Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice / 国际口腔科学杂志·英文版
International Journal of Oral Science
; (4): 33-33, 2022.
Article
ي En
| WPRIM
| ID: wpr-939852
المكتبة المسؤولة:
WPRO
ABSTRACT
The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint (TMJ) osteoarthritis (OA); however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4 (Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2 and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore, Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.
النص الكامل:
1
الفهرس:
WPRIM
الموضوع الرئيسي:
Osteoarthritis
/
Temporomandibular Joint
/
Cartilage, Articular
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Chondrocytes
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Cytoskeletal Proteins
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Aggrecans
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Muscle Proteins
نوع الدراسة:
Etiology_studies
المحددات:
Animals
اللغة:
En
مجلة:
International Journal of Oral Science
السنة:
2022
نوع:
Article