Abstract
Influence of taurolithocholate 3-sulphate on calcium content in cytosol and store of isolated mice hepatocytes
Highlights
Bile salts are synthesized from cholesterol in liver and represent the main driving force of the bile flow
TLC-S opens the ryanodine receptor type 1 (RyR) through activation of Nicotinic acid adenine dinucleotide phosphate (NAADP) [8]. It is still unclear if NAADP-sensitive acidic store is involved in TLC-S-induced Ca2+-signals
We have shown that TLC-S (50, 100 and 200 μM) elicited cytosolic Ca2+-signals, consistent with the previous findings described early [1, 2]
Summary
Bile salts are synthesized from cholesterol in liver and represent the main driving force of the bile flow. Previous work has shown that application of bile acids can cause the increase in the levels of cytosolic [Ca2+]i in hepatocytes [1, 4]. Bile acids activate calcium entry into the cells and cause depletion of internal calcium store [5]. It was shown that bile acids can release calcium from both ER and acidic stores in secretory granular areas. In both stores TLC-S interacts with both the IP3Rs and the RyRs. TLC-S opens the RyRs through activation of NAADP [8]. The main purpose of this study was to examine such possibility
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