کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10802433 | 1055694 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of c-Jun NH2-terminal kinase stimulates mu opioid receptor expression via p38 MAPK-mediated nuclear NF-κB activation in neuronal and non-neuronal cells
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کلمات کلیدی
Dnmt1PCBPMecp2PI3-KCREBBrg1c-Jun NH2-terminal kinaseU0126SP600125AP2NRSFLY294002Activator protein 2PDTCSAPKSB2035801,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadienemitogen-activated protein/extracellular signal-regulated kinaseRT-PCRNF-κBJnkDRGMORHDACqRT-PCRIFN-γdorsal root ganglion - گانگلیون ریشه پشتیDNA methyltransferase - DNA متیل ترانسفرازMAPK - MAPKSOx - SOXSp1 - SP1Aceh - آچهOct-1 - اکتبر 1interferon-gamma - اینترفرون گاماtumor necrosis factor-alpha - تومور نکروز عامل آلفاTNF-α - فاکتور نکروز توموری آلفاnuclear factor-kappaB - فاکتور هسته ای - kappaBphosphoinositide 3-kinase - فسفینوزیتید 3-کینازMEK - مجاهدین خلقSpecificity protein 1 - مشخصات پروتئین 1histone deacetylase - هیستون داستیلازquantitative reverse transcription-polymerase chain reaction - واکنش زنجیره ای رونویسی معکوس و پلیمریزا معکوسreverse transcription-polymerase chain reaction - واکنش زنجیره ای رونویسی-پلیمراز معکوسcAMP response element binding protein - پروتئین اتصال دهنده عنصر پاسخ cAMPmethyl-CpG-binding protein 2 - پروتئین متصل CpG متیل 2mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenStress-activated protein kinase - پروتئین کیناز فعال شده با استرسProximal promoter - پرومیکور پروگزیمالMu opioid receptor - گیرنده اپیدمی م
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Despite its potential side effects of addiction, tolerance and withdrawal symptoms, morphine is widely used for reducing moderate and severe pain. Previous studies have shown that the analgesic effect of morphine depends on mu opioid receptor (MOR) expression levels, but the regulatory mechanism of MOR is not yet fully understood. Several in vivo and in vitro studies have shown that the c-Jun NH2-terminal kinase (JNK) pathway is closely associated with neuropathic hyperalgesia, which closely resembles the neuroplastic changes observed with morphine antinociceptive tolerance. In this study, we show that inhibition of JNK by SP600125, its inhibitory peptide, or JNK-1 siRNA induced MOR at both mRNA and protein levels in neuronal cells. This increase in MOR expression was reversed by inhibition of the p38 mitogen-activated protein kinase (MAPK) pathway, but not by inhibition of the mitogen-activated protein/extracellular signal-regulated kinase (MEK) pathway. Further experiments using cell signaling inhibitors showed that MOR upregulation by JNK inhibition involved nuclear factor-kappa B (NF-κB). The p38 MAPK dependent phosphorylation of p65 NF-κB subunit in the nucleus was increased by SP600125 treatment. We also observed by chromatin immunoprecipitation (ChIP) analysis that JNK inhibition led to increased bindings of CBP and histone-3 dimethyl K4, and decreased bindings of HDAC-2, MeCP2, and histone-3 trimethyl K9 to the MOR promoter indicating a transcriptional regulation of MOR by JNK inhibition. All these results suggest a regulatory role of the p38 MAPK and NF-κB pathways in MOR gene expression and aid to our better understanding of the MOR gene regulation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 6, June 2013, Pages 1476-1488
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 6, June 2013, Pages 1476-1488
نویسندگان
Yadav Wagley, Cheol Kyu Hwang, Hong-Yiou Lin, Angel F.Y. Kam, Ping-Yee Law, Horace H. Loh, Li-Na Wei,