Chondrocytes Promote Vascularization in Fracture Healing Through a FOXO1-Dependent Mechanism.
Animals
Cell Line
Chondrocytes
/ metabolism
Collagen Type II
/ biosynthesis
Down-Regulation
Endothelial Cells
/ pathology
Forkhead Box Protein O1
/ genetics
Fracture Healing
Gene Deletion
Mice
Mice, Transgenic
Neovascularization, Physiologic
Platelet Endothelial Cell Adhesion Molecule-1
/ biosynthesis
Transcription, Genetic
Vascular Endothelial Growth Factor A
/ biosynthesis
BONE
CHONDROCYTE AND CARTILAGE BIOLOGY
ChIP
FRACTURE HEALING
GENETIC ANIMAL MODELS
Journal
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
ISSN: 1523-4681
Titre abrégé: J Bone Miner Res
Pays: United States
ID NLM: 8610640
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
27
02
2018
revised:
08
10
2018
accepted:
11
10
2018
pubmed:
23
10
2018
medline:
23
6
2020
entrez:
23
10
2018
Statut:
ppublish
Résumé
Chondrocytes play an essential role in fracture healing by producing cartilage, which forms an anlage for endochondral ossification that stabilizes the healing fracture callus. More recently it has been appreciated that chondrocytes have the capacity to produce factors that may affect the healing process. We examined the role of chondrocytes in angiogenesis during fracture healing and the role of the transcription factor forkhead box-O 1 (FOXO1), which upregulates wound healing in soft tissue. Closed fractures were induced in experimental mice with lineage-specific FOXO1 deletion by Cre recombinase under the control of a collagen-2α1 promoter element (Col2α1Cre
Identifiants
pubmed: 30347467
doi: 10.1002/jbmr.3610
pmc: PMC6414243
mid: NIHMS1004521
doi:
Substances chimiques
Col2a1 protein, mouse
0
Collagen Type II
0
Forkhead Box Protein O1
0
Foxo1 protein, mouse
0
Pecam1 protein, mouse
0
Platelet Endothelial Cell Adhesion Molecule-1
0
Vascular Endothelial Growth Factor A
0
vascular endothelial growth factor A, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
547-556Subventions
Organisme : NIAMS NIH HHS
ID : R01 AR060055
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR069044
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE017732
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE019108
Pays : United States
Informations de copyright
© 2018 American Society for Bone and Mineral Research.
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