Document Detail


Loss of transforming growth factor β adaptor protein β-2 spectrin leads to delayed liver regeneration in mice.
MedLine Citation:
PMID:  21520177     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Liver regeneration, following partial hepatectomy (PHx), occurs through precisely controlled and synchronized cell proliferation, in which quiescent hepatocytes undergo one to two rounds of replication, with restoration of liver mass and function. We previously demonstrated that loss of the Smad3/4 adaptor protein β-2 spectrin (β2SP) is associated with faster entry into S phase, and hepatocellular cancer formation. These observations led us to further pursue the role of β2SP in cell cycle progression in vivo. Liver regeneration studies with PHx in β2SP(+/-) mice reveal a surprising and significant decrease in liver/body weight ratio at 48 hours after PHx in β2SP(+/-) mice in comparison to wildtype mice. At 48 hours after PHx we also observe decreased levels of cyclin E (2.4-fold, P < 0.05), Cdk1 (7.2-fold, P < 0.05), cyclin A, pRb (Ser249/Thr252), proliferative cell nuclear antigen (PCNA), cyclin D1 with elevated levels of pCdk1 (Thr14) (3.6-fold, P < 0.05). Strikingly, at 24 hours elevated levels of p53 (4-fold, P < 0.05), phospho-p53 (ser15 and ser20), and p21 (200-fold, P < 0.05) persisting to 48 hours after PHx further correlated with raised expression of the DNA damage markers pChk2 (Thr68) and γH2AX (S139). However, compromised cell cycle progression with loss of β2SP is not rescued by inhibiting p53 function, and that G(2) /M phase arrest observed is independent and upstream of p53. CONCLUSION: β2SP deficiency results in dysfunctional hepatocyte cell cycle progression and delayed liver regeneration at 48 hours after PHx, which is p53-independent. β2SP loss may increase susceptibility to DNA damage, impair cell cycle progression, and ultimately lead to hepatocellular cancer.
Authors:
Arun Thenappan; Vivek Shukla; Feras J Abdul Khalek; Ying Li; Kirti Shetty; Pu Liu; Lu Li; Randy L Johnson; Lynt Johnson; Lopa Mishra
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  53     ISSN:  1527-3350     ISO Abbreviation:  Hepatology     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-04-26     Completed Date:  2011-07-19     Revised Date:  2012-05-02    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1641-50     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 American Association for the Study of Liver Diseases.
Affiliation:
Department of Surgery, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carrier Proteins / physiology*
Cell Cycle / physiology
Cyclin-Dependent Kinase Inhibitor p21 / physiology
Liver Regeneration / physiology*
Mice
Microfilament Proteins / physiology*
Receptors, Transforming Growth Factor beta / physiology*
Time Factors
Tumor Suppressor Protein p53 / physiology
Grant Support
ID/Acronym/Agency:
P01 CA130821-01A1/CA/NCI NIH HHS; P01CA130821/CA/NCI NIH HHS; R01 CA042857-21/CA/NCI NIH HHS; R01 CA106614-04/CA/NCI NIH HHS; R01CA042857/CA/NCI NIH HHS; R01CA106614/CA/NCI NIH HHS; RC2-AA019392/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Microfilament Proteins; 0/Receptors, Transforming Growth Factor beta; 0/Tumor Suppressor Protein p53; 0/fodrin

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