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Int J Clin Exp Pathol 2013;6(12):2872-2879

Original Article
Mouse p63 variants and chondrogenesis

Junxia Gu, Yaojuan Lu, Longwei Qiao, Deyuan Ran, Na Li, Hong Cao, Yan Gao, Qiping Zheng

Department of Hematology and Hematological Laboratory Science, School of Medical Science and Laboratory Medicine, Jiangsu University,
Zhenjiang 212013, China; Department of Anatomy and Cell Biology, Rush University Medical Center, Chicago, IL 60612, USA. Equal
contributors.

Received October 9, 2013; Accepted November 8, 2013; Epub November 15, 2013; Published December 1, 2013

Abstract: As a critical member of the p53 family of transcription factors, p63 has been implicated a role in development than in tumor formation,
because p63 is seldom mutated in human cancers, while p63 null mice exhibit severe developmental abnormalities without increasing cancer
susceptibility. Notably, besides the major epithelial and cardiac defect, p63 deficient mice show severe limb and craniofacial abnormalities. In
addition, humans with p63 mutations also show severe limb and digit defects, suggesting a putative role of p63 in skeletal development. There
are eight p63 variants which encode for the TAp63 and ΔNp63 isoforms by alternative promoters. How these isoforms function during skeletal
development is currently largely unknown. Our recent transgenic studies suggest a role of TAP63α, but not ΔNP63α, during embryonic long
bone development. However, the moderate skeletal phenotypes in the TAP63α transgenic mice suggest requirement of additional p63 isoform
(s) for the limb defects in p63 null mice. Here, we report analysis of mouse p63 variants in MCT and ATDC5 cells, two cell models undergo
hypertrophic differentiation and mimic the process of endochondral bone formation upon growth arrest or induction. We detected increased
level of p63 variants in hypertrophic MCT cells by regular RT-PCR analysis. Further analysis by qRT-PCR, we detected significantly upregulated
level of γ variant (p<0.05), but not α or β variant (p>0.05), in hypertrophic MCT cells than in proliferative MCT cells. Moreover, we detected
upregulated TAP63γ in ATDC5 cells undergoing hypertrophic differentiation. Our results suggest that TAp63γ plays a positive role during
endochondral bone formation. (IJCEP1310022).

Keywords: Mouse chondrocytes, p63 variants, TAp63γ, qRT-PCR

Address correspondence to: Dr. Qiping Zheng, Department of Anatomy and Cell Biology, Rush University Medical Center, Chicago, IL 60612,
USA. E-mail: qiping_zheng@rush.edu; Dr. Yaojuan Lu, Department of Hematology and Hematological Laboratory Science, School of Medical
Science and Laboratory Medicine, Jiangsu University, Zhenjiang 212013, China. E-mail: luyaojuan19@gmail.com