| pubmed-article:19166859 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19166859 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:19166859 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:19166859 | lifeskim:mentions | umls-concept:C1415072 | lld:lifeskim |
| pubmed-article:19166859 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:19166859 | lifeskim:mentions | umls-concept:C1705241 | lld:lifeskim |
| pubmed-article:19166859 | lifeskim:mentions | umls-concept:C1705242 | lld:lifeskim |
| pubmed-article:19166859 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19166859 | pubmed:dateCreated | 2009-3-10 | lld:pubmed |
| pubmed-article:19166859 | pubmed:abstractText | A polymorphism in the human Cx37 gene (C1019T), resulting in a non-conservative amino acid change in the regulatory C-terminus of the Cx37 protein (P319S), has been proposed as a prognostic marker for atherosclerosis. We have recently demonstrated that Cx37 hemichannels control the initiation of atherosclerotic plaque development by regulating ATP-dependent monocyte adhesion in atherosclerosis-susceptible apolipoprotein E-deficient mice. In this study, we have measured the electrical properties of Cx37 hemichannels (HCs) and gap junction channels (GJCs) with voltage-clamp methods. To this end, we have transfected hCx37-P319, hCx37-S319 or empty pIRES-eGFP vector cDNA into communication-deficient HeLa cells. In clones expressing similar levels of Cx37, exposure of single cells to low-Ca(2+) solution induced a voltage-sensitive HC current. The analysis yielded a bell-shaped function g(hc)=f(V(m)) (g(hc): normalized conductance at steady state; V(m): membrane potential) with a maximum around V(m)=-30 mV. The peak g(hc) of Cx37-P319 was 3-fold larger than that of Cx37-S319 HCs. Experiments on cell pairs revealed that Cx37-P319 GJCs exhibited a 1.5-fold larger unitary conductance than Cx37-S319 GJCs. Hence, the larger peak g(hc) of the former may reflect a larger conductance of their HCs. Using the same clones, we found that Cx37-P319 cells released more ATP and were less adhesive than Cx37-S319 cells. The reduction in adhesiveness of Cx37-expressing cells was prevented by extracellular apyrase. We conclude that the differences in biophysical properties between polymorphic HCs may be responsible for inequality in ATP release between Cx37-P319 and Cx37-S319 cells, which results in differential cell adhesion. | lld:pubmed |
| pubmed-article:19166859 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19166859 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19166859 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19166859 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19166859 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19166859 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19166859 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19166859 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19166859 | pubmed:issn | 1095-8584 | lld:pubmed |
| pubmed-article:19166859 | pubmed:author | pubmed-author:KwakBrenda... | lld:pubmed |
| pubmed-article:19166859 | pubmed:author | pubmed-author:WeingartRober... | lld:pubmed |
| pubmed-article:19166859 | pubmed:author | pubmed-author:DesplantezTho... | lld:pubmed |
| pubmed-article:19166859 | pubmed:author | pubmed-author:RothIsabelleI | lld:pubmed |
| pubmed-article:19166859 | pubmed:author | pubmed-author:WongCindy WCW | lld:pubmed |
| pubmed-article:19166859 | pubmed:author | pubmed-author:DerouetteJean... | lld:pubmed |
| pubmed-article:19166859 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19166859 | pubmed:volume | 46 | lld:pubmed |
| pubmed-article:19166859 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19166859 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19166859 | pubmed:pagination | 499-507 | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:meshHeading | pubmed-meshheading:19166859... | lld:pubmed |
| pubmed-article:19166859 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19166859 | pubmed:articleTitle | Functional differences between human Cx37 polymorphic hemichannels. | lld:pubmed |
| pubmed-article:19166859 | pubmed:affiliation | Department of Internal Medicine, Division of Cardiology, Faculty of Medicine, University of Geneva, Geneva, Switzerland. | lld:pubmed |
| pubmed-article:19166859 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19166859 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:2701 | entrezgene:pubmed | pubmed-article:19166859 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19166859 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19166859 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:19166859 | lld:pubmed |
