Microarray analysis of gene expression during the inflammation and endochondral bone formation stages of rat femur fracture repair

Bone ◽  
2006 ◽  
Vol 38 (4) ◽  
pp. 521-529 ◽  
Author(s):  
Charles H. Rundle ◽  
Hali Wang ◽  
Hongrun Yu ◽  
Robert B. Chadwick ◽  
Emile I. Davis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Formation ◽  
Microarray Analysis ◽  
Femur Fracture ◽  
Fracture Repair ◽  
Rat Femur ◽  
Endochondral Bone Formation ◽  
Endochondral Bone

scholarly journals Prolyl Hydroxylase Domain-Containing Protein 3 Gene Expression in Chondrocytes Is Not Essential for Bone Development in Mice

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2200
Author(s):  
Weirong Xing ◽  
Sheila Pourteymoor ◽  
Gustavo A. Gomez ◽  
Yian Chen ◽  
Subburaman Mohan
Keyword(s):  
Gene Expression ◽  
Bone Formation ◽  
Bone Mass ◽  
Trabecular Bone ◽  
Bone Volume ◽  
Endochondral Bone Formation ◽  
Chondrocyte Differentiation ◽  
Trabecular Bone Volume ◽  
Endochondral Bone ◽  
Trabecular Bone Mass

We previously showed that conditional disruption of the Phd2 gene in chondrocytes led to a massive increase in long bone trabecular bone mass. Loss of Phd2 gene expression or inhibition of PHD2 activity by a specific inhibitor resulted in a several-fold compensatory increase in Phd3 expression in chondrocytes. To determine if expression of PHD3 plays a role in endochondral bone formation, we conditionally disrupted the Phd3 gene in chondrocytes by crossing Phd3 floxed (Phd3flox/flox) mice with Col2α1-Cre mice. Loss of Phd3 expression in the chondrocytes of Cre+; Phd3flox/flox conditional knockout (cKO) mice was confirmed by real time PCR. At 16 weeks of age, neither body weight nor body length was significantly different in the Phd3 cKO mice compared to Cre−; Phd3flox/flox wild-type (WT) mice. Areal BMD measurements of total body as well as femur, tibia, and lumbar skeletal sites were not significantly different between the cKO and WT mice at 16 weeks of age. Micro-CT measurements revealed significant gender differences in the trabecular bone volume adjusted for tissue volume at the secondary spongiosa of the femur and the tibia for both genotypes, but no genotype difference was found for any of the trabecular bone measurements of either the femur or the tibia. Trabecular bone volume of distal femur epiphysis was not different between cKO and WT mice. Histology analyses revealed Phd3 cKO mice exhibited a comparable chondrocyte differentiation and proliferation, as evidenced by no changes in cartilage thickness and area in the cKO mice as compared to WT littermates. Consistent with the in vivo data, lentiviral shRNA-mediated knockdown of Phd3 expression in chondrocytes did not affect the expression of markers of chondrocyte differentiation (Col2, Col10, Acan, Sox9). Our study found that Phd2 but not Phd3 expressed in chondrocytes regulates endochondral bone formation, and the compensatory increase in Phd3 expression in the chondrocytes of Phd2 cKO mice is not the cause for increased trabecular bone mass in Phd2 cKO mice.

scholarly journals Roles of Chondrocytes in Endochondral Bone Formation and Fracture Repair

2016 ◽  
Vol 96 (1) ◽  
pp. 23-30 ◽  
Author(s):  
R.J. Hinton ◽  
Y. Jing ◽  
J. Jing ◽  
J.Q. Feng
Keyword(s):  
Bone Formation ◽  
Fracture Repair ◽  
Endochondral Bone Formation ◽  
Endochondral Bone

Microarray analysis on Runx2-deficient mouse embryos reveals novel Runx2 functions and target genes during intramembranous and endochondral bone formation

Bone ◽  
2006 ◽  
Vol 39 (4) ◽  
pp. 724-738 ◽  
Author(s):  
Bart L.T. Vaes ◽  
Patricia Ducy ◽  
Anneke M. Sijbers ◽  
José M.A. Hendriks ◽  
Eugene P. van Someren ◽  
...  
Keyword(s):  
Bone Formation ◽  
Microarray Analysis ◽  
Target Genes ◽  
Mouse Embryos ◽  
Endochondral Bone Formation ◽  
Deficient Mouse ◽  
Endochondral Bone

scholarly journals Ablation of Ephrin B2 in Col2 Expressing Cells Delays Fracture Repair

Endocrinology ◽  
2020 ◽  
Vol 161 (12) ◽  
Author(s):  
Yongmei Wang ◽  
Lin Ling ◽  
Faming Tian ◽  
Sun Hee Won Kim ◽  
Sunita Ho ◽  
...  
Keyword(s):  
Bone Formation ◽  
Cell Activation ◽  
Bone Development ◽  
Type Ii Collagen ◽  
Fracture Site ◽  
Fracture Repair ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Intramembranous Bone ◽  
Endothelial Growth Factor

Abstract Ephrin B2 is critical for endochondral bone development. In this study, we investigated its role in fracture repair by deleting ephrin B2 in type II collagen (Col.2) expressing cells. We used a nonstable tibia fracture model to evaluate fracture repair at 3 sites: intramembranous bone formation, endochondral bone formation, and intramedullary bone formation. We observed that during fracture repair, deletion of ephrin B2 impaired periosteal stem cell activation, inhibited their proliferation, decreased their survival, and blocked their differentiation into osteoblasts and chondrocytes. In addition, deletion of ephrin B2 decreased vascular endothelial growth factor production as well as vascular invasion into the fracture site. These changes led to reduced cartilage to bone conversion in the callus with decreased new bone formation, resulting in impaired fracture repair. Our data indicate that ephrin B2 in Col2-expressing cells is a critical regulator of fracture repair, pointing to a new and potentially targetable mechanism to enhance fracture repair.

scholarly journals The culture microenvironment of juvenile idiopathic arthritis synovial fibroblasts is favorable for endochondral bone formation through BMP4 and repressed by chondrocytes

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Megan M. Simonds ◽  
Amanda R. Schlefman ◽  
Suzanne M. McCahan ◽  
Kathleen E. Sullivan ◽  
Carlos D. Rose ◽  
...  
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Bone Formation ◽  
Synovial Fibroblasts ◽  
Conditioned Media ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Member Gene ◽  
Bmp Antagonist ◽  
Fibroblast Like Synoviocytes ◽  
Tgfβ Superfamily

Abstract Background We examined influences of conditioned media from chondrocytes (Ch) on juvenile idiopathic arthritis synovial fibroblasts (JFLS) and potential for JFLS to undergo endochondral bone formation (EBF). Methods Primary cells from three control fibroblast-like synoviocytes (CFLS) and three JFLS were cultured in Ch-conditioned media and compared with untreated fibroblast-like synoviocytes (FLS). RNA was analyzed by ClariomS microarray. FLS cells cultured in conditioned media were exposed to either TGFBR1 inhibitor LY3200882 or exogenous BMP4 and compared with FLS cultured in conditioned media from Ch (JFLS-Ch). Media supernatants were analyzed by ELISA. Results In culture, JFLS downregulate BMP2 and its receptor BMPR1a while upregulating BMP antagonists (NOG and CHRD) and express genes (MMP9, PCNA, MMP12) and proteins (COL2, COLX, COMP) associated with chondrocytes. Important TGFβ superfamily member gene expression (TGFBI, MMP9, COL1A1, SOX6, and MMP2) is downregulated when JFLS are cultured in Ch-conditioned media. COL2, COLX and COMP protein expression decreases in JFLS-Ch. BMP antagonist protein (NOG, CHRD, GREM, and FST) secretion is significantly increased in JFLS-Ch. Protein phosphorylation increases in JFLS-Ch exposed to exogenous BMP4, and chondrocyte-like phenotype is restored in BMP4 presence, evidenced by increased secretion of COL2 and COLX. Inhibition of TGFBR1 in JFLS-Ch results in overexpression of COL2. Conclusions JFLS are chondrocyte-like, and Ch-conditioned media can abrogate this phenotype. The addition of exogenous BMP4 causes JFLS-Ch to restore this chondrocyte-like phenotype, suggesting that JFLS create a microenvironment favorable for endochondral bone formation, thereby contributing to joint growth disturbances in juvenile idiopathic arthritis.

scholarly journals Intraflagellar transport is essential for endochondral bone formation

Development ◽  
2007 ◽  
Vol 134 (2) ◽  
pp. 307-316 ◽  
Author(s):  
C. J. Haycraft ◽  
Q. Zhang ◽  
B. Song ◽  
W. S. Jackson ◽  
P. J. Detloff ◽  
...  
Keyword(s):  
Bone Formation ◽  
Intraflagellar Transport ◽  
Endochondral Bone Formation ◽  
Endochondral Bone

scholarly journals Osteoblast‐Specific Loss of IGF1R Signaling Results in Impaired Endochondral Bone Formation During Fracture Healing

2015 ◽  
Vol 30 (9) ◽  
pp. 1572-1584 ◽  
Author(s):  
Tao Wang ◽  
Yongmei Wang ◽  
Alicia Menendez ◽  
Chak Fong ◽  
Muriel Babey ◽  
...  
Keyword(s):  
Bone Formation ◽  
Fracture Healing ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Specific Loss ◽  
Igf1r Signaling
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