Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Medina, J.F. (Juan Francisco) | es_ES |
dc.creator | Ardura-Fabregat, A. (Alberto) | es_ES |
dc.creator | Lopez-Martinez, M. (María) | es_ES |
dc.creator | Concepcion, A.R. (Axel Rolando) | es_ES |
dc.date.accessioned | 2014-09-26T11:19:08Z | - |
dc.date.available | 2014-09-26T11:19:08Z | - |
dc.date.issued | 2014 | es_ES |
dc.identifier.citation | Concepcion AR, Lopez M, Ardura-Fabregat A, Medina JF. Role of AE2 for pHi regulation in biliary epithelial cells. Front Physiol. 2014 Jan 17;4:413. | - |
dc.identifier.issn | 1664-042X | - |
dc.identifier.uri | https://hdl.handle.net/10171/36753 | - |
dc.description.abstract | The Cl(-)/HCO(-) 3anion exchanger 2 (AE2) is known to be involved in intracellular pH (pHi) regulation and transepithelial acid-base transport. Early studies showed that AE2 gene expression is reduced in liver biopsies and blood mononuclear cells from patients with primary biliary cirrhosis (PBC), a disease characterized by chronic non-suppurative cholangitis associated with antimitochondrial antibodies (AMA) and other autoimmune phenomena. Microfluorimetric analysis of the Cl(-)/HCO(-) 3 anion exchange (AE) in isolated cholangiocytes showed that the cAMP-stimulated AE activity is diminished in PBC compared to both healthy and diseased controls. More recently, it was found that miR-506 is upregulated in cholangiocytes of PBC patients and that AE2 may be a target of miR-506. Additional evidence for a pathogenic role of AE2 dysregulation in PBC was obtained with Ae2 (-/-) a,b mice, which develop biochemical, histological, and immunologic alterations that resemble PBC (including development of serum AMA). Analysis of HCO(-) 3 transport systems and pHi regulation in cholangiocytes from normal and Ae2 (-/-) a,b mice confirmed that AE2 is the transporter responsible for the Cl(-)/HCO(-) 3exchange in these cells. On the other hand, both Ae2 (+/+) a,b and Ae2 (-/-) a,b mouse cholangiocytes exhibited a Cl(-)-independent bicarbonate transport system, essentially a Na(+)-bicarbonate cotransport (NBC) system, which could contribute to pHi regulation in the absence of AE2. | - |
dc.language.iso | eng | en_EN |
dc.rights | info:eu-repo/semantics/openAccess | - |
dc.subject | Primary biliary cirrhosis | - |
dc.subject | Cholangiocytes | - |
dc.subject | Biliary HCO−3 secretion | - |
dc.subject | Bile flow | - |
dc.subject | Cl−/HCO−3 anion exchange | - |
dc.title | Role of AE2 for pHi regulation in biliary epithelial cells | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.publisher.place | FRONTIERS IN PHYSIOLOGY174413 | es_ES |
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