ArticleWorld journal of gastroenterology2002
Effect of cholesterol liposomes on calcium mobilization in muscle cells from the rabbit sphincter of Oddi.
Article in World journal of gastroenterology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Sphincter of Oddi Dysfunction Induces Gallstone by Inhibiting the Expression of ABCB11 via PKC-α.Applied biochemistry and biotechnology · 2024Article
- Expression and alteration of BKChannels (Austin, Tex.) · 2017Article
- Effects of sphincter of Oddi motility on the formation of cholesterol gallstones.World journal of gastroenterology · 2016Article
- Effects of cholesterol on proliferation and functional protein expression in rabbit bile duct fibroblasts.World journal of gastroenterology · 2004Article
- The study between the dynamics and the X-ray anatomy and regularizing effect of gallbladder on bile duct sphincter of the dog.World journal of gastroenterology · 2003Article
- Effect of pinaverium bromide on stress-induced colonic smooth muscle contractility disorder in rats.World journal of gastroenterology · 2003Article
- Effects of cholesterol on the phenotype of rabbit bile duct fibroblasts.World journal of gastroenterology · 2003Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimTo analyze the influence of cholesterol liposome on the Ca2+ mobilization of cultured muscle cells in the rabbit sphincter of Oddi's.
methodsNew Zealand rabbit was sacrificed and the sphincter of Oddi (SO) segment was obtained aseptically. The SO segment was cut into pieces and cultured in DMEM solution. Then the smooth muscle cells were subcultured, and the 4th-7th passage cells were used for further investigation. The intracellular Ca2+ increase was measured under confocal microscope after the addition of 20 mmol x L(-1) KCl, 10(-7) mol x L(-1) acetylcholine and 10(-7) mol x L(-1) cholecystokinin, and different antagonists were added to analyze the Ca2+ mobilization pathway. After the cells were incubated with 1g x L(-1) cholesterol liposome (CL)(molar ratio was -2:1), the intracellular Ca2+ increase was measured again to determine the effect of CL on cellular Ca(2+) mobilization.
resultsThe resting cellular calcium concentration of cultured SO cell was 108+/-21 nmol x L(-1).The intracellular Ca2+ increases induced by 20 mmol x L(-1) KCl, 10(-7) mol x L(-1) ACh and 10(-7) mol x L(-1) CCK were 183+/-56% 161+/-52% and 130+/-43%, respectively. When the extracellular Ca2+ was eliminated by 2 mmol x L(-1) EGTA and 5 micromol x L(-1) verapamil, the intracellular Ca2+ increases induced by KCl, ACh and CCK were 20+/-14%,82+/-21% and 104+/-23%, respectively. After the preincubation with heparin, the Ca2+ increases were 62+/-23% and 23+/-19% induced by ACh and CCK, as for preincubation with procaine they were 72+/-28% and 85+/-37% induced by ACh and CCK, respectively. Pretreatment with CL for 18 h, the resting cellular Ca2+ concentration elevated to 152+/-26 nmol x L(-1), however, the cellular Ca2+ increase percentages in response to these agonists were 67+/-32%,56+/-33% and 34+/-15%.
conclusionKCl elicit the SO cellular Ca2+ increase depends on influx of extracellular Ca2+, ACh evoked the SO cellular Ca2+ increase is through the mobilization of intracellular Ca2+ pool and influx of extracellular Ca2+ as well, CCK excites the SO cells mainly through mobilization of intracellular IP3-sensitive Ca2+ store. After the incorporation with cholesterol liposome, KCl,ACh and CCK induced cellular Ca2+ increase percentages decreased.
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