| http://purl.uniprot.org/citations/21840940 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21840940 | http://www.w3.org/2000/01/rdf-schema#comment | "Activation of matrix metalloproteinase-9 (MMP-9) is involved in HIV-1-induced disruption of the blood-brain barrier (BBB). In the present study, we hypothesize that peroxisome proliferator-activated receptor (PPAR)-α or PPARγ can protect against HIV-1-induced MMP-9 overexpression in brain endothelial cells (hCMEC cell line) by attenuating cellular oxidative stress and down-regulation of caveolae-associated redox signaling. Exposure to HIV-1-infected monocytes induced phosphorylation of ERK1/2 and Akt in hCMEC by 2.5- and 3.6-fold, respectively; however, these effects were attenuated by overexpression of PPARα or PPARγ and by silencing of caveolin-1 (cav-1). Coculture of hCMEC with HIV-1-infected monocytes significantly induced MMP-9 promoter and enzyme activity by 3-to 3.5-fold. Promoter mutation studies indicated that SP-1 (g1940t_g1941t) is an essential transcription factor involved in induction of MMP-9 promoter by HIV-1. In addition, HIV-1-stimulated activity of MMP-9 promoter was inhibited by mutation of AP-1 site 2 (c1918t_a1919g) and both (but not individual) NF-κB binding sites (g1389c and g1664c). PPAR overexpression, ERK1/2 or Akt inhibition, and silencing of cav-1 all effectively protected against HIV-1-induced MMP-9 promoter activity, indicating a close relationship among HIV-1-induced cerebrovascular toxicity, redox-regulated mechanisms, and functional caveolae. Such a link was further confirmed in MMP-9-deficient mice exposed to PPARα or PPARγ agonist and injected with the HIV-1-specific protein Tat into cerebral vasculature. Overall, our results indicate that ERK1/2, Akt, and cav-1 are involved in the regulatory mechanisms of PPAR-mediated protection against HIV-1-induced MMP-9 expression in brain endothelial cells."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.org/dc/terms/identifier | "doi:10.1096/fj.11-188607"xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/author | "Huang W."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/author | "Hennig B."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/author | "Rha G.B."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/author | "Toborek M."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/author | "Andras I.E."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/name | "FASEB J"xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/pages | "3979-3988"xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/title | "PPARalpha and PPARgamma protect against HIV-1-induced MMP-9 overexpression via caveolae-associated ERK and Akt signaling."xsd:string |
| http://purl.uniprot.org/citations/21840940 | http://purl.uniprot.org/core/volume | "25"xsd:string |
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