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Related Concept Videos

Healing I: Introduction01:11

Healing I: Introduction

Healing is the physiological process by which the body restores the integrity and function of damaged tissues following injury. It involves a coordinated interplay of cellular proliferation, extracellular matrix remodeling, and growth factor signaling. The extent and nature of the tissue damage determine whether healing occurs by resolution, regeneration, or replacement.ResolutionResolution represents the most complete form of healing, occurring when the injury is minimal and tissue...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
Phases of Wound Repair01:28

Phases of Wound Repair

Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
Formation of Blood Clot
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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Related Experiment Video

Updated: May 9, 2026

Separation of Rat Epidermis and Dermis with Thermolysin to Detect Site-Specific Inflammatory mRNA and Protein
08:45

Separation of Rat Epidermis and Dermis with Thermolysin to Detect Site-Specific Inflammatory mRNA and Protein

Published on: September 29, 2021

Wound-healing growth factor, basic FGF, induces Erk1/2-dependent mechanical hyperalgesia.

Christine Andres1, Jan Hasenauer, Hye-Sook Ahn

  • 1Max Planck Institute for Molecular Genetics, Berlin, Germany Institute of Chemistry and Biochemistry, Freie Universität Berlin, Berlin, Germany Institute for Systems Theory and Automatic Control, University of Stuttgart, Stuttgart, Germany Institute of Bioinformatics and Systems Biology, Helmholtz Zentrum München, Germany Department of Neurology, Yale University School of Medicine, New Haven, CT, USA Center for Neuroscience and Regeneration Research, New Haven, CT, USA Division of Neuroscience, Departments of Medicine and Oral & Maxillofacial Surgery, University of California, San Francisco, CA, USA Klinik für Anästhesiologie und Operative Intensivmedizin, Experimentelle Anästhesiologie und Schmerzforschung, Uniklinik Köln, Köln, Germany.

Pain
|July 23, 2013
PubMed
Summary

Basic fibroblast growth factor (bFGF), a wound-healing factor, sensitizes pain neurons by activating FGFR1 and increasing NaV1.8 channel currents. This leads to mechanical hyperalgesia, highlighting bFGF

Keywords:
Erk1/2FGF-2FGF-βInflammatory painMAP kinaseNa(V)1.8NociceptionPainPeripheral sensory neuronQuantitative automated microscopyRandall SelittoSensitization signalingVoltage gated sodium channelsWound healingbFGF

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Methods for Skin Wounding and Assays for Wound Responses in C. elegans
09:06

Methods for Skin Wounding and Assays for Wound Responses in C. elegans

Published on: December 3, 2014

Related Experiment Videos

Last Updated: May 9, 2026

Separation of Rat Epidermis and Dermis with Thermolysin to Detect Site-Specific Inflammatory mRNA and Protein
08:45

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Published on: September 29, 2021

A Human Corneal Organ Culture Model of Descemet's Stripping Only with Accelerated Healing Stimulated by Engineered Fibroblast Growth Factor 1
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Methods for Skin Wounding and Assays for Wound Responses in C. elegans
09:06

Methods for Skin Wounding and Assays for Wound Responses in C. elegans

Published on: December 3, 2014

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Known pain sensitizers include nerve growth factor and glial cell line-derived neurotrophic factor.
  • Numerous growth factors involved in wound healing are released during inflammation and tissue regeneration.
  • The role of many wound-healing factors in altering nociceptive neuron sensitivity remains largely unknown.

Purpose of the Study:

  • To investigate the role of basic fibroblast growth factor (bFGF), a key wound-healing factor, in pain sensitization.
  • To determine if bFGF affects the sensitivity of nociceptive neurons.

Main Methods:

  • Reverse transcription polymerase chain reaction (RT-PCR) to detect FGFR1 mRNA in rat dorsal root ganglia (DRG).
  • Quantitative automated immunofluorescence microscopy to confirm FGFR1 protein expression in DRG neurons.
  • Electrophysiological recordings to assess bFGF's effect on NaV1.8 channel currents in DRG neurons.
  • Intradermal injection of bFGF in rats to induce and assess mechanical hyperalgesia.

Main Results:

  • FGFR1, the receptor for bFGF, is expressed in lumbar rat DRG neurons at both mRNA and protein levels.
  • bFGF treatment induced Erk1/2 phosphorylation in nociceptive neurons, dependent on FGF receptor inhibition.
  • bFGF activated Erk1/2 in a dose- and time-dependent manner.
  • bFGF increased the current density of NaV1.8 channels in DRG neurons, an effect abrogated by Erk1/2 inhibitors.
  • Intradermal bFGF injection in rats resulted in Erk1/2-dependent mechanical hyperalgesia.

Conclusions:

  • Basic fibroblast growth factor (bFGF) acts as a novel pain sensitizing factor.
  • Intracellular signaling dynamics in nociceptive neurons are crucial for identifying pain modulators.
  • Wound-healing factors represent a potential avenue for investigating novel mechanisms of nociception.