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Article: D-Glucose upregulates adenosine transport in cultured human aortic smooth muscle cells

TitleD-Glucose upregulates adenosine transport in cultured human aortic smooth muscle cells
Authors
KeywordsDiabetes
Nucleoside transporter
Issue Date2005
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 288 n. 6 57-6, p. H2756-H2762 How to Cite?
AbstractThe etiology of the atherosclerosis that occurs in diabetes mellitus is unclear. Adenosine has been shown to inhibit growth of rat aortic smooth muscle cells. Nucleoside transporters play an integral role in adenosine function by regulating adenosine levels in the vicinity of adenosine receptors. Therefore, we studied the effect of 25 mM D-glucose, which mimics hyperglycemia of diabetes, on adenosine transport in cultured human aortic smooth muscle cells (HASMCs). Although RT-PCR demonstrated the presence of equilibrative nucleoside transporter-1 (ENT-1) and ENT-2 mRNA, functional studies revealed that adenosine transport in HASMCs was predominantly mediated by ENT-1 and inhibited by nitrobenzylmercaptopurine riboside (NBMPR, IC 50 = 0.69 ± 0.05 nM). Adenosine transport in HASMCs was increased by >30% after treatment for 48 h with 25 mM D-glucose, but not with equimolar D-mannitol and L-glucose. Kinetic studies showed that D-glucose increased V max of adenosine transport without affecting K m. Similarly, D-glucose increased B max of high-affinity [ 3H]NBMPR binding, while the dissociation constant (K d) was not changed. Consistent with these observations, 25 mM D-glucose increased mRNA and protein expression of ENT-1. Treatment of serum-starved cells with the selective inhibitors of MAPK/ERK, PD-98059 (40 μM) and U-0126 (10 μM), abolished the effect of D-glucose on ENT-1. We conclude that D-glucose upregulates the protein and message expression and functional activity of ENT-1 in HASMCs, possibly via MAPK/ ERK-dependent pathways. Pathologically, the increase in ENT-1 activity in diabetes may affect the availability of adenosine in the vicinity of adenosine receptors and, thus, alter vascular functions in diabetes. Copyright © 2005 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/80278
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorTse, CMen_HK
dc.date.accessioned2010-09-06T08:04:31Z-
dc.date.available2010-09-06T08:04:31Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 2005, v. 288 n. 6 57-6, p. H2756-H2762en_HK
dc.identifier.issn0363-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80278-
dc.description.abstractThe etiology of the atherosclerosis that occurs in diabetes mellitus is unclear. Adenosine has been shown to inhibit growth of rat aortic smooth muscle cells. Nucleoside transporters play an integral role in adenosine function by regulating adenosine levels in the vicinity of adenosine receptors. Therefore, we studied the effect of 25 mM D-glucose, which mimics hyperglycemia of diabetes, on adenosine transport in cultured human aortic smooth muscle cells (HASMCs). Although RT-PCR demonstrated the presence of equilibrative nucleoside transporter-1 (ENT-1) and ENT-2 mRNA, functional studies revealed that adenosine transport in HASMCs was predominantly mediated by ENT-1 and inhibited by nitrobenzylmercaptopurine riboside (NBMPR, IC 50 = 0.69 ± 0.05 nM). Adenosine transport in HASMCs was increased by >30% after treatment for 48 h with 25 mM D-glucose, but not with equimolar D-mannitol and L-glucose. Kinetic studies showed that D-glucose increased V max of adenosine transport without affecting K m. Similarly, D-glucose increased B max of high-affinity [ 3H]NBMPR binding, while the dissociation constant (K d) was not changed. Consistent with these observations, 25 mM D-glucose increased mRNA and protein expression of ENT-1. Treatment of serum-starved cells with the selective inhibitors of MAPK/ERK, PD-98059 (40 μM) and U-0126 (10 μM), abolished the effect of D-glucose on ENT-1. We conclude that D-glucose upregulates the protein and message expression and functional activity of ENT-1 in HASMCs, possibly via MAPK/ ERK-dependent pathways. Pathologically, the increase in ENT-1 activity in diabetes may affect the availability of adenosine in the vicinity of adenosine receptors and, thus, alter vascular functions in diabetes. Copyright © 2005 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_HK
dc.subjectDiabetesen_HK
dc.subjectNucleoside transporteren_HK
dc.titleD-Glucose upregulates adenosine transport in cultured human aortic smooth muscle cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0363-6135&volume=288&spage=H2576&epage=2762&date=2005&atitle=D-Glucose+upregulates+adenosine+transport+in+cultured+human+aortic+smooth+muscle+cells.en_HK
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityLeung, GPH=rp00234en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajpheart.00921.2004en_HK
dc.identifier.pmid15695555-
dc.identifier.scopuseid_2-s2.0-19344364430en_HK
dc.identifier.hkuros100440en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19344364430&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume288en_HK
dc.identifier.issue6 57-6en_HK
dc.identifier.spageH2756en_HK
dc.identifier.epageH2762en_HK
dc.identifier.isiWOS:000229139900028-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeung, GPH=35963668200en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridTse, CM=7103295076en_HK

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