Expression of Intracellular Calcium Channels and Pumps after Partial Hepatectomy in Rat

Magnino, Fabrice; St‐Pierre, Marie V.; Lüthi, Michael; Hilly, Mauricette; Mauger, Jean‐Pierre; Dufour, Jean‐François

doi:10.1006/mcbr.2000.0242

Cited by 17 publications

(13 citation statements)

References 28 publications

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“…Conflicting results on the InsP 3 receptor expression modification after partial hepatectomy have been reported [10,11], although Magnino et al [12] reported a type II InsP 3 receptor downregulation associated with an up-regulation of type I expression. However, this affected only mRNA levels, with protein expression being only slightly modified [12]. As already stated for cell desensitisation, hepatocyte over-stimulation by agonists and the resulting over-production of .…”

Section: Insp 3 Receptor Is Downregulated During Hepatocyte Desensitimentioning

confidence: 99%

“…Intracellular calcium is also crucial for cell proliferation [8], including during liver regeneration, as suggested by early studies on hypocalcaemic rats [9]. Alterations in the calcium signalling machinery have been reported to occur during liver regeneration, although the data remain limited and conflicting [10][11][12]. Other reports have both directly and indirectly suggested that agonist-induced calcium signals are modified after partial hepatectomy in the rat [13,14].…”

Section: Introductionmentioning

confidence: 99%

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Remodelling of calcium signalling during liver regeneration in the rat

Nicou

Serrière

Hilly

et al. 2007

Journal of Hepatology

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Section: Insp 3 Receptor Is Downregulated During Hepatocyte Desensitimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Remodelling of calcium signalling during liver regeneration in the rat

Nicou

Serrière

Hilly

et al. 2007

Journal of Hepatology

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“…2+ concentrations occur during cell cycle entry in hepatocytes during liver regeneration (33)(34)(35). Of relevance to cell proliferation, this increase in intracellular Ca 2+ has been correlated with activation of the calmodulin-dependent phosphatase calcineurin (36,37).…”

Section: Elevations In Intracellular Camentioning

confidence: 99%

Mice Lacking bi-1 Gene Show Accelerated Liver Regeneration

et al. 2007

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The liver has enormous regenerative capacity such that, after partial hepatectomy, hepatocytes rapidly replicate to restore liver mass, thus providing a context for studying in vivo mechanisms of cell growth regulation. Bax inhibitor-1 (BI-1) is an evolutionarily conserved endoplasmic reticulum (ER) protein that suppresses cell death. Interestingly, the BI-1 protein has been shown to regulate Ca 2+ handling by the ER similar to antiapoptotic Bcl-2 family proteins. Effects on cell cycle entry by Bcl-2 family proteins have been described, prompting us to explore whether bi-1-deficient mice display alterations in the in vivo regulation of cell cycle entry using a model of liver regeneration. Accordingly, we compared bi-1 +/+ and bi-1 À/À mice subjected to partial hepatectomy with respect to the kinetics of liver regeneration and molecular events associated with hepatocyte proliferation. We found that bi-1 deficiency accelerates liver regeneration after partial hepatectomy. Regenerating hepatocytes in bi-1 À/À mice enter cell cycle faster, as documented by more rapid incorporation of deoxynucleotides, associated with earlier increases in cyclin D1, cyclin D3, cyclin-dependent kinase (Cdk) 2, and Cdk4 protein levels, more rapid hyperphosphorylation of retinoblastoma protein, and faster degradation of p27 Kip1. Dephosphorylation and nuclear translocation of nuclear factor of activated T cells 1 (NFAT1), a substrate of the Ca 2+ -sensitive phosphatase calcineurin, were also accelerated following partial hepatectomy in BI-1-deficient hepatocytes. These findings therefore reveal additional similarities between BI-1 and Bcl-2 family proteins, showing a role for BI-1 in regulating cell proliferation in vivo, in addition to its previously described actions as a regulator of cell survival.

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“…In hepatocytes, IP 3 receptor isoform 2 is predominant and IP 3 receptor isoform 3 virtually absent. 31,32 In contrast, biliary epithelial cells express a substantial fraction of their IP 3 receptor as isoform 3. 12,31 The role of gap junctions in biliary epithelial cells has been difficult to study.…”

Section: Discussionmentioning

confidence: 99%