ArticleBMC musculoskeletal disorders2017
GIT1 gene deletion delays chondrocyte differentiation and healing of tibial plateau fracture through suppressing proliferation and apoptosis of chondrocyte.
Article in BMC musculoskeletal disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Decoding Geniposide's Mechanism: From miR-208a-3p/SMAD5 Modulation To Osteoblast Proliferation and Differentiation.Applied biochemistry and biotechnology · 2026Article
- Dendronized chitosan hydrogel with GIT1 to accelerate bone defect repair through increasing local neovascular amount.Bone reports · 2023Article
- Temporal Pattern of micro-CT Angiography Vascular Parameters and VEGF mRNA Expression in Fracture Healing: a Radiograph and Molecular Comparison.European journal of dentistry · 2023Article
- Emerging role of mesenchymal stem/stromal cells (MSCs) and MSCs-derived exosomes in bone- and joint-associated musculoskeletal disorders: a new frontier.European journal of medical research · 2023Review
- Exosomes rewire the cartilage microenvironment in osteoarthritis: from intercellular communication to therapeutic strategies.International journal of oral science · 2022Review
- Single-cell RNA Seq reveals cellular landscape-specific characteristics and potential etiologies for adolescent idiopathic scoliosis.JOR spine · 2021Article
- GIT1 overexpression promotes epithelial-mesenchymal transition and predicts poor prognosis in hepatocellular carcinoma.Bioengineered · 2021Article
- LncRNA HAGLR absorbing miR-214-3p promotes BMP2 expression and improves tibial fractures.American journal of translational research · 2021Article
- Inhibiting GIT1 reduces the growth, invasion, and angiogenesis of osteosarcoma.Cancer management and research · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough tibial plateau fracture is an uncommon injury, its regulation is challenging and there are some influencing factors, including the effects of severe bone displacement, depression and cancellous bone cartilage, and inevitable cartilage damage. And GIT1 plays an important role in bone mass and 78 osteoblast cell migration.
methodsThe study used 72 C57/BL6 mice. A tibial plateau fracture model was established by using mice with the same number of GIT1 gene deletions (the experimental group) and their wild-type littermates (the control group). Joint and bone callus recovery were evaluated by X-ray and CT thin layer scans. Micro CT assay and histomorphometry were conducted in order to evaluate the volume of newly formed blood vessels. Type II collagen expression in tibial tissues after tibial plateau fracture were detected by immunohistochemistry after 7, 14 and 21 days. The number of proliferating cell nuclear antigen (PCNA) positive cells after tibial plateau fracture was tested by immunohistochemistry after 14 and 21 days. The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was conducted after 14 and 21 days in order to test chondrocyte apoptosis in tibial tissues after tibial plateau fracture.
resultsThe GIT1 gene deletion group mice spent less time on the rotating rod than the control group mice (P < 0.05). Compared with the control group, postoperative recovery was retarded, because GIT1 gene deletion slowed down neovascularization after tibial plateau fracture (P < 0.05). Compared with the control group, mouse type II collagen expression significantly decreased in the GIT1 gene deletion group, and the proportion of PCNA positive cells significantly decreased (P < 0.05). The TUNEL results indicate that GIT1 gene deletion led to reduced chondrocyte apoptosis.
conclusionGIT1 gene deletion can inhibit chondrocyte proliferation and apoptosis during the recovery of tibial plateau fracture, so as to delay chondrocyte differentiation and tibial plateau fracture healing.
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