Effects of taurolithocholate, a Ca2+-mobilizing agent, on cell Ca2+ in rat hepatocytes, human platelets and neuroblastoma NG108-15 cell line

Coquil, Jean-François; Berthon, B; Chomiki, Nathalie; Combettes, Laurent; Jourdon, Philippe; Schteingart, Claudio D.; Erlinger, S; Claret, M

doi:10.1042/bj2730153

Cited by 19 publications

(14 citation statements)

References 37 publications

(46 reference statements)

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“…We have previously shown 14 that BA uptake by ABAT is required for BA to alter cholangiocyte proliferation. Other studies 37,38 have shown that BA signal cellular processes only if BA are internalized in cells. Experimental insertion of ABAT into cells, which normally do not respond to BA, markedly increases BA-signaling.…”

Section: Discussionmentioning

confidence: 99%

Bile acid feeding increased proliferative activity and apical bile acid transporter expression in both small and large rat cholangiocytes

2001

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Section: Discussionmentioning

confidence: 99%

Bile acid feeding increased proliferative activity and apical bile acid transporter expression in both small and large rat cholangiocytes

2001

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“…Second, the cells continued to respond to TDC in the absence ofbath Ca2 , which would not be likely if a detergentinduced leak pathway for Ca2+ was responsible for the secretory effects ofTDC. Third, bile acid exposure does not cause an increase in (Ca2+)i in some cell types, e.g., platelets or neuroblastoma cells (43), whereas increased (Ca2+)i would be expected in all cells if the effects were nonspecific. Fourth, there was no detectable leak of fura-2 from the cells during the Ca2" measurements.…”

Section: Discussionmentioning

confidence: 99%

Taurodeoxycholate activates potassium and chloride conductances via an IP3-mediated release of calcium from intracellular stores in a colonic cell line (T84)

Devor¹,

Sekar²,

Frizzell³

et al. 1993

J. Clin. Invest.

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Whole-cell patch-clamp techniques and fluorescence measurements of intracellular Ca2" concentration, (Ca2+)i, were used to investigate the mechanism oftaurodeoxycholate (TDC) stimulation of Cl-secretion in the T84 colonic cell line. During perforated whole-cell recordings, the cell membrane voltage was alternately clamped to EK and Ea. Initially, TDC (0.75 mM) stimulated inward nonselective cation currents that were composed of discrete large conductance single-channel events. This initial response was followed by activation of K+ and C0-currents with peak values of385±41 pA and 98±28 pA, respectively (n = 12). The K+ and Cl-currents oscillated while TDC was present and returned to baseline levels upon its removal. The threshold for activation of the oscillatory currents was 0.1 mM TDC. Taurocholate TDC-induced (Ca2")i oscillations were observed in the absence of bath Ca2"; however, removal of bath Ca2" during the TDC response caused (Ca2+); to return to near baseline values. Simultaneous K+ current and (Ca2+)i measurements confirmed that the initial nonselective cation current was independent of (Ca2`)j, while K+ current oscillations were in phase with the (Ca2+)i oscillations. TDC induced inositol monophosphate (IP) accumulation, reflecting production of inositol 1,4,5-trisphosphate (IP3) during TDC stimulation. The response to TDC during standard whole-cell patch-clamp was similar to that observed with perforated whole-cell recordings, except the nonselective cation current was prolonged. When heparin (1 mg/ml) was added to the pipette under these conditions, the Ca2-activated currents were inhibited, but the nonselective cat- Clin. Invest. 1993. 92:2173-2181

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“…Hydrophobic bile acids are classic hepatotoxicants in vivo, causing cholestatic liver injury. Numerous studies have demonstrated that hydrophobic bile acids, including TLC, elevate hepatocyte Ca 2ϩ (72)(73)(74)(91)(92)(93) and calpain activity (20), which play a key role in bile acid hepatotoxicity (20,(72)(73)(74)(91)(92)(93).…”

Section: Discussionmentioning

confidence: 99%

“…3E). TLC elevates hepatocyte Ca 2ϩ (72)(73)(74) through release from intracellular stores by directly increasing store Ca 2ϩ permeability (73).…”

Section: Anp Stimulates Cgmp Production In Atp-treated Ratmentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Elevations in Ca2+ and Protects Hepatocytes by Stimulating Net Plasma Membrane Ca2+ Efflux

Green

Stratton

Squires

et al. 2007

Journal of Biological Chemistry

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Elevations in intracellular Ca2؉ concentration and calpain activity are common early events in cellular injury, including that of hepatocytes. Atrial natriuretic peptide is a circulating hormone that has been shown to be hepatoprotective. The aim of this study was to examine the effects of atrial natriuretic peptide on potentially harmful elevations in cytosolic free Ca 2؉ (24) that plays a key role in initiation of cellular injury and subsequent necrosis or apoptosis (6,(25)(26)(27)(28)(29)(30). In hepatocytes, calpain promotes hepatocyte plasma membrane blebbing (31), induces the mitochondrial permeability transition in hepatocyte necrosis (32), and contributes to hepatocyte necrosis in anoxia (33). Calpain has been implicated in hepatotoxicity in ischemia-reperfusion injury (34, 35), hemorrhagic shock (36), and bile acid toxicity (20).In the search for cytoprotective agents and therapeutic interventions, those which suppress injurious [Ca 2ϩ ] i rises are considered highly promising (2-6, 30). Natriuretic peptides attenuate elevations in cytosolic free Ca 2ϩ concentration ([Ca 2ϩ ] c ) in many cell types (37-50), including rat hepatocytes (51). Atrial natriuretic peptide (ANP) 3 is a circulating hormone released mainly by atrial myocytes (52) in response to stress conditions such as volume expansion or cardiac hypoxia. In addition to its hypotensive, vasodilatory, and natriuretic effects in the cardiovascular and renal systems (53), increasing evidence supports a more widespread role for ANP in several other organs (54), including the liver. ANP elevates cGMP in rat hepatocytes (51,(55)(56) through the guanylyl cyclase A receptor (57), and is cytoprotective in both isolated hepatocytes (51,55,58) and perfused liver (57, 59 -62). An early preliminary study showed that ANP attenuated both oxidant-induced cell injury and the accompanying [Ca 2ϩ ] i rise (51), suggesting that the hepatoprotective effects of ANP may be mediated by mechanisms involved in Ca 2ϩ homeostasis (51, 55, 57). We have since examined the effects of ANP on physiological alterations in [Ca 2ϩ ] c ; we showed that ANP, through protein kinase G (PKG), attenuates [Ca 2ϩ ] c oscillations, dramatically increases the basal rate of plasma membrane Ca 2ϩ efflux and modestly inhibits basal Ca 2ϩ influx in rat hepatocytes (56).

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Effects of taurolithocholate, a Ca2+-mobilizing agent, on cell Ca2+ in rat hepatocytes, human platelets and neuroblastoma NG108-15 cell line

Cited by 19 publications

References 37 publications

Bile acid feeding increased proliferative activity and apical bile acid transporter expression in both small and large rat cholangiocytes

Bile acid feeding increased proliferative activity and apical bile acid transporter expression in both small and large rat cholangiocytes

Taurodeoxycholate activates potassium and chloride conductances via an IP3-mediated release of calcium from intracellular stores in a colonic cell line (T84)

Atrial Natriuretic Peptide Attenuates Elevations in Ca2+ and Protects Hepatocytes by Stimulating Net Plasma Membrane Ca2+ Efflux

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