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Introduction to Fibroblasts

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...

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Related Experiment Video

Updated: Oct 12, 2025

A Human Corneal Organ Culture Model of Descemet's Stripping Only with Accelerated Healing Stimulated by Engineered Fibroblast Growth Factor 1

A Human Corneal Organ Culture Model of Descemet's Stripping Only with Accelerated Healing Stimulated by Engineered Fibroblast Growth Factor 1

Published on: July 22, 2022

FAK Inhibition Attenuates Corneal Fibroblast Differentiation In Vitro.

Vincent Yeung¹, Sriniwas Sriram¹, Jennifer A Tran¹

¹Department of Ophthalmology, Schepens Eye Research Institute of Mass Eye and Ear, Harvard Medical School, Boston, MA 02114, USA.

|November 27, 2021

Summary

This summary is machine-generated.

Transforming growth factor-beta (TGF-β)1 and TGF-β3 influence corneal wound healing. Focal adhesion kinase (FAK) inhibition reduces TGF-β1-induced myofibroblast differentiation, offering a potential therapy for corneal scarring.

Keywords:

3D cell culture corneal scarring extracellular matrix (ECM)focal adhesion kinase (FAK)α-smooth muscle actin (αSMA)

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Corneal Tissue Engineering: An In Vitro Model of the Stromal-nerve Interactions of the Human Cornea

Corneal Tissue Engineering: An In Vitro Model of the Stromal-nerve Interactions of the Human Cornea

Published on: January 24, 2018

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Last Updated: Oct 12, 2025

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Corneal Tissue Engineering: An In Vitro Model of the Stromal-nerve Interactions of the Human Cornea

Corneal Tissue Engineering: An In Vitro Model of the Stromal-nerve Interactions of the Human Cornea

Published on: January 24, 2018

Area of Science:

Ophthalmology
Cell Biology
Biomedical Engineering

Background:

Corneal fibrosis, a leading cause of vision impairment, results from ocular trauma or infection.
Transforming growth factor-beta (TGF)-β1 and TGF-β3 are key modulators of corneal wound healing and fibrosis.
These factors influence extracellular matrix deposition and α-smooth muscle actin (αSMA) expression, a marker of myofibroblast differentiation.

Purpose of the Study:

To investigate the distinct roles of TGF-β1 and TGF-β3 in corneal fibroblast behavior.
To evaluate the impact of focal adhesion kinase (FAK) inhibition on TGF-β1-mediated responses.
To explore novel therapeutic strategies for mitigating corneal scarring.

Main Methods:

Human corneal fibroblasts (hCF) were cultured in 2D monolayer and 3D stromal constructs.
Cultures were treated with TGF-β1, TGF-β3, or a combination of TGF-β1 and a FAK inhibitor (FAKi).
Gene expression (ITGAV, ITGB1, SRC, ACTA2) and protein levels (αSMA, FAK) were analyzed.

Main Results:

TGF-β1 and TGF-β3 induced distinct gene expression profiles related to wound healing and fibrosis in 3D constructs.
TGF-β1 significantly increased αSMA and FAK protein expression in 3D models, while TGF-β3 did not.
Combined treatment with TGF-β1 and FAKi effectively attenuated TGF-β1-induced αSMA expression in both 2D and 3D models.

Conclusions:

FAK signaling plays a critical role in TGF-β1-driven myofibroblast differentiation in corneal fibroblasts.
FAK inhibition presents a promising therapeutic approach to suppress TGF-β1-mediated corneal scarring.
Differential effects of TGF-β isoforms highlight the complexity of corneal wound healing regulation.