RNA-Seq Analysis of Spinal Cord Tissues from hPFN1(G118V) Transgenic Mouse Model of ALS at Pre-symptomatic and End-Stages of Disease.
RNA-Seq Analysis of Spinal Cord Tissues from hPFN1(G118V) Transgenic Mouse Model of ALS at Pre-symptomatic and End-Stages of Disease.
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DOI：
10.1038/s41598-018-31132-y
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发表时间：
2018-09-13
影响因子：
4.6
通讯作者：
Kiaei M
中科院分区：
文献类型：
--
作者：
Barham C;Fil D;Byrum SD;Rahmatallah Y;Glazko G;Kiaei M
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that leads to the loss of motor neurons. The molecular mechanisms of motor neuron degeneration are largely unknown and there are currently no effective therapies to treat this disease. In this work, we report whole transcriptome profiling of spinal cords of mutant transgenic hPFN1G118V mice and their wildtype transgenic hPFN1WT controls at a pre-symptomatic stage and at the end-stage of disease. Analyses revealed that end-stage hPFN1G118V mice had 890 differentially expressed genes (747 up-regulated, 143 down-regulated) when compared to pre-symptomatic hPFN1G118V mice, and they had 836 differentially expressed genes (742 up-regulated, 94 down-regulated) when compared to age-matched hPFN1WT controls. Pre-symptomatic hPFN1G118V mice were not significantly different from age-matched hPFN1WT controls. Ingenuity Pathway Analysis identified inflammatory pathways significantly activated in end-stage hPFN1G118V samples, suggesting an excess of glial activation at end-stage disease, possibly due to an increase in glial composition within the spinal cord during disease progression. In conclusion, our RNA-Seq data identified molecules and pathways involved in the mechanisms of neurodegeneration that could potentially serve as therapeutic targets for ALS.
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影响因子：
4.2
作者：
Smith BN;Vance C;Scotter EL;Troakes C;Wong CH;Topp S;Maekawa S;King A;Mitchell JC;Lund K;Al-Chalabi A;Ticozzi N;Silani V;Sapp P;Brown RH Jr;Landers JE;Al-Sarraj S;Shaw CE
通讯作者：
Shaw CE
影响因子：
14.9
作者：
Ritchie ME;Phipson B;Wu D;Hu Y;Law CW;Shi W;Smyth GK
通讯作者：
Smyth GK
影响因子：
5.3
作者：
Heath PR;Kirby J;Shaw PJ
通讯作者：
Shaw PJ
影响因子：
3.5
作者：
Fil D;DeLoach A;Yadav S;Alkam D;MacNicol M;Singh A;Compadre CM;Goellner JJ;O'Brien CA;Fahmi T;Basnakian AG;Calingasan NY;Klessner JL;Beal FM;Peters OM;Metterville J;Brown RH Jr;Ling KKY;Rigo F;Ozdinler PH;Kiaei M
通讯作者：
Kiaei M
影响因子：
3.1
作者：
D'Arrigo, Antonello;Colavito, Davide;Leon, Alberta
通讯作者：
Leon, Alberta