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Published on: December 3, 2016
Fibroblast growth factor 7 (FGF7) causes cartilage destruction, subchondral bone remodeling, and the premature growth
Youngnim Shin1, Ji-Sun Kwak1, Seul Ki Kim1
1National Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 61005, Republic of Korea.
Objective:
Fibroblast growth factor (FGF) signaling plays a significant role in osteoarthritis (OA) pathogenesis, though the OA-related functions of only a few FGFs have been fully elucidated. This study investigates the specific roles of FGF7 in OA development.
Methods:
FGF7 expression was analyzed in human (n=6) and mouse (n=10) cartilage. Experimental OA was induced by destabilization of the medial meniscus (DMM). The roles of FGF7 were explored using intra-articular (IA) injection of recombinant FGF7 (rFGF7) and whole-body Fgf7 knockout mice (Fgf7-/-). Subchondral bone remodeling and growth plate morphology were assessed micro computed tomography (µCT) and histological analysis.
Results:
FGF7 was upregulated in OA cartilage. IA injection of rFGF7 led to OA cartilage destruction (OARSI [Osteoarthritis Research Society International] grade; 0.61 [95% CI 0.00-5.33]), while Fgf7-/- mice showed reduced DMM-induced cartilage erosion (OARSI grade; 1.89 [95% CI 1.08-3.00]) compared to wild-type mice (4.92 [95% CI 3.83-5.33]). These effects were associated with changes in matrix-degrading enzyme expression in chondrocytes. Mice receiving IA injection of rFGF7 (20 μg) exhibited increased subchondral bone thickness (68.01 µm [95% CI 61.55-74.46]) and decreased osteoclastogenesis (tartrate-resistant acid phosphatase positivity; 1.94% [95% CI 1.41-2.47]) compared to controls (38.33 µm [95% CI 33.71-42.96]) and (4.23% [95% CI 3.28-5.19]), respectively. Additionally, rFGF7 treatment caused premature closure of growth plates, whereas Fgf7-/- mice exhibited significantly increased growth plate thickness.
Conclusions:
FGF7 exerts multiple functions in various joint tissues, including promoting cartilage destruction, inducing subchondral bone remodeling (SBP thickening), and triggering premature growth plate closure.
Insights
Fibroblast growth factor 7 (FGF7) promotes osteoarthritis by damaging cartilage and altering bone. FGF7 knockout mice show reduced osteoarthritis, highlighting FGF7
Area of Science:
- Biochemistry
- Cell Biology
- Orthopedics
Background:
- Fibroblast growth factor (FGF) signaling is crucial in osteoarthritis (OA) pathogenesis.
- The specific roles of many FGFs in OA remain unclear.
- This study focuses on the function of FGF7 in OA development.
Purpose of the Study:
- To investigate the specific roles of FGF7 in osteoarthritis development.
- To analyze FGF7 expression in human and mouse cartilage.
- To explore the effects of FGF7 manipulation on OA pathogenesis.
Main Methods:
- Analyzed FGF7 expression in human and mouse cartilage.
- Induced experimental osteoarthritis using destabilization of the medial meniscus (DMM) in mice.
- Administered intra-articular (IA) injection of recombinant FGF7 (rFGF7) and utilized whole-body Fgf7 knockout mice (Fgf7-/-).
- Assessed subchondral bone remodeling and growth plate morphology via micro computed tomography (µCT) and histological analysis.
Main Results:
- FGF7 expression was upregulated in OA cartilage.
- IA injection of rFGF7 exacerbated OA cartilage destruction, while Fgf7-/- mice exhibited reduced DMM-induced cartilage erosion compared to wild-type controls.
- rFGF7 treatment increased subchondral bone thickness and decreased osteoclastogenesis, whereas Fgf7-/- mice showed altered growth plate morphology, including premature closure with rFGF7 and increased thickness in knockout mice.
Conclusions:
- FGF7 plays a significant role in osteoarthritis pathogenesis.
- FGF7 promotes cartilage destruction and subchondral bone remodeling.
- FGF7 influences growth plate closure, indicating its multifaceted role in joint tissue homeostasis.
