KDELR2 promotes bone marrow mesenchymal stem cell osteogenic differentiation via GSK3β/β-catenin signaling pathway

被引：2

作者：

Wu, Xiaoyong ^{[1
,2
,3
,4
]}

Zhang, Weijun ^{[1
,2
,3
,4
]}

Long, Long ^{[1
,2
,3
,4
,5
]}

Wang, Yibo ^{[6
,7
]}

Chen, Hongyu ^{[1
,2
,3
,4
]}

Wang, Kanbin ^{[1
,2
,3
,4
]}

Wang, Zhongxiang ^{[1
,2
,3
,4
]}

Bai, Jinwu ^{[1
,2
,3
,4
]}

Xue, Deting ^{[1
,2
,3
,4
]}

Pan, Zhijun ^{[1
,2
,3
,4
]}

机构：

[1] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Orthoped Surg, 88 Jiefang Rd, Hangzhou 310009, Peoples R China

[2] Zhejiang Univ, Orthoped Res Inst, 88 Jiefang Rd, Hangzhou 310009, Peoples R China

[3] Key Lab Motor Syst Dis Res & Precis Therapy Zhejia, Hangzou City, Zhejiang, Peoples R China

[4] Clin Res Ctr Motor Syst Dis Zhejiang Prov, Hangzhou, Peoples R China

[5] Linping Hosp Integrated Chinese & Western Med, 60,Baojian Rd, Hangzhou 310009, Peoples R China

[6] Sun Yat Sen Univ, Affiliated Hosp 1, Guangdong Prov Key Lab Orthoped & Traumatol, Guangzhou 510080, Peoples R China

[7] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Spine Surg, Guangzhou, Peoples R China

来源：

CELL AND TISSUE RESEARCH | 2024年 / 396卷 / 02期

基金：

中国国家自然科学基金;

关键词：

KDELR2; Osteogenesis; mBMSCs; GSK3; beta/beta-catenin; BOVINE ENDOMETRIUM; CHEMOKINE CCL2; INTERFERON; EXPRESSION; PROLIFERATION; PREGNANCY; GENES; ROLES; CCR2;

D O I：

10.1007/s00441-024-03884-9

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Nonunion is a challenging complication of fractures for the surgeon. Recently the Lys-Asp-Glu-Leu (KDEL) endoplasmic reticulum protein retention receptor 2 (KDELR2) has been found that involved in osteogenesis imperfecta. However, the exact mechanism is still unclear. In this study, we used lentivirus infection and mouse fracture model to investigate the role of KDELR2 in osteogenesis. Our results showed that KDELR2 knockdown inhibited the osteogenic differentiation of mBMSCs, whereas KDELR2 overexpression had the opposite effect. Furthermore, the levels of active-beta-catenin and phospho-GSK3 beta (Ser9) were upregulated by KDELR2 overexpression and downregulated by KDELR2 knockdown. In the fracture model, mBMSCs overexpressing KDELR2 promoted healing. In conclusion, KDELR2 promotes the osteogenesis of mBMSCs by regulating the GSK3 beta/beta-catenin signaling pathway.

引用

页码：269 / 281

页数：13

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