Discovery of Sonic hedgehog expression in postnatal growth plate chondrocytes: Differential regulation of Sonic and Indian hedgehog by retinoic acid

2002 ◽  
Vol 87 (2) ◽  
pp. 173-187 ◽  
Author(s):  
Licia N.Y. Wu ◽  
Min Lu ◽  
Brian R. Genge ◽  
George Y. Guo ◽  
Daotai Nie ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Growth Plate ◽  
Sonic Hedgehog ◽  
Postnatal Growth ◽  
Differential Regulation ◽  
Indian Hedgehog ◽  
Growth Plate Chondrocytes

Both retinoic acid and 1,25(OH)2 vitamin D3 inhibit thyroid hormone-induced terminal differentiaton of growth plate chondrocytes

2001 ◽  
Vol 19 (1) ◽  
pp. 43-49 ◽  
Author(s):  
R. Tracy Ballock ◽  
Xiaolan Zhou ◽  
Lynn M. Mink ◽  
Daniel H. C. Chen ◽  
Barry C. Mita
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Growth Plate ◽  
Vitamin D3 ◽  
Growth Plate Chondrocytes

scholarly journals Role of G-proteins in the differentiation of epiphyseal chondrocytes

2014 ◽  
Vol 53 (2) ◽  
pp. R39-R45 ◽  
Author(s):  
Andrei S Chagin ◽  
Henry M Kronenberg
Keyword(s):  
G Protein ◽  
G Proteins ◽  
Growth Plate ◽  
Current Knowledge ◽  
Postnatal Growth ◽  
Chondrocyte Differentiation ◽  
Growth Plate Chondrocytes ◽  
Α Subunit ◽  
G Protein Coupled

Herein, we review the regulation of differentiation of the growth plate chondrocytes by G-proteins. In connection with this, we summarize the current knowledge regarding each family of G-protein α subunit, specifically, Gαs, Gαq/11, Gα12/13, and Gαi/o. We discuss different mechanisms involved in chondrocyte differentiation downstream of G-proteins and different G-protein-coupled receptors (GPCRs) activating G-proteins in the epiphyseal chondrocytes. We conclude that among all G-proteins and GPCRs expressed by chondrocytes, Gαshas the most important role and prevents premature chondrocyte differentiation. Receptor for parathyroid hormone (PTHR1) appears to be the major activator of Gαsin chondrocytes and ablation of either one leads to accelerated chondrocyte differentiation, premature fusion of the postnatal growth plate, and ultimately short stature.

scholarly journals Organization of the Indian hedgehog – parathyroid hormone-related protein system in the postnatal growth plate

2011 ◽  
Vol 47 (1) ◽  
pp. 99-107 ◽  
Author(s):  
Michael Chau ◽  
Patricia Forcinito ◽  
Anenisia C Andrade ◽  
Anita Hegde ◽  
Sohyun Ahn ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Growth Plate ◽  
Feedback Loop ◽  
Postnatal Growth ◽  
Indian Hedgehog ◽  
Related Protein ◽  
Functional Changes ◽  
Growth Cartilage ◽  
Embryonic Growth ◽  
Parathyroid Hormone Related Protein

In embryonic growth cartilage, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP) participate in a negative feedback loop that regulates chondrocyte differentiation. Postnatally, this region undergoes major structural and functional changes. To explore the organization of the Ihh–PTHrP system in postnatal growth plate, we microdissected growth plates of 7-day-old rats into their constituent zones and assessed expression of genes participating in the Ihh–PTHrP feedback loop.Ihh, Patched 1, Smoothened,Gli1, Gli2, Gli3, andPthr1were expressed in regions analogous to the expression domains in embryonic growth cartilage. However, PTHrP was expressed in resting zone cartilage, a site that differs from the embryonic source, the periarticular cells. We then used mice in whichlacZhas replaced coding sequences ofGli1and thus serves as a marker for active hedgehog signaling. At 1, 4, 8, and 12 weeks of age,lacZexpression was detected in a pattern analogous to that of embryonic cartilage. The findings support the hypothesis that the embryonic Ihh–PTHrP feedback loop is maintained in the postnatal growth plate except that the source of PTHrP has shifted to a more proximal location in the resting zone.

Static Compressive Loading Reduces the mRNA Expression of Type II and X Collagen in Rat Growth-Plate Chondrocytes During Postnatal Growth

2005 ◽  
Vol 46 (4-5) ◽  
pp. 211-219 ◽  
Author(s):  
I. Villemure ◽  
M. A. Chung ◽  
C. S. Seck ◽  
M. H. Kimm ◽  
J. R. Matyas ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Growth Plate ◽  
Compressive Loading ◽  
Postnatal Growth ◽  
Type Ii ◽  
Growth Plate Chondrocytes ◽  
Rat Growth

scholarly journals Retinoic acid stimulates annexin-mediated growth plate chondrocyte mineralization

2002 ◽  
Vol 157 (6) ◽  
pp. 1061-1070 ◽  
Author(s):  
Wei Wang ◽  
Thorsten Kirsch
Keyword(s):  
Gene Expression ◽  
Alkaline Phosphatase ◽  
Retinoic Acid ◽  
Growth Plate ◽  
Calcium Concentration ◽  
Matrix Vesicles ◽  
Cytosolic Calcium ◽  
Annexin Ii ◽  
Growth Plate Chondrocytes ◽  
Cytosolic Calcium Concentration

Biomineralization is a highly regulated process that plays a major role during the development of skeletal tissues. Despite its obvious importance, little is known about its regulation. Previously, it has been demonstrated that retinoic acid (RA) stimulates terminal differentiation and mineralization of growth plate chondrocytes (Iwamoto, M., I.M. Shapiro, K. Yagumi, A.L. Boskey, P.S. Leboy, S.L. Adams, and M. Pacifici. 1993. Exp. Cell Res. 207:413–420). In this study, we provide evidence that RA treatment of growth plate chondrocytes caused a series of events eventually leading to mineralization of these cultures: increase in cytosolic calcium concentration, followed by up-regulation of annexin II, V, and VI gene expression, and release of annexin II–, V–, VI– and alkaline phosphatase–containing matrix vesicles. Cotreatment of growth plate chondrocytes with RA and BAPTA-AM, a cell permeable Ca2+ chelator, inhibited the up-regulation of annexin gene expression and mineralization of these cultures. Interestingly, only matrix vesicles isolated from RA-treated cells that contained annexins, were able to take up Ca2+ and mineralize, whereas vesicles isolated from untreated or RA/BAPTA-treated cells, that contained no or only little annexins were not able to take up Ca2+ and mineralize. Cotreatment of chondrocytes with RA and EDTA revealed that increases in the cytosolic calcium concentration were due to influx of extracellular calcium. Interestingly, the novel 1,4-benzothiazepine derivative K-201, a specific annexin Ca2+ channel blocker, or antibodies specific for annexin II, V, or VI inhibited the increases in cytosolic calcium concentration in RA-treated chondrocytes. These findings indicate that annexins II, V, and VI form Ca2+ channels in the plasma membrane of terminally differentiated growth plate chondrocytes and mediate Ca2+ influx into these cells. The resulting increased cytosolic calcium concentration leads to a further up-regulation of annexin II, V, and VI gene expression, the release of annexin II–, V–, VI– and alkaline phosphatase–containing matrix vesicles, and the initiation of mineralization by these vesicles.

scholarly journals Growth Plate Chondrocytes: Skeletal Development, Growth and Beyond

2019 ◽  
Vol 20 (23) ◽  
pp. 6009 ◽  
Author(s):  
Shawn A. Hallett ◽  
Wanida Ono ◽  
Noriaki Ono
Keyword(s):  
Growth Plate ◽  
Bone Marrow Stromal Cells ◽  
Skeletal Development ◽  
Cell Types ◽  
Postnatal Growth ◽  
Lineage Tracing ◽  
Molecular Characteristics ◽  
Growth Plate Chondrocytes ◽  
Parathyroid Hormone Related Protein

Growth plate chondrocytes play central roles in the proper development and growth of endochondral bones. Particularly, a population of chondrocytes in the resting zone expressing parathyroid hormone-related protein (PTHrP) is now recognized as skeletal stem cells, defined by their ability to undergo self-renewal and clonally give rise to columnar chondrocytes in the postnatal growth plate. These chondrocytes also possess the ability to differentiate into a multitude of cell types including osteoblasts and bone marrow stromal cells during skeletal development. Using single-cell transcriptomic approaches and in vivo lineage tracing technology, it is now possible to further elucidate their molecular properties and cellular fate changes. By discovering the fundamental molecular characteristics of these cells, it may be possible to harness their functional characteristics for skeletal growth and regeneration. Here, we discuss our current understanding of the molecular signatures defining growth plate chondrocytes.

scholarly journals Basic Helix-loop-helix Protein DEC1 Promotes Chondrocyte Differentiation at the Early and Terminal Stages

2002 ◽  
Vol 277 (51) ◽  
pp. 50112-50120 ◽  
Author(s):  
Ming Shen ◽  
Eri Yoshida ◽  
Weiqun Yan ◽  
Takeshi Kawamoto ◽  
Ketut Suardita ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Growth Plate ◽  
Chondrogenic Differentiation ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Indian Hedgehog ◽  
Chondrocyte Differentiation ◽  
Growth Plate Chondrocytes ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix

The mRNA level of basic helix-loop-helix transcription factor DEC1 (BHLHB2)/Stra13/Sharp2 was up-regulated during chondrocyte differentiation in cultures of ATDC5 cells and growth plate chondrocytes, and in growth plate cartilagein vivo. Forced expression of DEC1 in ATDC5 cells induced chondrogenic differentiation, and insulin increased this effect of DEC1 overexpression. Parathyroid hormone (PTH) and PTH-related peptide (PTHrP) suppressed DEC1 expression and the differentiation of ATDC5 cells, but DEC1 overexpression antagonized this inhibitory action of PTH/PTHrP. Transforming growth factor-β or bone morphogenetic protein-2, as well as insulin, induced DEC1 expression in ATDC5 cultures where it induced chondrogenic differentiation. In pellet cultures of bone marrow mesenchymal stem cells exposed to transforming growth factor-β and insulin, DEC1 was induced at the earliest stage of chondrocyte differentiation and also at the hypertrophic stage. Overexpression of DEC1 in the mesenchymal cells induced the mRNA expressions of type II collagen, Indian hedgehog, and Runx2, as well as cartilage matrix accumulation; overexpression of DEC1 in growth plate chondrocytes at the prehypertrophic stage increased the mRNA levels of Indian hedgehog, Runx2, and type X collagen, and also increased alkaline phosphatase activity and mineralization. To our knowledge, DEC1 is the first transcription factor that can promote both chondrogenic differentiation and terminal differentiation.

Sign in / Sign up

Export Citation Format

Share Document