strategy for lung tissue repair.