RGD Reference Report - The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury. - Rat Genome Database

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The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury.

Authors: Sevelsted Møller, Linda  Fialla, Annette Dam  Schierwagen, Robert  Biagini, Matteo  Liedtke, Christian  Laleman, Wim  Klein, Sabine  Reul, Winfried  Koch Hansen, Lars  Rabjerg, Maj  Singh, Vikrant  Surra, Joaquin  Osada, Jesus  Reinehr, Roland  de Muckadell, Ove B Schaffalitzky  Köhler, Ralf  Trebicka, Jonel 
Citation: Sevelsted Møller L, etal., Sci Rep. 2016 Jun 29;6:28770. doi: 10.1038/srep28770.
RGD ID: 329955558
Pubmed: PMID:27354175   (View Abstract at PubMed)
PMCID: PMC4926059   (View Article at PubMed Central)
DOI: DOI:10.1038/srep28770   (Journal Full-text)

The calcium-activated potassium channel KCa3.1 controls different cellular processes such as proliferation and volume homeostasis. We investigated the role of KCa3.1 in experimental and human liver fibrosis. KCa3.1 gene expression was investigated in healthy and injured human and rodent liver. Effect of genetic depletion and pharmacological inhibition of KCa3.1 was evaluated in mice during carbon tetrachloride induced hepatic fibrogenesis. Transcription, protein expression and localisation of KCa3.1 was analysed by reverse transcription polymerase chain reaction, Western blot and immunohistochemistry. Hemodynamic effects of KCa3.1 inhibition were investigated in bile duct-ligated and carbon tetrachloride intoxicated rats. In vitro experiments were performed in rat hepatic stellate cells and hepatocytes. KCa3.1 expression was increased in rodent and human liver fibrosis and was predominantly observed in the hepatocytes. Inhibition of KCa3.1 aggravated liver fibrosis during carbon tetrachloride challenge but did not change hemodynamic parameters in portal hypertensive rats. In vitro, KCa3.1 inhibition leads to increased hepatocyte apoptosis and DNA damage, whereas proliferation of hepatic stellate cells was stimulated by KCa3.1 inhibition. Our data identifies KCa3.1 channels as important modulators in hepatocellular homeostasis. In contrast to previous studies in vitro and other tissues this channel appears to be anti-fibrotic and protective during liver injury.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
KCNN4HumanExperimental Liver Cirrhosis exacerbatesISOKcnn4 (Mus musculus) RGD 
KCNN4HumanExperimental Liver Cirrhosis  ISOKcnn4 (Rattus norvegicus)mRNA:increased expression:liver (rat)RGD 
Kcnn4RatExperimental Liver Cirrhosis exacerbatesISOKcnn4 (Mus musculus) RGD 
Kcnn4RatExperimental Liver Cirrhosis  IEP mRNA:increased expression:liver (rat)RGD 
Kcnn4MouseExperimental Liver Cirrhosis exacerbatesIMP  RGD 
Kcnn4MouseExperimental Liver Cirrhosis  ISOKcnn4 (Rattus norvegicus)mRNA:increased expression:liver (rat)RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Kcnn4Rathepatocyte apoptotic process  IMP  RGD 
Kcnn4Ratnegative regulation of cell volume  IMP  RGD 
Kcnn4Ratnegative regulation of hepatic stellate cell proliferation  IMP  RGD 
Kcnn4Ratresponse to tetrachloromethane  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Kcnn4  (potassium calcium-activated channel subfamily N member 4)

Genes (Mus musculus)
Kcnn4  (potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4)

Genes (Homo sapiens)
KCNN4  (potassium calcium-activated channel subfamily N member 4)


Additional Information