| pubmed-article:11756339 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C0227651 | lld:lifeskim |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C0596138 | lld:lifeskim |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:11756339 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11756339 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11756339 | pubmed:dateCreated | 2001-12-28 | lld:pubmed |
| pubmed-article:11756339 | pubmed:abstractText | Mesangial cells isolated from NOD mice after the onset of diabetes have undergone a stable phenotypic change. This phenotype is characterized by increased expression of IGF-I and downregulation of collagen degradation, which is associated with decreased MMP-2 activity. Here, we investigated the IGF-I signaling pathway in mesangial cells isolated from NOD mice before (nondiabetic NOD mice [ND-NOD]) and after (diabetic NOD mice [D-NOD]) the onset of diabetes. We found that the IGF-I signaling pathway in D-NOD cells was activated by autocrine IGF-I. They had phosphorylation of the IGF-I receptor beta-subunit, phosphorylation of insulin receptor substrate (IRS)-1, and association of the p85 subunit (phosphatidylinositol 3-kinase [PI3K]) with the IGF-I receptor and IRS-1 in D-NOD cells in the basal state. This was also associated with increased phosphorylation of ERK2 in D-NOD mesangial cells. Inhibiting autocrine IGF-I from binding to its receptor using an IGF-I-neutralizing antibody or inhibiting IGF-I signaling pathways using a specific PI3K inhibitor or a specific mitogen-activated protein kinase/extracellular response kinase kinase inhibitor decreased phosphorylated ERKs in D-NOD cells. Importantly, this was associated with increased MMP-2 activity. The addition of exogenous IGF-I to ND-NOD activated signal transduction. Therefore, we conclude that the IGF-I signaling pathway is intact in both D-NOD and ND-NOD cells. However, the phenotypic change in D-NOD cells is associated with constitutive activation of the IGF-I signaling pathways, which may participate in the development and progression of diabetic glomerulosclerosis. | lld:pubmed |
| pubmed-article:11756339 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11756339 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11756339 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11756339 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:11756339 | pubmed:issn | 0012-1797 | lld:pubmed |
| pubmed-article:11756339 | pubmed:author | pubmed-author:TackIvanI | lld:pubmed |
| pubmed-article:11756339 | pubmed:author | pubmed-author:ElliotSharon... | lld:pubmed |
| pubmed-article:11756339 | pubmed:author | pubmed-author:PotierMyleneM | lld:pubmed |
| pubmed-article:11756339 | pubmed:author | pubmed-author:RiveraAnaA | lld:pubmed |
| pubmed-article:11756339 | pubmed:author | pubmed-author:StrikerGary... | lld:pubmed |
| pubmed-article:11756339 | pubmed:author | pubmed-author:StrikerLilian... | lld:pubmed |
| pubmed-article:11756339 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11756339 | pubmed:volume | 51 | lld:pubmed |
| pubmed-article:11756339 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11756339 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11756339 | pubmed:pagination | 182-8 | lld:pubmed |
| pubmed-article:11756339 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:meshHeading | pubmed-meshheading:11756339... | lld:pubmed |
| pubmed-article:11756339 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11756339 | pubmed:articleTitle | Autocrine activation of the IGF-I signaling pathway in mesangial cells isolated from diabetic NOD mice. | lld:pubmed |
| pubmed-article:11756339 | pubmed:affiliation | Physiology Laboratory, University of Toulouse School of Medicine, Toulouse, France. | lld:pubmed |
| pubmed-article:11756339 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11756339 | pubmed:publicationType | Comparative Study | lld:pubmed |
| entrez-gene:16000 | entrezgene:pubmed | pubmed-article:11756339 | lld:entrezgene |
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