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Positive‐Feedback Regulation of Subchondral H‐Type Vessel Formation by Chondrocyte Promotes Osteoarthritis Development in Mice
Journal of bone and mineral research, 2018-05, Vol.33 (5), p.909-920
Lu, Jiansen
Zhang, Haiyan
Cai, Daozhang
Zeng, Chun
Lai, Pinglin
Shao, Yan
Fang, Hang
Li, Delong
Ouyang, Jiayao
Zhao, Chang
Xie, Denghui
Huang, Bin
Yang, Jian
Jiang, Yu
Bai, Xiaochun
2018
Details
Autor(en) / Beteiligte
Lu, Jiansen
Zhang, Haiyan
Cai, Daozhang
Zeng, Chun
Lai, Pinglin
Shao, Yan
Fang, Hang
Li, Delong
Ouyang, Jiayao
Zhao, Chang
Xie, Denghui
Huang, Bin
Yang, Jian
Jiang, Yu
Bai, Xiaochun
Titel
Positive‐Feedback Regulation of Subchondral H‐Type Vessel Formation by Chondrocyte Promotes Osteoarthritis Development in Mice
Ist Teil von
Journal of bone and mineral research, 2018-05, Vol.33 (5), p.909-920
Ort / Verlag
United States: Wiley Subscription Services, Inc
Erscheinungsjahr
2018
Link zum Volltext
Quelle
Wiley Online Library
Beschreibungen/Notizen
ABSTRACT Vascular‐invasion‐mediated interactions between activated articular chondrocytes and subchondral bone are essential for osteoarthritis (OA) development. Here, we determined the role of nutrient sensing mechanistic target of rapamycin complex 1 (mTORC1) signaling in the crosstalk across the bone cartilage interface and its regulatory mechanisms. Then mice with chondrocyte‐specific mTORC1 activation (Tsc1 CKO and Tsc1 CKOER) or inhibition (Raptor CKOER) and their littermate controls were subjected to OA induced by destabilization of the medial meniscus (DMM) or not. DMM or Tsc1 CKO mice were treated with bevacizumab, a vascular endothelial growth factor (VEGF)‐A antibody that blocks angiogenesis. Articular cartilage degeneration was evaluated using the Osteoarthritis Research Society International score. Immunostaining and Western blotting were conducted to detect H‐type vessels and protein levels in mice. Primary chondrocytes from mutant mice and ADTC5 cells were treated with interleukin‐1β to investigate the role of chondrocyte mTORC1 in VEGF‐A secretion and in vitro vascular formation. Clearly, H‐type vessels were increased in subchondral bone in DMM‐induced OA and aged mice. Cartilage mTORC1 activation stimulated VEGF‐A production in articular chondrocyte and H‐type vessel formation in subchondral bone. Chondrocyte mTORC1 promoted OA partially through formation of VEGF‐A–stimulated subchondral H‐type vessels. In particular, vascular‐derived nutrients activated chondrocyte mTORC1, and stimulated chondrocyte activation and production of VEGF, resulting in further angiogenesis in subchondral bone. Thus a positive‐feedback regulation of H‐type vessel formation in subchondral bone by articular chondrocyte nutrient‐sensing mTORC1 signaling is essential for the pathogenesis and progression of OA. © 2018 American Society for Bone and Mineral Research
Sprache
Englisch
Identifikatoren
ISSN: 0884-0431
eISSN: 1523-4681
DOI: 10.1002/jbmr.3388
Titel-ID: cdi_proquest_miscellaneous_1989582387
Format
–
Schlagworte
ANGIOGENESIS
,
Arthritis
,
Bevacizumab
,
Bone growth
,
Cartilage (articular)
,
Cartilage diseases
,
CHONDROCYTE
,
Chondrocytes
,
Degeneration
,
Feedback
,
H‐TYPE VESSELS
,
Knee
,
Meniscus
,
Monoclonal antibodies
,
MTORC1
,
Nutrients
,
OSTEOARTHRITIS
,
Rapamycin
,
Subchondral bone
,
TOR protein
,
Tuberous Sclerosis Complex 1
,
Vascular endothelial growth factor
,
Western blotting
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