کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8923808 | 1643501 | 2017 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Environmental toxin acrolein alters levels of endogenous lipids, including TRP agonists: A potential mechanism for headache driven by TRPA1 activation
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کلمات کلیدی
2-AGN-arachidonoyl ethanolamineN-Acyl ethanolamineN-arachidonoyl glycineFAAH2-arachidonyl glyceroleCBPLCmaglNAELEADMEMFBSAEAPEADEAHPLC/MS/MS - HPLC / MS / MSOEA - OASArachidonic acid - اسید آراشیدونیکFatty acid amide hydrolase - اسید آمینه هیدرولاز اسید چربCNS - دستگاه عصبی مرکزیdiacylglycerol - دیسیل گلیسیرینDAG - روزCer - سرfetal bovine serum - سرم جنین گاوcentral nervous system - سیستم عصبی مرکزیphospholipase C - فسفولیپاز Cmonoacylglycerol lipase - لیپاز monoacylglycerol لیپازDulbecco’s modified eagle’s medium - محیط عقاب اصلاح شده DulbeccoCerebellum - مخچهknockout - ناکاوتNAgly - ناگلیprostaglandin - پروستاگلاندینهاEndogenous cannabinoid - کانابینوئید آندوژنیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Exposure to airborne toxins can trigger headaches, but the mechanisms are not well understood. Some environmental toxins, such as acrolein, activate transient receptor potential ankyrin 1 (TRPA1), a receptor involved in pain sensation that is highly expressed in the trigeminovascular system. It has been shown in rat models that repeated exposure to acrolein induces trigeminovascular sensitization to both TRPA1 and TRP vanilloid 1 (TRPV1) agonists, a phenomenon linked to headache. In this study, we test the hypothesis that the sensitization of trigeminovascular responses in rats after acrolein exposure via inhalation is associated with changes in levels of endogenous lipids, including TRPV1 agonists, in the trigeminal ganglia, trigeminal nucleus, and cerebellum. Lipidomics analysis of 80 lipids was performed on each tissue after acute acrolein, chronic acrolein, or room air control. Both acute and chronic acrolein exposure drove widespread alterations in lipid levels. After chronic acrolein exposure, levels of all 6Â N-acyl ethanolamines in the screening library, including the endogenous cannabinoid and TRPV1 agonist, N-arachidonoyl ethanolamine, were elevated in trigeminal tissue and in the cerebellum. This increase in TRPV1 ligands by acrolein exposure may indicate further downstream signaling, in that we also show here that a combination of these TRPV1 endogenous agonists increases the potency of the individual ligands in TRPV1-HEK cells. In addition to these TRPV1 agonists, 3 TRPV3 antagonists, 4 TRPV4 agonists, and 25 orphan lipids were up and down regulated after acrolein exposure. These data support the hypothesis that lipid signaling may represent a mechanism by which repeated exposure to the TRPA1 agonist and environmental toxin, acrolein, drives trigeminovascular sensitization.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Pain - Volume 1, JanuaryâJuly 2017, Pages 28-36
Journal: Neurobiology of Pain - Volume 1, JanuaryâJuly 2017, Pages 28-36
نویسندگان
Emma Leishman, Phillip E. Kunkler, Meera Manchanda, Kishan Sangani, Jordyn M. Stuart, Gerry S. Oxford, Joyce H. Hurley, Heather B. Bradshaw,