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硬化蛋白调节纤维软骨附着点的矿化程度和硬度分布，以维持组织的机械完整性。

Sclerostin modulates mineralization degree and stiffness profile in the fibrocartilaginous enthesis for mechanical tissue integrity.

作者信息

Yambe Shinsei, Yoshimoto Yuki, Ikeda Kazutaka, Maki Koichiro, Takimoto Aki, Tokuyama Akihide, Higuchi Shinnosuke, Yu Xinyi, Uchibe Kenta, Miura Shigenori, Watanabe Hitomi, Sakuma Tetsushi, Yamamoto Takashi, Tanimoto Kotaro, Kondoh Gen, Kasahara Masataka, Mizoguchi Toshihide, Docheva Denitsa, Adachi Taiji, Shukunami Chisa

机构信息

Department of Molecular Biology and Biochemistry, Division of Dental Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Department of Orthodontics and Craniofacial Developmental Biology, Applied Life Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

出版信息

Front Cell Dev Biol. 2024 Jun 4;12:1360041. doi: 10.3389/fcell.2024.1360041. eCollection 2024.

DOI:10.3389/fcell.2024.1360041
PMID:38895158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11183276/
Abstract

Fibrocartilaginous entheses consist of tendons, unmineralized and mineralized fibrocartilage, and subchondral bone, each exhibiting varying stiffness. Here we examined the functional role of sclerostin, expressed in mature mineralized fibrochondrocytes. Following rapid mineralization of unmineralized fibrocartilage and concurrent replacement of epiphyseal hyaline cartilage by bone, unmineralized fibrocartilage reexpanded after a decline in alkaline phosphatase activity at the mineralization front. Sclerostin was co-expressed with osteocalcin at the base of mineralized fibrocartilage adjacent to subchondral bone. In -deficient mice with less mechanical loading due to defects of the Achilles tendon, sclerostin fibrochondrocyte count significantly decreased in the defective enthesis where chondrocyte maturation was markedly impaired in both fibrocartilage and hyaline cartilage. Loss of the gene, encoding sclerostin, elevated mineral density in mineralized zones of fibrocartilaginous entheses. Atomic force microscopy analysis revealed increased fibrocartilage stiffness. These lines of evidence suggest that sclerostin in mature mineralized fibrochondrocytes acts as a modulator for mechanical tissue integrity of fibrocartilaginous entheses.

摘要

纤维软骨附着点由肌腱、未矿化和矿化的纤维软骨以及软骨下骨组成，每一部分都表现出不同的硬度。在这里，我们研究了在成熟矿化纤维软骨细胞中表达的硬化蛋白的功能作用。在未矿化纤维软骨快速矿化以及骨骺透明软骨同时被骨替代后，矿化前沿碱性磷酸酶活性下降，未矿化纤维软骨重新扩张。硬化蛋白与骨钙素在靠近软骨下骨的矿化纤维软骨基部共同表达。在由于跟腱缺陷导致机械负荷较小的 - 缺陷小鼠中，硬化蛋白纤维软骨细胞数量在缺陷附着点显著减少，在该附着点，纤维软骨和透明软骨中的软骨细胞成熟均明显受损。编码硬化蛋白的 基因缺失导致纤维软骨附着点矿化区域的矿物质密度升高。原子力显微镜分析显示纤维软骨硬度增加。这些证据表明，成熟矿化纤维软骨细胞中的硬化蛋白作为纤维软骨附着点机械组织完整性的调节因子发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/fdbeb563b30e/fcell-12-1360041-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/1204334464ce/fcell-12-1360041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/4563736a0098/fcell-12-1360041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/598c61fb6b19/fcell-12-1360041-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/3fe63a54dfcf/fcell-12-1360041-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/f9755eedfee9/fcell-12-1360041-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/d8b9031b793a/fcell-12-1360041-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/9d985654234e/fcell-12-1360041-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/fdbeb563b30e/fcell-12-1360041-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/1204334464ce/fcell-12-1360041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/4563736a0098/fcell-12-1360041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/598c61fb6b19/fcell-12-1360041-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/3fe63a54dfcf/fcell-12-1360041-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/f9755eedfee9/fcell-12-1360041-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/d8b9031b793a/fcell-12-1360041-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/9d985654234e/fcell-12-1360041-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5630/11183276/fdbeb563b30e/fcell-12-1360041-g008.jpg

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