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Yue XI, Qifeng JIANG, Wei DAI, Chaozhen CHEN, Yang WANG, Xiaoyan MIAO, Kaichen LAI, Zhiwei JIANG, Guoli YANG, Ying WANG. SP7 transcription factor ameliorates bone defect healing in low-density lipoprotein receptor-related protein 5-dependent osteoporosis mice[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .
@article{title="SP7 transcription factor ameliorates bone defect healing in low-density lipoprotein receptor-related protein 5-dependent osteoporosis mice",
author="Yue XI, Qifeng JIANG, Wei DAI, Chaozhen CHEN, Yang WANG, Xiaoyan MIAO, Kaichen LAI, Zhiwei JIANG, Guoli YANG, Ying WANG",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2300531"
}
%0 Journal Article
%T SP7 transcription factor ameliorates bone defect healing in low-density lipoprotein receptor-related protein 5-dependent osteoporosis mice
%A Yue XI
%A Qifeng JIANG
%A Wei DAI
%A Chaozhen CHEN
%A Yang WANG
%A Xiaoyan MIAO
%A Kaichen LAI
%A Zhiwei JIANG
%A Guoli YANG
%A Ying WANG
%J Journal of Zhejiang University SCIENCE B
%V -1
%N -1
%P
%@ 1673-1581
%D 1998
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2300531
TY - JOUR
T1 - SP7 transcription factor ameliorates bone defect healing in low-density lipoprotein receptor-related protein 5-dependent osteoporosis mice
A1 - Yue XI
A1 - Qifeng JIANG
A1 - Wei DAI
A1 - Chaozhen CHEN
A1 - Yang WANG
A1 - Xiaoyan MIAO
A1 - Kaichen LAI
A1 - Zhiwei JIANG
A1 - Guoli YANG
A1 - Ying WANG
J0 - Journal of Zhejiang University Science B
VL - -1
IS - -1
SP -
EP -
%@ 1673-1581
Y1 - 1998
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2300531
Abstract: Loss-of-function variants in the low-density lipoprotein receptor-related protein 5 (LRP5) can lead to reduced bone formation, culminating in diminished bone mass. Our previous study reported SP7 transcription factor (SP7) binding sites on the LRP5 promoter and its pivotal role in upregulating LRP5 expression during implant osseointegration. However, the potential role of SP7 in ameliorating LRP5-dependent osteoporosis remained unknown. In this study, we used mice with a conditional knockout (cKO) of LRP5 in mature osteoblasts, which presented decreased osteogenesis. The in vitro experimental results showed that SP7 could promote LRP5 expression, thereby upregulating the osteogenic markers such as alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2) and β-catenin (P < 0.05). For the in vivo experiment, the SP7 overexpression virus was injected into a bone defect model of LRP5 cKO mice, resulting in increased bone mineral density (BMD) (P < 0.001), volumetric density (bone volume (BV) / total volume (TV)) (P < 0.001) and decreased trabecular separation (Tb. Sp) (P < 0.05). These data suggested that SP7 could ameliorate bone defect healing in LRP5 cKO mice. Our study provides new insights into potential therapeutic opportunities for ameliorating LRP5-dependent osteoporosis.
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