کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5508631 | 1400393 | 2017 | 41 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A crosstalk between muscarinic and CRF2 receptors regulates cellular adhesion properties of human colon cancer cells
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کلمات کلیدی
ECMCRF2cTnRT-PCRFAKUCNMMPGPRCEGFRG protein coupled receptor - G پروتئین همراه با پروتئینStress - استرس یا فشار روانیAcetylcholine - استیل کولینUrocortin - اوروکورتینEMT - تکنسین فوریتهای پزشکیColorectal cancer - سرطان روده بزرگcorticotrophin releasing factor - عامل آزاد کننده کورتیکوتروپینExtracellular matrix - ماتریکس خارج سلولیreverse transcription polymerase chain reaction - واکنش زنجیره ای پلیمراز رونویسی معکوسTumor progression - پیشرفت تومورadherens junctions - پیوندها را پیگیری می کندCell adhesion - چسبندگی سلولیCatenin - کاتنینCRC - کد افزونگی دورهای focal adhesion kinase - کیناز چسبندگی کانونیEpithelial-mesenchymal transition - گذار اپیتلیال-مزانشیمیMuscarinic receptor - گیرنده MuscarinicEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Patients with inflammatory bowel disease often suffer from chronic and relapsing intestinal inflammation that favor the development of colitis associated cancer. An alteration of the epithelial intestinal barrier function observed in IBD is supposed to be a consequence of stress. It has been proposed that corticotrophin-releasing factor receptor (CRF2), one of the two receptors of CRF, the principal neuromediator of stress, acts on cholinergic nerves to induce stress-mediated epithelial barrier dysfunction. Non-neuronal acetylcholine (Ach) and muscarinic receptors (mAchR) also contribute to alterations of epithelial cell functions. In this study, we investigated the mechanisms through which stress and Ach modulate epithelial cell adhesive properties. We show that Ach-induced activation of mAchR in HT-29 cells results in cell dissociation together with changes in cell-matrix contacts, which correlates with the acquisition of invasive potential consistent with a matrix metalloproteinase (MMP) mode of invasion. These processes result from mAchR subsequent stimulation of the cascade of src/Erk and FAK activation. Ach-induced secretion of laminin 332 leads to α3β1 integrin activation and RhoA-dependent reorganization of the actin cytoskeleton. We show that Ach-mediated effects on cell adhesion are blocked by astressin 2b, a CRF2 antagonist, suggesting that Ach action depends partly on CRF2 signaling. This is reinforced by the fact that Ach-mediated activation of mAchR stimulates both the synthesis and the release of CRF2 ligands in HT-29 cells (effects blocked by atropine). In summary, our data provides evidence for a novel intracellular circuit involving mAchR acting on CRF2-signaling that could mediate colonic mucosal barrier dysfunction and exacerbate mucosal inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1864, Issue 7, July 2017, Pages 1246-1259
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1864, Issue 7, July 2017, Pages 1246-1259
نویسندگان
M. Pelissier-Rota, N.T. Chartier, B. Bonaz, M.R. Jacquier-Sarlin,