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Introduction to Fibroblasts01:09

Introduction to Fibroblasts

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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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Joints form during embryonic development in conjunction with the formation and growth of the associated bones. The embryonic tissue that gives rise to all bones, cartilage, and connective tissues of the body is called mesenchyme.
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Structural Joints: Synovial Joints01:16

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Synovial joints are the most common type of joint in the body. A key structural characteristic for a synovial joint is the presence of a joint cavity. This fluid-filled space is where the articulating surfaces of the bones contact each other. Also, unlike fibrous or cartilaginous joints, the articulating bone surfaces at a synovial joint are not directly connected to each other with fibrous connective tissue or cartilage. This gives the bones of a synovial joint the ability to move smoothly...
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Fibronectin is an adhesive glycoprotein present in the extracellular matrix of embryogenic and adult tissue. These molecules primarily aid in regulating cell motility and attachment. A fibronectin molecule is composed of two identical polypeptide chains attached to each other by a pair of disulfide bonds at the C-terminal.
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Glycosaminoglycans01:23

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Glycosaminoglycans (GAGs), also known as mucopolysaccharides, are long and linear polymers comprising of specific repeating disaccharides - the amino sugar that can be N-acetylglucosamine or N-acetylgalactosamine, and a uronic acid that is usually glucuronic acid or iduronic acid.
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Hyaluronic...
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Fibril-associated Collagen01:11

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Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
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Related Experiment Video

Updated: Feb 19, 2026

Author Spotlight: Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue
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Author Spotlight: Isolation and Culture of Primary Synovial Macrophages and Fibroblasts from Murine Arthritis Tissue

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Synovial fibroblasts in 2017.

Caroline Ospelt1

  • 1Department of Rheumatology, Center of Experimental Rheumatology, University Hospital and University of Zurich, Zurich, Switzerland.

RMD Open
|October 31, 2017
PubMed
Summary
This summary is machine-generated.

Synovial fibroblasts are key players in rheumatoid arthritis (RA) inflammation and cartilage damage. This review explores their innate immune roles, epigenetic alterations, and distinct subsets in RA.

Keywords:
fibroblastsinflammationrheumatoidarthritis

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Area of Science:

  • Immunology
  • Cell Biology
  • Rheumatology

Background:

  • Synovial fibroblasts are crucial stromal cells influencing their microenvironment.
  • Their role extends beyond structural support to active participation in immune responses.

Purpose of the Study:

  • To review the role of synovial fibroblasts in the innate immune system.
  • To detail their involvement in rheumatoid arthritis (RA) pathogenesis, including inflammation and cartilage destruction.
  • To discuss epigenetic modifications and subset identification within RA synovial fibroblasts.

Main Methods:

  • Literature review of existing studies on synovial fibroblasts in RA.
  • Analysis of the immunological functions of synovial fibroblasts.
  • Examination of epigenetic changes and cellular heterogeneity in RA synovial fibroblasts.

Main Results:

  • Synovial fibroblasts function as innate immune cells, contributing significantly to RA.
  • They are implicated in driving both inflammation and the destruction of cartilage in RA.
  • Epigenetic alterations and distinct fibroblast subsets characterize the RA synovium.

Conclusions:

  • Synovial fibroblasts are critical mediators of RA pathogenesis.
  • Understanding their immune functions, epigenetic landscape, and heterogeneity is vital for RA treatment strategies.
  • Further research into synovial fibroblast subsets may reveal novel therapeutic targets for rheumatoid arthritis.