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.

10.3892/mmr.2018.9002 http://scihub22266oqcxt.onion/10.3892/mmr.2018.9002 C6059687!6059687!29749529     free     free     free 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 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 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 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Med+Rep 2018 ; 18 (1): 322-32 Nephropedia Template TP {{tp|p=29749529|t=2018. ?-synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum-Golgi compartment |pdf=|usr=}}{{29749529}} gab.com Text -synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum-Golgi compartment JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=29749529 #FOAvip Although previous work has demonstrated that the overexpression of wild-type or mutant ?-synuclein (?-syn) can induce cell death via a number of different mechanisms, including oxidative stress, dysfunction of the ubiquitin-proteasome degradation system, mitochondrial damage and endoplasmic reticulum (ER) stress, research interest has primarily focused on neurons. However, there is accumulating evidence that suggests that astrocytes may be involved in the earliest changes, as well as the progression of Parkinson's disease (PD), though the role of ?-syn in astrocytes has not been widely studied. In the present study, it was revealed that the mutant ?-syn (A53T and A30P) in astrocytes triggered ER stress via the protein kinase RNA-like ER kinase/eukaryotic translation initiation factor 2? signaling pathway. Astrocyte apoptosis was induced through a CCAAT-enhancer-binding protein homologous protein-mediated pathway. In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal-astroglial co-culture system, that the overexpression of ?-syn significantly decreased the levels of glia-derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER-Golgi compartment in astrocytes overexpressing ?-syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. Twit Text FOAVip -synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum-Golgi compartment ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=29749529 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29749529 #FOAvip English Wikipedia <ref>{{Cite pmid|29749529}}</ref> ?-synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum-Golgi compartment #MMPMID29749529 Liu M; Qin L; Wang L; Tan J; Zhang H; Tang J; Shen X; Tan L; Wang C Mol Med Rep 2018[Jul]; 18 (1): 322-32 PMID29749529show ga Although previous work has demonstrated that the overexpression of wild-type or mutant ?-synuclein (?-syn) can induce cell death via a number of different mechanisms, including oxidative stress, dysfunction of the ubiquitin-proteasome degradation system, mitochondrial damage and endoplasmic reticulum (ER) stress, research interest has primarily focused on neurons. However, there is accumulating evidence that suggests that astrocytes may be involved in the earliest changes, as well as the progression of Parkinson's disease (PD), though the role of ?-syn in astrocytes has not been widely studied. In the present study, it was revealed that the mutant ?-syn (A53T and A30P) in astrocytes triggered ER stress via the protein kinase RNA-like ER kinase/eukaryotic translation initiation factor 2? signaling pathway. Astrocyte apoptosis was induced through a CCAAT-enhancer-binding protein homologous protein-mediated pathway. In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal-astroglial co-culture system, that the overexpression of ?-syn significantly decreased the levels of glia-derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER-Golgi compartment in astrocytes overexpressing ?-syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future. ä?-synuclein induces apoptosis of astrocytes by causing dysfunction of (epmc).pdf DeepDyve Pubget Overpricing