4.7 Article

Collagen XXIV (Col24α1) Promotes Osteoblastic Differentiation and Mineralization through TGF-β/Smads Signaling Pathway

期刊

INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 8, 期 10, 页码 1310-1322

出版社

IVYSPRING INT PUBL
DOI: 10.7150/ijbs.5136

关键词

COLLAGEN XXIV; Osteoblast differentiation; Bone mineralization; SMAD; Integrin

资金

  1. National Institutes of Health [AR055678, AR061052]
  2. NIAMS/NIH [AR055678, AR061052]

向作者/读者索取更多资源

Collagen XXIV (Col24 alpha 1) is a recently discovered fibrillar collagen. It is known that mouse Col24 alpha 1 is predominantly expressed in the forming skeleton of the mouse embryo, as well as in the trabecular bone and periosteum of the newborn mouse. However, the role and mechanism of Col24 alpha 1 in osteoblast differentiation and mineralization remains unclear. By analyzing the expression pattern of Col24 alpha 1, we confirmed that it is primarily expressed in bone tissues, and this expression gradually increased concomitant with the progression of osteoblast differentiation. Through the use of a lentivirus vector-mediated interference system, silencing Col24a1 expression in MC3T3-E1 murine preosteoblastic cells resulted in significant inhibition of alkaline phosphatase (ALP) activity, cell mineralization, and the expression of osteoblast marker genes such as runt-related transcription factor 2 (Runx2), osteocalcin (OCN), ALP, and type I collagen (Col I). Subsequent overexpression not only rescued the deficiency in osteoblast differentiation from Col24 alpha 1 silenced cells, but also enhanced osteoblastic differentiation in control cells. We further revealed that Col24 alpha 1 interacts with integrin beta 3, and silencing Col24 alpha 1 up-regulated the expression of Smad7 during osteoblast differentiation while at the same time inhibiting the phosphorylation of the Smad2/3 complex. These results suggest that Col24 alpha 1 imparts some of its regulatory control on osteoblast differentiation and mineralization at least partially through interaction with integrin beta 3 and the transforming growth factor beta (TGF-beta) / Smads signaling pathway.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据