当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Gain-of-function mutation of FGFR3 results in impaired fracture healing due to inhibition of chondrocyte differentiation.

Gain-of-function mutation of FGFR3 results in impaired fracture healing due to inhibition of chondrocyte differentiation.

Abstract：

:Fracture healing is a complicated regeneration process which to some extent recapitulates bone development. Fibroblast growth factor receptor 3 (FGFR3) has a negative regulatory effect on endochondral ossification, and FGFR3 is also expressed in prehypertrophic and hypertrophic chondrocytes during fracture healing. However, the actual role of FGFR3 during bone regeneration is not fully understood. Therefore we investigated the role of FGFR3 in fracture repair using a non-stabilized fracture model. Fracture repair in gain-of-function mutation of FGFR3 (Fgfr3(G369C/+)) mice was delayed, with more cartilage callus on day 14 and residue of cartilage in the callus on day 21. Histologic, in-situ hybridization and qRT-PCR analysis showed that differentiation of mesenchymal cells into chondrocytes and hypertrophic differentiation was delayed in Fgfr3(G369C/+) mice during fracture healing. These results indicated that activating mutation of FGFR3 could lead to impaired bone repair due to inhibition of chondrocyte differentiation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Su N,Yang J,Xie Y,Du X,Lu X,Yin Z,Yin L,Qi H,Zhao L,Feng J,Chen L

doi

10.1016/j.bbrc.2008.08.165

subject

Has Abstract

pub_date

2008-11-21 00:00:00

pages

454-9

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)01702-6

journal_volume

376

pub_type

杂志文章

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