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Article: The presence and activity of SP-D in porcine coronary endothelial cells depend on Akt/PI3K, Erk and nitric oxide and decrease after multiple passaging

TitleThe presence and activity of SP-D in porcine coronary endothelial cells depend on Akt/PI3K, Erk and nitric oxide and decrease after multiple passaging
Authors
KeywordsEndothelial cells
Nitric oxide
SP-D
TNF-α
Issue Date2009
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/molimm
Citation
Molecular Immunology, 2009, v. 46 n. 6, p. 1050-1057 How to Cite?
Abstract
Surfactant protein D (SP-D) mediates clearance of microorganisms and modulates inflammation in response to cytotoxic stimulation. It is present in various epithelia, but also in vascular smooth muscle and endothelial cells. Experiments were designed to determine whether or not SP-D is present in porcine coronary arterial endothelial cells and if so, to investigate the molecular mechanisms underlying this presence. The expression of SP-D, NO synthase, Akt 1/2 and Erk 1/2 proteins was determined in cultures at passages 1 (#1) and 4 (#4). SP-D in primary cells existed in three isoforms (37-38 kDa and 50 kDa). The 37-38 kDa SP-D forms were the dominant isoforms in the porcine endothelium and were prominent at #1 but partially lost at #4. Tumor necrosis factor-α (TNF-α) significantly augmented the level of SP-D expression at #1 but not at #4. The basal level of 37-38 kDa SP-D isoforms at #1 was reduced by L-NAME, wortmannin and PD 98059. The low basal expression at #4 could be increased by DETA NONOate (donor of NO) or insulin (activator of PI3K/Akt). The presence of nitric oxide synthase was reduced while that of Akt 1/2 and Erk 1/2 was increased at #4. In cells both at passages 1 and 4, TNF-α downregulated NO synthase and up-regulated p-Erk 1/2 protein. The present findings demonstrate the presence of SP-D in endothelial cells which is NO-, PI3K/Akt- and Erk-dependent. They suggest a protective role of SP-D in these cells. © 2008 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/59549
ISSN
2013 Impact Factor: 3.003
2013 SCImago Journal Rankings: 1.474
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council of Hong KongHKU7490/06M
Research Centre of Heart, Brain, Hormone & Healthy Aging of The University of Hong Kong
Funding Information:

We thank Ms. Chung Yee Hat for her technical support in the laboratory. This work was supported by grants from the Research Grant Council of Hong Kong (HKU7490/06M) and the Research Centre of Heart, Brain, Hormone & Healthy Aging of The University of Hong Kong.

References

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Syddansk Universitet
DC FieldValueLanguage
dc.contributor.authorLee, MYKen_HK
dc.contributor.authorSørensen, GLen_HK
dc.contributor.authorHolmskov, Uen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-05-31T03:52:31Z-
dc.date.available2010-05-31T03:52:31Z-
dc.date.issued2009en_HK
dc.identifier.citationMolecular Immunology, 2009, v. 46 n. 6, p. 1050-1057en_HK
dc.identifier.issn0161-5890en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59549-
dc.description.abstractSurfactant protein D (SP-D) mediates clearance of microorganisms and modulates inflammation in response to cytotoxic stimulation. It is present in various epithelia, but also in vascular smooth muscle and endothelial cells. Experiments were designed to determine whether or not SP-D is present in porcine coronary arterial endothelial cells and if so, to investigate the molecular mechanisms underlying this presence. The expression of SP-D, NO synthase, Akt 1/2 and Erk 1/2 proteins was determined in cultures at passages 1 (#1) and 4 (#4). SP-D in primary cells existed in three isoforms (37-38 kDa and 50 kDa). The 37-38 kDa SP-D forms were the dominant isoforms in the porcine endothelium and were prominent at #1 but partially lost at #4. Tumor necrosis factor-α (TNF-α) significantly augmented the level of SP-D expression at #1 but not at #4. The basal level of 37-38 kDa SP-D isoforms at #1 was reduced by L-NAME, wortmannin and PD 98059. The low basal expression at #4 could be increased by DETA NONOate (donor of NO) or insulin (activator of PI3K/Akt). The presence of nitric oxide synthase was reduced while that of Akt 1/2 and Erk 1/2 was increased at #4. In cells both at passages 1 and 4, TNF-α downregulated NO synthase and up-regulated p-Erk 1/2 protein. The present findings demonstrate the presence of SP-D in endothelial cells which is NO-, PI3K/Akt- and Erk-dependent. They suggest a protective role of SP-D in these cells. © 2008 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/molimmen_HK
dc.relation.ispartofMolecular Immunologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectEndothelial cellsen_HK
dc.subjectNitric oxideen_HK
dc.subjectSP-Den_HK
dc.subjectTNF-αen_HK
dc.subject.meshEndothelial Cells - metabolism-
dc.subject.meshEndothelium, Vascular - cytology - metabolism-
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - metabolism-
dc.subject.meshNitric Oxide - metabolism-
dc.subject.meshProto-Oncogene Proteins c-akt - metabolism-
dc.titleThe presence and activity of SP-D in porcine coronary endothelial cells depend on Akt/PI3K, Erk and nitric oxide and decrease after multiple passagingen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0161-5890&volume=46&issue=6&spage=1050&epage=1057&date=2009&atitle=The+presence+and+activity+of+SP-D+in+porcine+coronary+endothelial+cells+depend+on+Akt/PI3K,+Erk+and+nitric+oxide+and+decrease+after+multiple+passagingen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.molimm.2008.09.027en_HK
dc.identifier.pmid19010548en_HK
dc.identifier.scopuseid_2-s2.0-61449196879en_HK
dc.identifier.hkuros161389en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-61449196879&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume46en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1050en_HK
dc.identifier.epage1057en_HK
dc.identifier.isiWOS:000264693200005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLee, MYK=22980015700en_HK
dc.identifier.scopusauthoridSørensen, GL=7102982904en_HK
dc.identifier.scopusauthoridHolmskov, U=7004526416en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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