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.

10.1172/JCI91301 http://scihub22266oqcxt.onion/10.1172/JCI91301 C5531407!5531407 !28737509     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28737509 &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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 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\28737509 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2017 ; 127 (8 ): 3136-3151 Nephropedia Template TP {{tp|p=28737509 |t=2017. Astrocytic tight junctions control inflammatory CNS lesion pathogenesis |pdf=|usr=}}{{28737509 }} gab.com Text Astrocytic tight junctions control inflammatory CNS lesion pathogenesis JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28737509 #FOAvip Lesions and neurologic disability in inflammatory CNS diseases such as multiple sclerosis (MS) result from the translocation of leukocytes and humoral factors from the vasculature, first across the endothelial blood-brain barrier (BBB) and then across the astrocytic glia limitans (GL). Factors secreted by reactive astrocytes open the BBB by disrupting endothelial tight junctions (TJs), but the mechanisms that control access across the GL are unknown. Here, we report that in inflammatory lesions, a second barrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctional adhesion molecule A (JAM-A) subunits is induced at the GL. In a human coculture model, CLDN4-deficient astrocytes were unable to control lymphocyte segregation. In models of CNS inflammation and MS, mice with astrocyte-specific Cldn4 deletion displayed exacerbated leukocyte and humoral infiltration, neuropathology, motor disability, and mortality. These findings identify a second inducible barrier to CNS entry at the GL. This barrier may be therapeutically targetable in inflammatory CNS disease. Twit Text FOAVip Astrocytic tight junctions control inflammatory CNS lesion pathogenesis ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28737509 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28737509 #FOAvip English Wikipedia <ref>{{Cite pmid|28737509 }}</ref> Astrocytic tight junctions control inflammatory CNS lesion pathogenesis #MMPMID28737509 Horng S ; Therattil A ; Moyon S ; Gordon A ; Kim K ; Argaw AT ; Hara Y ; Mariani JN ; Sawai S ; Flodby P ; Crandall ED ; Borok Z ; Sofroniew MV ; Chapouly C ; John GR J Clin Invest 2017[Aug]; 127 (8 ): 3136-3151 PMID28737509 show ga Lesions and neurologic disability in inflammatory CNS diseases such as multiple sclerosis (MS) result from the translocation of leukocytes and humoral factors from the vasculature, first across the endothelial blood-brain barrier (BBB) and then across the astrocytic glia limitans (GL). Factors secreted by reactive astrocytes open the BBB by disrupting endothelial tight junctions (TJs), but the mechanisms that control access across the GL are unknown. Here, we report that in inflammatory lesions, a second barrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctional adhesion molecule A (JAM-A) subunits is induced at the GL. In a human coculture model, CLDN4-deficient astrocytes were unable to control lymphocyte segregation. In models of CNS inflammation and MS, mice with astrocyte-specific Cldn4 deletion displayed exacerbated leukocyte and humoral infiltration, neuropathology, motor disability, and mortality. These findings identify a second inducible barrier to CNS entry at the GL. This barrier may be therapeutically targetable in inflammatory CNS disease. |*Inflammation [MESH] |*Tight Junctions [MESH] |Animals [MESH] |Astrocytes/*cytology [MESH] |Blood-Brain Barrier/pathology [MESH] |Cell Adhesion Molecules/metabolism [MESH] |Central Nervous System/*pathology [MESH] |Claudin-1/metabolism [MESH] |Claudin-4/metabolism [MESH] |Coculture Techniques [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Encephalomyelitis, Autoimmune, Experimental/pathology [MESH] |Female [MESH] |Humans [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Multiple Sclerosis/pathology [MESH] |Nervous System Diseases/*pathology [MESH]Astrocytic tight junctions control inflammatory CNS lesion pathogenesi(epmc).pdf DeepDyve Pubget Overpricing