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Article: Effects of octreotide on expression of L-type voltage-operated calcium channels and on intracellular Ca2+ in activated hepatic stellate cells

TitleEffects of octreotide on expression of L-type voltage-operated calcium channels and on intracellular Ca2+ in activated hepatic stellate cells
Authors
Issue Date2004
PublisherChinese Medical Association. The Journal's web site is located at http://www.cmj.org/
Citation
Chinese Medical Journal, 2004, v. 117 n. 6, p. 913-916 How to Cite?
AbstractBackground. The contractility of hepatic stellate cells (HSCs) may play an important role in the pathogenesis of cirrhosis with portal hypertension. The aim of this study was to research the effects of octreotide, an analogue of somatostatin, on intracellular Ca2+ and on the expression of L-type voltage-operated calcium channels (L-VOCCs) in activated HSCs, and to try to survey the use of octreotide in treatment and prevention of cirrhosis with portal hypertension complications. Methods. HSC-T6, an activated HSCs line, was plated on small glass coverslips in 35-mm culture dishes at a density of 1 × 105/ml, and incubated in DMEM media for 24 hours. After the cells were loaded with Fluo-3/AM, intracellular Ca2+ was measured by Laser Scanning Confocal Microscopy (LSCM). The dynamic changes in activated HSCs of intracellular Ca2+, stimulated by octreotide, endothelin-1, and KCI, respectively, were also determined by LSCM. Each experiment was repeated six times. L-VOCC expression in HSCs was estimated by immunocytochemistry. Results. After octreotide stimulation, a signifcant decrease in the intracellular Ca2+ of activated HSCs was observed. However, octreotide did not inhibit the increases in intracellular Ca2+ after stimulation by KCI and endothelin-1. Moreover, octreotide did not significantly affect L-VOCC expression. These results suggest that neither L-VOCC nor endothelin-1 receptors in activated HSCs are inhibited by octreotide. Conclusions. Octreotide may decrease portal hypertension and intrahepatic vascular tension by inhibiting activated HSCs contractility through decreases in intracellular Ca2+. The somatostatin receptors in activated HSCs may be inhibited by octreotide.
Persistent Identifierhttp://hdl.handle.net/10722/162939
ISSN
2015 Impact Factor: 0.957
2015 SCImago Journal Rankings: 0.428
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDing, HGen_US
dc.contributor.authorWang, BEen_US
dc.contributor.authorJia, JDen_US
dc.contributor.authorXia, HHXen_US
dc.contributor.authorWong, BCYen_US
dc.contributor.authorZhao, CHen_US
dc.contributor.authorXu, YLen_US
dc.date.accessioned2012-09-05T05:25:36Z-
dc.date.available2012-09-05T05:25:36Z-
dc.date.issued2004en_US
dc.identifier.citationChinese Medical Journal, 2004, v. 117 n. 6, p. 913-916en_US
dc.identifier.issn0366-6999en_US
dc.identifier.urihttp://hdl.handle.net/10722/162939-
dc.description.abstractBackground. The contractility of hepatic stellate cells (HSCs) may play an important role in the pathogenesis of cirrhosis with portal hypertension. The aim of this study was to research the effects of octreotide, an analogue of somatostatin, on intracellular Ca2+ and on the expression of L-type voltage-operated calcium channels (L-VOCCs) in activated HSCs, and to try to survey the use of octreotide in treatment and prevention of cirrhosis with portal hypertension complications. Methods. HSC-T6, an activated HSCs line, was plated on small glass coverslips in 35-mm culture dishes at a density of 1 × 105/ml, and incubated in DMEM media for 24 hours. After the cells were loaded with Fluo-3/AM, intracellular Ca2+ was measured by Laser Scanning Confocal Microscopy (LSCM). The dynamic changes in activated HSCs of intracellular Ca2+, stimulated by octreotide, endothelin-1, and KCI, respectively, were also determined by LSCM. Each experiment was repeated six times. L-VOCC expression in HSCs was estimated by immunocytochemistry. Results. After octreotide stimulation, a signifcant decrease in the intracellular Ca2+ of activated HSCs was observed. However, octreotide did not inhibit the increases in intracellular Ca2+ after stimulation by KCI and endothelin-1. Moreover, octreotide did not significantly affect L-VOCC expression. These results suggest that neither L-VOCC nor endothelin-1 receptors in activated HSCs are inhibited by octreotide. Conclusions. Octreotide may decrease portal hypertension and intrahepatic vascular tension by inhibiting activated HSCs contractility through decreases in intracellular Ca2+. The somatostatin receptors in activated HSCs may be inhibited by octreotide.en_US
dc.languageengen_US
dc.publisherChinese Medical Association. The Journal's web site is located at http://www.cmj.org/en_US
dc.relation.ispartofChinese Medical Journalen_US
dc.subject.meshCalcium - Analysisen_US
dc.subject.meshCalcium Channels, L-Type - Analysisen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshHepatocytes - Chemistry - Cytology - Drug Effectsen_US
dc.subject.meshMicroscopy, Confocalen_US
dc.subject.meshOctreotide - Pharmacologyen_US
dc.titleEffects of octreotide on expression of L-type voltage-operated calcium channels and on intracellular Ca2+ in activated hepatic stellate cellsen_US
dc.typeArticleen_US
dc.identifier.emailBenjamin Wong, CY:bcywong@hku.hken_US
dc.identifier.authorityBenjamin Wong, CY=rp00429en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid15198898-
dc.identifier.scopuseid_2-s2.0-3242698812en_US
dc.identifier.hkuros99194-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3242698812&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume117en_US
dc.identifier.issue6en_US
dc.identifier.spage913en_US
dc.identifier.epage916en_US
dc.identifier.isiWOS:000222457800024-
dc.publisher.placeChinaen_US
dc.identifier.scopusauthoridDing, HG=36848276800en_US
dc.identifier.scopusauthoridWang, BE=7405917909en_US
dc.identifier.scopusauthoridJia, JD=7202343661en_US
dc.identifier.scopusauthoridHarry Xia, HX=6504358303en_US
dc.identifier.scopusauthoridBenjamin Wong, CY=7402023340en_US
dc.identifier.scopusauthoridZhao, CH=7403563984en_US
dc.identifier.scopusauthoridXu, YL=8275451100en_US
dc.customcontrol.immutablejt 131009-

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