Oncotarget

Research Papers:

The tissue dependent interactions between p53 and Bcl-2 in vivo

Xin Li _, Xiao Miao, Hongshen Wang, Zhixiang Xu and Bin Li

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Oncotarget. 2015; 6:35699-35709. https://doi.org/10.18632/oncotarget.5372

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Abstract

Xin Li1,*, Xiao Miao2,*, Hongshen Wang2, Zhixiang Xu3, Bin Li1

1Department of Dermatology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China, 200437

2Shanghai University of Traditional Chinese Medicine, Shanghai, China, 201203

3Division of Hematology/Oncology, Department of Medicine, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35233, USA

*These authors have contributed equally to this work

Correspondence to:

Xin Li, e-mail: 13661956326@163.com

Bin Li, e-mail: 18930568129@163.com

Keywords: p53, Bcl-2, apoptosis, interaction, mice

Received: June 28, 2015     Accepted: September 24, 2015     Published: October 06, 2015

ABSTRACT

To further investigate the role of p53 in apoptosis in vivo and the interaction between p53 and Bcl-2 in the regulation of cellular apoptosis in vivo, we depleted p53 in Bcl-2-null mice. We found that the interaction between p53 and Bcl-2 are tissue dependent. Specifically, loss of p53 in Bcl-2−/− mice inhibits apoptotic induction in spleen and subsequently inhibits the Bcl-2-null-induced spleen atrophy. Furthermore, p53 deficiency overcomes loss of melanocyte stem cell (MSC)-induced apoptosis and subsequently prevents hair graying in Bcl-2- null mice. In addition, p53 deletion partly inhibits apoptosis in hair follicle keratinocytes, leading to the alleviation of hair growth delay in Bcl-2-null mice. However, p53 absence in Bcl-2-null mice cannot restore other defects in Bcl-2-null mice, including retardation of growth, short ears and polycystic kidney disease.


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