TRPV2 is involved in induction of lubricin and suppression of ectopic endochondral ossification in articular joints

2021 ◽  
Author(s):  
Hideki Nakamoto ◽  
Yuki Katanosaka ◽  
Ryota Chijimatsu ◽  
Daisuke Mori ◽  
Fengjun Xuan ◽  
...  
Keyword(s):  
Endochondral Ossification

scholarly journals Activation of β–catenin-LEF/TCF signal pathway in chondrocytes stimulates ectopic endochondral ossification

2003 ◽  
Vol 11 (1) ◽  
pp. 36-43 ◽  
Author(s):  
J. Kitagaki ◽  
M. Iwamoto ◽  
J.-G. Liu ◽  
Y. Tamamura ◽  
M. Pacifci ◽  
...  
Keyword(s):  
Endochondral Ossification ◽  
Signal Pathway

scholarly journals PP2A in LepR+ mesenchymal stem cells contributes to embryonic and postnatal endochondral ossification through Runx2 dephosphorylation

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yu-Ting Yen ◽  
May Chien ◽  
Pei-Yi Wu ◽  
Shih-Chieh Hung
Keyword(s):  
Stem Cells ◽  
Alkaline Phosphatase ◽  
Mesenchymal Stem Cells ◽  
Bone Density ◽  
Endochondral Ossification ◽  
Bone Growth ◽  
Leptin Receptor ◽  
Trabecular Bone Density ◽  
Mature Adipocyte ◽  
Ossification Centers

AbstractIt has not been well studied which cells and related mechanisms contribute to endochondral ossification. Here, we fate mapped the leptin receptor-expressing (LepR+) mesenchymal stem cells (MSCs) in different embryonic and adult extremities using Lepr-cre; tdTomato mice and investigated the underling mechanism using Lepr-cre; Ppp2r1afl/fl mice. Tomato+ cells appear in the primary and secondary ossification centers and express the hypertrophic markers. Ppp2r1a deletion in LepR+ MSCs reduces the expression of Runx2, Osterix, alkaline phosphatase, collagen X, and MMP13, but increases that of the mature adipocyte marker perilipin, thereby reducing trabecular bone density and enhancing fat content. Mechanistically, PP2A dephosphorylates Runx2 and BRD4, thereby playing a major role in positively and negatively regulating osteogenesis and adipogenesis, respectively. Our data identify LepR+ MSC as the cell origin of endochondral ossification during embryonic and postnatal bone growth and suggest that PP2A is a therapeutic target in the treatment of dysregulated bone formation.

scholarly journals The Skull’s Girder: A Brief Review of the Cranial Base

2021 ◽  
Vol 9 (1) ◽  
pp. 3
Author(s):  
Shankar Rengasamy Venugopalan ◽  
Eric Van Otterloo
Keyword(s):  
Birth Defects ◽  
Vertebral Column ◽  
Endochondral Ossification ◽  
Cranial Base ◽  
Facial Skeleton ◽  
The Core ◽  
Skull Vault ◽  
Congenital Birth Defects ◽  
Intimate Association ◽  
The Brain

The cranial base is a multifunctional bony platform within the core of the cranium, spanning rostral to caudal ends. This structure provides support for the brain and skull vault above, serves as a link between the head and the vertebral column below, and seamlessly integrates with the facial skeleton at its rostral end. Unique from the majority of the cranial skeleton, the cranial base develops from a cartilage intermediate—the chondrocranium—through the process of endochondral ossification. Owing to the intimate association of the cranial base with nearly all aspects of the head, congenital birth defects impacting these structures often coincide with anomalies of the cranial base. Despite this critical importance, studies investigating the genetic control of cranial base development and associated disorders lags in comparison to other craniofacial structures. Here, we highlight and review developmental and genetic aspects of the cranial base, including its transition from cartilage to bone, dual embryological origins, and vignettes of transcription factors controlling its formation.

scholarly journals Bone defect reconstruction via endochondral ossification: A developmental engineering strategy

2021 ◽  
Vol 12 ◽  
pp. 204173142110042
Author(s):  
Rao Fu ◽  
Chuanqi Liu ◽  
Yuxin Yan ◽  
Qingfeng Li ◽  
Ru-Lin Huang
Keyword(s):  
Bone Regeneration ◽  
Bone Defect ◽  
Bone Repair ◽  
Endochondral Ossification ◽  
Current Knowledge ◽  
Endochondral Bone ◽  
Defect Reconstruction ◽  
Hypoxic Conditions ◽  
Bone Defect Reconstruction

Traditional bone tissue engineering (BTE) strategies induce direct bone-like matrix formation by mimicking the embryological process of intramembranous ossification. However, the clinical translation of these clinical strategies for bone repair is hampered by limited vascularization and poor bone regeneration after implantation in vivo. An alternative strategy for overcoming these drawbacks is engineering cartilaginous constructs by recapitulating the embryonic processes of endochondral ossification (ECO); these constructs have shown a unique ability to survive under hypoxic conditions as well as induce neovascularization and ossification. Such developmentally engineered constructs can act as transient biomimetic templates to facilitate bone regeneration in critical-sized defects. This review introduces the concept and mechanism of developmental BTE, explores the routes of endochondral bone graft engineering, highlights the current state of the art in large bone defect reconstruction via ECO-based strategies, and offers perspectives on the challenges and future directions of translating current knowledge from the bench to the bedside.

scholarly journals Transcutaneous CO2 application accelerates fracture repair in streptozotocin-induced type I diabetic rats

2020 ◽  
Vol 8 (2) ◽  
pp. e001129
Author(s):  
Takahiro Oda ◽  
Takahiro Niikura ◽  
Tomoaki Fukui ◽  
Keisuke Oe ◽  
Yu Kuroiwa ◽  
...  
Keyword(s):  
Endochondral Ossification ◽  
Callus Formation ◽  
Femoral Shaft ◽  
Shaft Fracture ◽  
Diabetic Rats ◽  
Fracture Repair ◽  
Female Rats ◽  
Control Group ◽  
Type I ◽  
Biomechanical Assessment

IntroductionDiabetes mellitus (DM) negatively affects fracture repair by inhibiting endochondral ossification, chondrogenesis, callus formation, and angiogenesis. We previously reported that transcutaneous CO2 application accelerates fracture repair by promoting endochondral ossification and angiogenesis. The present study aimed to determine whether CO2 treatment would promote fracture repair in cases with type I DM.Research design and methodsA closed femoral shaft fracture was induced in female rats with streptozotocin-induced type I DM. CO2 treatment was performed five times a week for the CO2 group. Sham treatment, where CO2 was replaced with air, was performed for the control group. Radiographic, histologic, genetic, and biomechanical measurements were taken at several time points.ResultsRadiographic assessment demonstrated that fracture repair was induced in the CO2 group. Histologically, accelerated endochondral ossification and capillary formation were observed in the CO2 group. Immunohistochemical assessment indicated that early postfracture proliferation of chondrocytes in callus was enhanced in the CO2 group. Genetic assessment results suggested that cartilage and bone formation, angiogenesis, and vasodilation were upregulated in the CO2 group. Biomechanical assessment revealed enhanced mechanical strength in the CO2 group.ConclusionsOur findings suggest that CO2 treatment accelerates fracture repair in type I DM rats. CO2 treatment could be an effective strategy for delayed fracture repair due to DM.

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