Unsaturated but not saturated fatty acids induce transcriptional regulation of CCL2 in pancreatic acini. A potential role in acute pancreatitis
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- 作者：A. Mateu ; I. De Dios ; M.A. Manso ; L. Ramudo ; ramudo@usal.es" class="auth_mail" title="E-mail the corresponding author
- 关键词：AP ; acute pancreatitis ; CCL2 ; chemokine (C&ndash ; C motif) ligand 2 ; ERK ; extracellular signal-regulated kinase ; FA ; fatty acid ; JAK ; Janus kinase ; JNK ; Jun NH2-terminal kinase ; LA ; linoleic acid ; MAPKs ; mitogen-activated protein kinases ; NF-魏B ; nuclear factor-kappa B ; OA ; oleic acid ; PA ; palmitic acid ; PPAR ; peroxisome proliferator-activated receptor ; SA ; stearic acid ; SFA ; saturated fatty acid ; STAT ; signal transducer and activator of transcription ; UFA ; unsaturated fatty acid ; 15d-PGJ2 ; 15-Deo
- 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：1852
- 期：12
- 页码：2671-2677
- 全文大小：903 K
文摘
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Palmitic and stearic acids do not change the CCL2 expression in pancreatic acini.
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The unsaturated fatty acids (UFAs) oleic and linoleic up-regulate CCL2 in acini.
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MAPKs and JAK act as upstreams in the acinar CCL2 expression induced by UFAs.
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UFAs-induced CCL2 up-regulation is synergically mediated by NF-魏B and STAT3.
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By blocking NF-魏B and STAT3, 15d-PGJ2 inhibits the UFA-induced CCL2 expression.