Document Detail


Mitochondrial calcium regulates rat liver regeneration through the modulation of apoptosis.
MedLine Citation:
PMID:  21503946     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Subcellular Ca(2+) signals control a variety of responses in the liver. For example, mitochondrial Ca(2+) (Ca(mit)(2+)) regulates apoptosis, whereas Ca(2+) in the nucleus regulates cell proliferation. Because apoptosis and cell growth can be related, we investigated whether Ca(mit)(2+) also affects liver regeneration. The Ca(2+)-buffering protein parvalbumin, which was targeted to the mitochondrial matrix and fused to green fluorescent protein, was expressed in the SKHep1 liver cell line; the vector was called parvalbumin-mitochondrial targeting sequence-green fluorescent protein (PV-MITO-GFP). This construct properly localized to and effectively buffered Ca(2+) signals in the mitochondrial matrix. Additionally, the expression of PV-MITO-GFP reduced apoptosis induced by both intrinsic and extrinsic pathways. The reduction in cell death correlated with the increased expression of antiapoptotic genes [B cell lymphoma 2 (bcl-2), myeloid cell leukemia 1, and B cell lymphoma extra large] and with the decreased expression of proapoptotic genes [p53, B cell lymphoma 2-associated X protein (bax), apoptotic peptidase activating factor 1, and caspase-6]. PV-MITO-GFP was also expressed in hepatocytes in vivo with an adenoviral delivery system. Ca(mit)(2+) buffering in hepatocytes accelerated liver regeneration after partial hepatectomy, and this effect was associated with the increased expression of bcl-2 and the decreased expression of bax. CONCLUSION: Together, these results reveal an essential role for Ca(mit)(2+) in hepatocyte proliferation and liver regeneration, which may be mediated by the regulation of apoptosis.
Authors:
Mateus T Guerra; Emerson A Fonseca; Flavia M Melo; Viviane A Andrade; Carla J Aguiar; Lídia M Andrade; Ana Cristina N Pinheiro; Marisa C F Casteluber; Rodrigo R Resende; Mauro C X Pinto; Simone O A Fernandes; Valbert N Cardoso; Elaine M Souza-Fagundes; Gustavo B Menezes; Ana M de Paula; Michael H Nathanson; Maria de Fátima Leite
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  54     ISSN:  1527-3350     ISO Abbreviation:  Hepatology     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-28     Completed Date:  2011-09-30     Revised Date:  2012-03-12    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  296-306     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 American Association for the Study of Liver Diseases.
Affiliation:
Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Calcium / metabolism*
Calcium Signaling / physiology
Cell Proliferation
Liver Regeneration / physiology*
Male
Mitochondria, Liver / metabolism*
Models, Animal
Proto-Oncogene Proteins c-bcl-2 / metabolism
Rats
Rats, Sprague-Dawley
bcl-2-Associated X Protein / metabolism
Grant Support
ID/Acronym/Agency:
DK34989/DK/NIDDK NIH HHS; DK45710/DK/NIDDK NIH HHS; DK57751/DK/NIDDK NIH HHS; P01 DK057751-10/DK/NIDDK NIH HHS; P30 DK034989-25S1/DK/NIDDK NIH HHS; R01 DK045710-10/DK/NIDDK NIH HHS; R01 DK045710-18/DK/NIDDK NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 7440-70-2/Calcium

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