Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.4049/jimmunol.1401372 http://scihub22266oqcxt.onion/10.4049/jimmunol.1401372 C4216178!4216178!25261473     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25261473&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25261473.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2014 ; 193 (9): 4558-67 Nephropedia Template TP {{tp|p=25261473|t=2014. miR-15a/16 Regulates Macrophage Phagocytosis After Bacterial Infection |pdf=|usr=}}{{25261473}} gab.com Text miR-15a/16 Regulates Macrophage Phagocytosis After Bacterial Infection JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25261473 #FOAvip Bacterial infection and its associated sepsis are devastating clinical entities which lead to high mortality and morbidity in critically ill patients. Phagocytosis, along with other innate immune responses, exerts crucial impacts on the outcomes of these patients. MicroRNAs (miRNAs) are a novel class of regulatory noncoding RNAs targeting specific mRNAs for modulation of translation and expression of a targeted protein. The roles of miRNAs in host defense against bacterial sepsis remain unclear. We found that bacterial infections and/or bacterial-derived LPS enhanced the level of miR-15a/16 in bone marrow derived macrophages (BMDMs). Deletion of miR-15a/16 (miR-15a/16-/-) in myeloid cells significantly decreased the bacterial infection associated mortality in sepsis mouse models. Moreover, miR-15a/16 deficiency (miR-15a/16-/-) resulted in augmented phagocytosis and generation of mitochondrial reactive oxygen species (ROS) in BMDMs. Supportively, over-expression of miR-15a/16 using miRNA mimics led to decreased phagocytosis and decreased generation of mitochondrial ROS. Mechanistically, deletion of miR-15a/16 up-regulated the expression of toll-like receptor 4 (TLR4) via targeting the principle transcriptional regulator PU.1 locating on the promoter region of TLR4, and further modulated TLR4's downstream signaling molecules, including Rho GTPase Cdc 42 and TRAF6. Additionally, deficiency of miR-15a/16 also facilitated TLR4-mediated pro-inflammatory cytokine/chemokine release from BMDMs at the initial phase of infections. Taken together, miR-15a/16 altered phagocytosis and bacterial clearance by targeting, at least partially, on the TLR4-associated pathways, subsequently affecting the survival of septic mice. Twit Text FOAVip miR-15a/16 Regulates Macrophage Phagocytosis After Bacterial Infection ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25261473 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25261473 #FOAvip English Wikipedia <ref>{{Cite pmid|25261473}}</ref> miR-15a/16 Regulates Macrophage Phagocytosis After Bacterial Infection #MMPMID25261473 Moon HG; Yang J; Zheng Y; Jin Y J Immunol 2014[Nov]; 193 (9): 4558-67 PMID25261473show ga Bacterial infection and its associated sepsis are devastating clinical entities which lead to high mortality and morbidity in critically ill patients. Phagocytosis, along with other innate immune responses, exerts crucial impacts on the outcomes of these patients. MicroRNAs (miRNAs) are a novel class of regulatory noncoding RNAs targeting specific mRNAs for modulation of translation and expression of a targeted protein. The roles of miRNAs in host defense against bacterial sepsis remain unclear. We found that bacterial infections and/or bacterial-derived LPS enhanced the level of miR-15a/16 in bone marrow derived macrophages (BMDMs). Deletion of miR-15a/16 (miR-15a/16-/-) in myeloid cells significantly decreased the bacterial infection associated mortality in sepsis mouse models. Moreover, miR-15a/16 deficiency (miR-15a/16-/-) resulted in augmented phagocytosis and generation of mitochondrial reactive oxygen species (ROS) in BMDMs. Supportively, over-expression of miR-15a/16 using miRNA mimics led to decreased phagocytosis and decreased generation of mitochondrial ROS. Mechanistically, deletion of miR-15a/16 up-regulated the expression of toll-like receptor 4 (TLR4) via targeting the principle transcriptional regulator PU.1 locating on the promoter region of TLR4, and further modulated TLR4's downstream signaling molecules, including Rho GTPase Cdc 42 and TRAF6. Additionally, deficiency of miR-15a/16 also facilitated TLR4-mediated pro-inflammatory cytokine/chemokine release from BMDMs at the initial phase of infections. Taken together, miR-15a/16 altered phagocytosis and bacterial clearance by targeting, at least partially, on the TLR4-associated pathways, subsequently affecting the survival of septic mice. �miR-15a/16 Regulates Macrophage Phagocytosis After Bacterial Infection(epmc).pdf DeepDyve Pubget Overpricing