Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Introduction to Fibroblasts01:09

Introduction to Fibroblasts

4.0K
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...
4.0K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

10.7K
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...
10.7K
Fibril-associated Collagen01:11

Fibril-associated Collagen

3.4K
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.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
3.4K
Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

4.4K
Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
4.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Linoleic acid accelerates osteoarthritis progression in male rats by targeting iron-sulfur clusters to drive ferroptosis in chondrocytes.

Nature communications·2026
Same author

Corrigendum to "Hyperoside ameliorates the progression of osteoarthritis: An in vitro and in vivo study" [Phytomedicine/volume80 (2021)/153387].

Phytomedicine : international journal of phytotherapy and phytopharmacology·2026
Same author

Intra-articular injection of Erastin induces OA pathological progression as an experimental model.

International immunopharmacology·2026
Same author

Correction: Immunological purification of rat precartilaginous stem cells and construction of the immortalized cell strain.

Archives of orthopaedic and trauma surgery·2026
Same author

Correction to: Low-intensity pulsed ultrasound delays the progression of osteoarthritis by regulating the YAP-RIPK1-NF-κB axis and influencing autophagy.

Journal of translational medicine·2026
Same author

RICTOR-mediated GPX4 downregulation regulates chondrocyte ferroptosis in osteoarthritis progression.

International immunopharmacology·2026

Related Experiment Video

Updated: Feb 23, 2026

Isolation of Chondrocytes and Chondroprogenitors Using Fibronectin Adhesion and Migratory Assay
08:09

Isolation of Chondrocytes and Chondroprogenitors Using Fibronectin Adhesion and Migratory Assay

Published on: October 4, 2024

1.3K

Basic fibroblast growth factor increases IFT88 expression in chondrocytes.

Daolu Zhan1, Wei Xiang2, Fengjing Guo2

  • 1Graduate School, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.

Molecular Medicine Reports
|September 14, 2017
PubMed
Summary
This summary is machine-generated.

Basic fibroblast growth factor (bFGF) boosts Intraflagellar transport protein 88 (IFT88) expression and primary cilia in chondrocytes. This process involves the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway.

More Related Videos

Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
08:30

Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity

Published on: February 24, 2017

10.1K
Differentiating Chondrocytes from Peripheral Blood-derived Human Induced Pluripotent Stem Cells
07:51

Differentiating Chondrocytes from Peripheral Blood-derived Human Induced Pluripotent Stem Cells

Published on: July 18, 2017

9.7K

Related Experiment Videos

Last Updated: Feb 23, 2026

Isolation of Chondrocytes and Chondroprogenitors Using Fibronectin Adhesion and Migratory Assay
08:09

Isolation of Chondrocytes and Chondroprogenitors Using Fibronectin Adhesion and Migratory Assay

Published on: October 4, 2024

1.3K
Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
08:30

Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity

Published on: February 24, 2017

10.1K
Differentiating Chondrocytes from Peripheral Blood-derived Human Induced Pluripotent Stem Cells
07:51

Differentiating Chondrocytes from Peripheral Blood-derived Human Induced Pluripotent Stem Cells

Published on: July 18, 2017

9.7K

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Primary cilia on chondrocytes are vital for mechanotransduction and chemosignaling.
  • The impact of cytokines on Intraflagellar transport protein 88 (IFT88) and cilia dynamics is not fully understood.

Purpose of the Study:

  • To investigate the role of basic fibroblast growth factor (bFGF) in regulating IFT88 expression and primary cilia formation in chondrocytes.
  • To elucidate the signaling pathways mediating bFGF's effects on IFT88 and cilia.

Main Methods:

  • ATDC5 chondrocytic cell line and primary chondrocytes were treated with bFGF.
  • IFT88 expression was analyzed using quantitative PCR and Western blotting.
  • Specific inhibitors (PD0325901 for ERK, BGJ398 for FGFR) and small interfering RNA (siRNA) targeting IFT88 were employed.
  • Cilia formation was assessed by counting ciliated cells.

Main Results:

  • bFGF dose- and time-dependently upregulated IFT88 mRNA and protein expression in ATDC5 cells and primary chondrocytes.
  • Inhibition of ERK or FGF receptor signaling, or IFT88 knockdown, suppressed bFGF-induced IFT88 upregulation.
  • bFGF treatment increased the number of ciliated cells, an effect abrogated by inhibiting the pathway or IFT88.
  • IFT88 knockdown also reduced ERK protein expression, suggesting a feedback loop.

Conclusions:

  • bFGF promotes IFT88 expression and primary cilia development in chondrocytes.
  • The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway is crucial for mediating bFGF's effects on IFT88.
  • These findings highlight a novel regulatory mechanism for cilia function in chondrocytes.