| pubmed-article:18363844 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0441247 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0010055 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0036186 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0442043 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C0694888 | lld:lifeskim |
| pubmed-article:18363844 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
| pubmed-article:18363844 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18363844 | pubmed:dateCreated | 2009-1-29 | lld:pubmed |
| pubmed-article:18363844 | pubmed:abstractText | Abstract Internal mammary artery (IMA) coronary artery bypass grafts (CABG) are remarkably resistant to intimal hyperplasia (IH) as compared to saphenous vein (SV) grafts following aorto-coronary anastomosis. The reason behind this puzzling difference still remains an enigma. In this study, we examined the effects of IGF-1 stimulation on the PI3K-AKT/PKB pathway mediating proliferation of smooth muscle cells (SMCs) of IMA and SV origin and the specific contribution of phosphatase and tensin homologue (PTEN) in regulating the IGF-1-PI3K-AKT/PKB axis under these conditions. Mitogenic activation with IGF-1, time-dependently stimulated the phosphorylation of PI3K and AKT/PKB in the SV SMCs to a much greater extent than the IMA. Conversely, PTEN was found to be significantly more active in IMA SMCs. Transient overexpression of PTEN in SMCs of SV and IMA inhibited AKT/PKB activity and upstream of AKT/PKB, caused a reduction of IGF-1 receptors. Downstream, PTEN overexpression in SV SMCs induced the transactivation of tumour suppressor protein p53 by down-regulating the expression of its inhibitor MDM2. However, PTEN overexpression had no significant effect on MDM2 and p53 expression in IMA SMCs. PTEN overexpression inhibited IGF-1-induced SMC proliferation in both SV and IMA. PTEN suppression, induced by siRNA transfection of IMA SMCs diminished the negative regulation of PI3K-PKB signalling leading to greater proliferative response induced by IGF-1 stimulation. Thus, we show for the first time that early inactivation of PTEN in SV SMCs leads to temporally increased activity of the pro-hyperplasia PI3K-AKT/PKB pathway leading to IH-induced vein graft occlusion. Therefore, modulation of the PI3K-AKT/PKB pathway via PTEN might be a novel and effective strategy in combating SV graft failure following CABG. | lld:pubmed |
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| pubmed-article:18363844 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18363844 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18363844 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18363844 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18363844 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:18363844 | pubmed:issn | 1582-4934 | lld:pubmed |
| pubmed-article:18363844 | pubmed:author | pubmed-author:AgrawalDevend... | lld:pubmed |
| pubmed-article:18363844 | pubmed:author | pubmed-author:GangaharDeepa... | lld:pubmed |
| pubmed-article:18363844 | pubmed:author | pubmed-author:MitraAmit KAK | lld:pubmed |
| pubmed-article:18363844 | pubmed:author | pubmed-author:JiaGuanghongG | lld:pubmed |
| pubmed-article:18363844 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18363844 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:18363844 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18363844 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18363844 | pubmed:pagination | 177-87 | lld:pubmed |
| pubmed-article:18363844 | pubmed:dateRevised | 2011-11-8 | lld:pubmed |
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