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10.1186/s12890-016-0247-8 http://scihub22266oqcxt.onion/10.1186/s12890-016-0247-8 C4877999!4877999 !27215284     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27215284 &cmd=llinks): Failed to open stream: HTTP request failed! 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The MK2/HuR signaling pathway regulates TNF-?-induced ICAM-1 expression by promoting the stabilization of ICAM-1 mRNA |pdf=|usr=}}{{27215284 }} gab.com Text The MK2/HuR signaling pathway regulates TNF- -induced ICAM-1 expression by promoting the stabilization of ICAM-1 mRNA JO: BMC Pulm Med http://www.kidney.de/pget.php?&tw=1&pmid=27215284 #FOAvip BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by acute lung inflammation. Intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) play an important role in the development of these diseases. Mitogen-activated protein kinase (MAPK) p38/activated protein kinase 2 (MK2) regulates the expression of ICAM-1 and IL-8 in human lung microvascular endothelial cells (HPMECs) stimulated by tumor necrosis factor-? (TNF-?); however, the underlying molecular mechanism remains unclear. Here, we show that human antigen R (HuR), an RNA binding protein which binds preferentially to AU-rich elements (AREs) and stabilizes mRNAs, regulates TNF-?-induced ICAM-1 expression in the MK2/HuR signaling pathway. METHOD: MK2 and HuR were silenced respectively in HPMECs and then HPMECs were stimulatied with TNF-?. Nucleo-cytoplasmic shuttling of HuR was detected by subcellular fractionation and confocal microscopy in MK2 knockdown HPMECs. In HuR silencing cells, protein and mRNA levels of ICAM-1 and IL-8 were measured by western blot analysis, ELISA and real-time PCR; mRNA stabilization were measured by real-time PCR after actinomycin D (ActD) blocking transcription. Furthermore, we performed neutrophil adhesion assay to assess the adhering capacity after HuR silencing. RESULTS: MK2 were subjected to a knockdown by interfering RNA, the mRNA and protein levels of HuR in human pulmonary microvascular endothelial cells (HPMECs) were not affected. However, after the stimulation of TNF-?, silencing MK2 inhibited HuR accumulation to cytoplasm from nucleus in HPMECs. Consequently, knockdown of HuR by RNA interference in HPMECs, there was reduction in the stability of ICAM-1 mRNA and ICAM-1 protein level. This event was accompanied by a decrease in the adhesion of neutrophils towards HPMECs. Nevertheless, HuR silencing had no effect on the mRNA and protein levels of IL-8. CONCLUSION: These results indicate that MK2 post-transcriptionally regulates TNF-?-induced ICAM-1 expression by altering the cytoplasmic localization of HuR in HPMECs. Twit Text FOAVip The MK2/HuR signaling pathway regulates TNF- -induced ICAM-1 expression by promoting the stabilization of ICAM-1 mRNA ????BMC Pulm Med http://www.kidney.de/pget.php?&tw=1&pmid=27215284 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27215284 #FOAvip English Wikipedia <ref>{{Cite pmid|27215284 }}</ref> The MK2/HuR signaling pathway regulates TNF-?-induced ICAM-1 expression by promoting the stabilization of ICAM-1 mRNA #MMPMID27215284 Wu T ; Shi JX ; Geng S ; Zhou W ; Shi Y ; Su X BMC Pulm Med 2016[May]; 16 (1 ): 84 PMID27215284 show ga BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by acute lung inflammation. Intercellular adhesion molecule-1 (ICAM-1) and interleukin-8 (IL-8) play an important role in the development of these diseases. Mitogen-activated protein kinase (MAPK) p38/activated protein kinase 2 (MK2) regulates the expression of ICAM-1 and IL-8 in human lung microvascular endothelial cells (HPMECs) stimulated by tumor necrosis factor-? (TNF-?); however, the underlying molecular mechanism remains unclear. Here, we show that human antigen R (HuR), an RNA binding protein which binds preferentially to AU-rich elements (AREs) and stabilizes mRNAs, regulates TNF-?-induced ICAM-1 expression in the MK2/HuR signaling pathway. METHOD: MK2 and HuR were silenced respectively in HPMECs and then HPMECs were stimulatied with TNF-?. Nucleo-cytoplasmic shuttling of HuR was detected by subcellular fractionation and confocal microscopy in MK2 knockdown HPMECs. In HuR silencing cells, protein and mRNA levels of ICAM-1 and IL-8 were measured by western blot analysis, ELISA and real-time PCR; mRNA stabilization were measured by real-time PCR after actinomycin D (ActD) blocking transcription. Furthermore, we performed neutrophil adhesion assay to assess the adhering capacity after HuR silencing. RESULTS: MK2 were subjected to a knockdown by interfering RNA, the mRNA and protein levels of HuR in human pulmonary microvascular endothelial cells (HPMECs) were not affected. However, after the stimulation of TNF-?, silencing MK2 inhibited HuR accumulation to cytoplasm from nucleus in HPMECs. Consequently, knockdown of HuR by RNA interference in HPMECs, there was reduction in the stability of ICAM-1 mRNA and ICAM-1 protein level. This event was accompanied by a decrease in the adhesion of neutrophils towards HPMECs. Nevertheless, HuR silencing had no effect on the mRNA and protein levels of IL-8. CONCLUSION: These results indicate that MK2 post-transcriptionally regulates TNF-?-induced ICAM-1 expression by altering the cytoplasmic localization of HuR in HPMECs. |*Signal Transduction [MESH] |Cells, Cultured [MESH] |ELAV-Like Protein 1/*metabolism [MESH] |Endothelial Cells/drug effects/*metabolism [MESH] |Gene Expression Regulation [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Intercellular Adhesion Molecule-1/genetics/*metabolism [MESH] |Interleukin-8/genetics/*metabolism [MESH] |Intracellular Signaling Peptides and Proteins/*metabolism [MESH] |Protein Serine-Threonine Kinases/*metabolism [MESH] |RNA Interference [MESH] |RNA, Messenger/genetics/metabolism [MESH]The MK2/HuR signaling pathway regulates TNF-?-induced ICAM-1 expressio(epmc).pdf DeepDyve Pubget Overpricing