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Article: Catecholamines Inhibit Gastric Epithelial [RGM-1] Cell Proliferation via Beta Adrenoceptors

TitleCatecholamines Inhibit Gastric Epithelial [RGM-1] Cell Proliferation via Beta Adrenoceptors
Authors
KeywordsCathecholamines
Cell cycle
Cell proliferation
Flow cytometry
RGM-1
Issue Date2010
PublisherUniversity of Calabar, College of Medical Sciences. The Journal's web site is located at http://www.bioline.org.br/np
Citation
Nigerian Journal of Physiological Sciences, 2010, v. 25 n. 1, p. 5-16 How to Cite?
AbstractCatecholamines have been implicated in the modulation of normal cell growth, exerting inhibitory or excitatory control depending on the cell type. However, there is a dearth of information on the role of adrenergic mediators in gastric cell proliferation. In the present study, the effects of adrenaline (ADR) and noradrenaline (NOR) on mucosal cell growth and the cell cycle were evaluated in vitro using a normal rat gastric mucosal cell line RGM-1. Cell proliferation was assessed using [3H]-thymidine incorporation and cell cycle patterns were determined by DNA labeling with propidium iodide and flow cytometric quantification. The expressions of adrenoceptors in RGM-1 were determined by Western blot. ADR (0.01 - 10microM) and NOR (0.01 - 10microM) inhibited the growth of RGM-1 cells in a concentration-dependent manner. Pre-treatment of cells with ADR and NOR also inhibited the proliferation stimulated by epidermal growth factor (EGF). Neither phentolamine (non-selective alpha-adrenergic blocker), methoxamine (alpha1-selective agonist) nor clonidine (alpha2-selective agonist) significantly affected the inhibition of cell proliferation produced by ADR and NOR. Propranolol (non-selective beta-adrenergic blocker) and butoxamine (selective beta2-adrenergic blocker) significantly (but not totally) reversed the inhibitory action of ADR on cell proliferation. Furthermore, procaterol (selective beta-2 agonist) but not dobutamine (selective beta-1 agonist) had effects similar to those produced by ADR and NOR. Exposure of RGM-1 cells to both ADR and NOR caused significant inhibition of the G1 - S cycle progression as evidenced by the higher percentage of the G0/G1 phase and a decreased S- phase. This effect was blocked by pre-treatment with propranolol but not phentolamine These results indicate that catecholamines inhibit the proliferation of RGM-1 cells probably partly through beta-2 receptors. ┬ęPhysiological Society of Nigeria.
Persistent Identifierhttp://hdl.handle.net/10722/183319
ISSN
2015 SCImago Journal Rankings: 0.169

 

DC FieldValueLanguage
dc.contributor.authorOlaleye, SB-
dc.contributor.authorWu, WKK-
dc.contributor.authorCho, CH-
dc.date.accessioned2013-05-23T02:28:16Z-
dc.date.available2013-05-23T02:28:16Z-
dc.date.issued2010-
dc.identifier.citationNigerian Journal of Physiological Sciences, 2010, v. 25 n. 1, p. 5-16-
dc.identifier.issn0794-859X-
dc.identifier.urihttp://hdl.handle.net/10722/183319-
dc.description.abstractCatecholamines have been implicated in the modulation of normal cell growth, exerting inhibitory or excitatory control depending on the cell type. However, there is a dearth of information on the role of adrenergic mediators in gastric cell proliferation. In the present study, the effects of adrenaline (ADR) and noradrenaline (NOR) on mucosal cell growth and the cell cycle were evaluated in vitro using a normal rat gastric mucosal cell line RGM-1. Cell proliferation was assessed using [3H]-thymidine incorporation and cell cycle patterns were determined by DNA labeling with propidium iodide and flow cytometric quantification. The expressions of adrenoceptors in RGM-1 were determined by Western blot. ADR (0.01 - 10microM) and NOR (0.01 - 10microM) inhibited the growth of RGM-1 cells in a concentration-dependent manner. Pre-treatment of cells with ADR and NOR also inhibited the proliferation stimulated by epidermal growth factor (EGF). Neither phentolamine (non-selective alpha-adrenergic blocker), methoxamine (alpha1-selective agonist) nor clonidine (alpha2-selective agonist) significantly affected the inhibition of cell proliferation produced by ADR and NOR. Propranolol (non-selective beta-adrenergic blocker) and butoxamine (selective beta2-adrenergic blocker) significantly (but not totally) reversed the inhibitory action of ADR on cell proliferation. Furthermore, procaterol (selective beta-2 agonist) but not dobutamine (selective beta-1 agonist) had effects similar to those produced by ADR and NOR. Exposure of RGM-1 cells to both ADR and NOR caused significant inhibition of the G1 - S cycle progression as evidenced by the higher percentage of the G0/G1 phase and a decreased S- phase. This effect was blocked by pre-treatment with propranolol but not phentolamine These results indicate that catecholamines inhibit the proliferation of RGM-1 cells probably partly through beta-2 receptors. ┬ęPhysiological Society of Nigeria.-
dc.languageeng-
dc.publisherUniversity of Calabar, College of Medical Sciences. The Journal's web site is located at http://www.bioline.org.br/np-
dc.relation.ispartofNigerian Journal of Physiological Sciences-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCathecholamines-
dc.subjectCell cycle-
dc.subjectCell proliferation-
dc.subjectFlow cytometry-
dc.subjectRGM-1-
dc.titleCatecholamines Inhibit Gastric Epithelial [RGM-1] Cell Proliferation via Beta Adrenoceptorsen_US
dc.typeArticleen_US
dc.identifier.emailWu, WKK: wukakei@graduate.hku.hk-
dc.identifier.emailCho, CH: chcho@hku.hk-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid22314897-
dc.identifier.scopuseid_2-s2.0-84863034174-
dc.identifier.volume25-
dc.identifier.issue1-
dc.identifier.spage5-
dc.identifier.epage16-
dc.publisher.placeNigeria-

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