Investigation of RARg Signaling in Human Growth-Plate Chondrocytes

Author(s):  
Joshua M. Abzug ◽  
Hongying Tian ◽  
Masatake Matsuoka ◽  
Danielle A. Hogarth ◽  
Casey M. Codd ◽  
...  
2013 ◽  
Vol 38 (4) ◽  
pp. 881-889 ◽  
Author(s):  
Karin Pichler ◽  
Tanja Kraus ◽  
Elisabeth Martinelli ◽  
Patrick Sadoghi ◽  
Giuseppe Musumeci ◽  
...  

1991 ◽  
Vol 99 (3) ◽  
pp. 641-649 ◽  
Author(s):  
A. Marriott ◽  
S. Ayad ◽  
M.E. Grant

Chondrocytes were isolated from bovine growth-plate cartilage and cultured within type I collagen gels. A major collagen with chains of Mr 59,000, decreasing to 47,000 on pepsinization, was synthesized and identified as type X collagen. This collagen was cleaved at two sites by mammalian collagenase, resulting in a major triple-helical fragment with chains of Mr 32,000. The species of Mr 59,000, 47,000 and 32,000 were not detected by SDS-polyacrylamide gel electrophoresis before reduction, indicating the presence of disulphide bonds within the triple helix. In contrast, similar biosynthetic studies with human growth-plate cartilage in organ culture, indicated that human type X collagen does not contain disulphide bonds. A polyclonal antiserum was raised to bovine type X collagen and used in immunolocalization studies to provide direct evidence for the association of type X collagen with the hypertrophic chondrocytes in both bovine and human growth plates during development.


2016 ◽  
Vol 53 (2) ◽  
pp. 141-148 ◽  
Author(s):  
Keming Sun ◽  
Fangna Liu ◽  
Junjian Wang ◽  
Zhanhao Guo ◽  
Zejuan Ji ◽  
...  

BMC Genomics ◽  
2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Bing Li ◽  
Karthika Balasubramanian ◽  
Deborah Krakow ◽  
Daniel H. Cohn

2004 ◽  
Vol 279 (35) ◽  
pp. 37103-37114 ◽  
Author(s):  
Antonio Marchini ◽  
Tiina Marttila ◽  
Anja Winter ◽  
Sandra Caldeira ◽  
Ilaria Malanchi ◽  
...  

2013 ◽  
Vol 95-B (4) ◽  
pp. 568-573 ◽  
Author(s):  
K. Pichler ◽  
V. Herbert ◽  
B. Schmidt ◽  
E. E. Fischerauer ◽  
A. Leithner ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Michael Guo ◽  
Zun Liu ◽  
Jessie Willen ◽  
Cameron P Shaw ◽  
Daniel Richard ◽  
...  

GWAS have identified hundreds of height-associated loci. However, determining causal mechanisms is challenging, especially since height-relevant tissues (e.g. growth plates) are difficult to study. To uncover mechanisms by which height GWAS variants function, we performed epigenetic profiling of murine femoral growth plates. The profiled open chromatin regions recapitulate known chondrocyte and skeletal biology, are enriched at height GWAS loci, particularly near differentially expressed growth plate genes, and enriched for binding motifs of transcription factors with roles in chondrocyte biology. At specific loci, our analyses identified compelling mechanisms for GWAS variants. For example, at CHSY1, we identified a candidate causal variant (rs9920291) overlapping an open chromatin region. Reporter assays demonstrated that rs9920291 shows allelic regulatory activity, and CRISPR/Cas9 targeting of human chondrocytes demonstrates that the region regulates CHSY1 expression. Thus, integrating biologically relevant epigenetic information (here, from growth plates) with genetic association results can identify biological mechanisms important for human growth.


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