کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10817080 | 1058655 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential modulation of COX-2 expression in A549 airway epithelial cells by structurally distinct PPARγ agonists: evidence for disparate functional effects which are independent of NF-κB and PPARγ
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کلمات کلیدی
15-deoxy-Δ12,14 prostaglandin J2PGDHCOXHRPPPAR15-Hydroxy-prostaglandin dehydrogenaseCBPPKBGSKmPGES15d-PGJ2Microsomal prostaglandin E synthasecyclooxygenase - آنزیم سیکلواکسیژنازBADGE - بدbisphenol A diglycidyl ether - بیسفنول A diglycidyl etherLung - ریهCell activation - فعال سازی سلولHorseradish peroxidase - پراکسیداز هوررادیشCREB binding protein - پروتئین اتصال CREBprotein kinase B - پروتئین کیناز Bglycogen synthase kinase - گلیکوزین سیتستاز کینازperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Differential modulation of COX-2 expression in A549 airway epithelial cells by structurally distinct PPARγ agonists: evidence for disparate functional effects which are independent of NF-κB and PPARγ Differential modulation of COX-2 expression in A549 airway epithelial cells by structurally distinct PPARγ agonists: evidence for disparate functional effects which are independent of NF-κB and PPARγ](/preview/png/10817080.png)
چکیده انگلیسی
Ligands of peroxisome proliferator-activated receptor-γ (PPARγ) are thought to possess anti-inflammatory properties mediated via both PPARγ dependent and independent mechanisms. This work investigates the effects of PPARγ ligands on the regulation of cyclooxygenase-2 (COX-2) in the human lung epithelial cell line, A549. The synthetic ligand troglitazone activated the phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase pathway (MAPK), whereas the endogenous ligand, 15-deoxy-Î12,14-prostaglandin J2 (15d-PGJ2), only activated the PI3K pathway. 15d-PGJ2 had no detectable effects on COX-2, mPGES expression, or PGE2 production. However, troglitazone induced time-dependent COX-2 expression, which was insensitive to PPARγ antagonists, but was abrogated by inhibitors of PI3K and the ERK MAP kinase pathway. Furthermore, troglitazone induced mPGES expression and PGE2 production. Neither troglitazone nor 15d-PGJ2 was able to convincingly activate NF-κB in A549 cells. Further heterogeneity in the responses to troglitazone and 15d-PGJ2 was observed in the regulation of gene expression as assessed by microarray analysis. In summary, this study provides compelling evidence that troglitazone (like 15d-PGJ2) can exert functional effects independently of actions via PPARγ. Moreover, we have identified unique biochemical and functional actions of troglitazone that are not shared by 15d-PGJ2, which may influence the therapeutic potential of this compound in inflammatory settings.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 17, Issue 9, September 2005, Pages 1098-1110
Journal: Cellular Signalling - Volume 17, Issue 9, September 2005, Pages 1098-1110
نویسندگان
Kajal M. Patel, Karen L. Wright, Paul Whittaker, Probir Chakravarty, Malcolm L. Watson, Stephen G. Ward,