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Plant toxin β-ODAP activates integrin β1 and focal adhesion : a critical pathway to cause neurolathyrism

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Abstract
Neurolathyrism is a unique neurodegeneration disease caused by beta-N-oxalyl-L-alpha, beta-diaminopropionic (beta-ODAP) present in grass pea seed (Lathyrus stativus L.) and its pathogenetic mechanism is unclear. This issue has become a critical restriction to take full advantage of drought-tolerant grass pea as an elite germplasm resource under climate change. We found that, in a human glioma cell line, beta-ODAP treatment decreased mitochondrial membrane potential, leading to outside release and overfall of Ca2+ from mitochondria to cellular matrix. Increased Ca2+ in cellular matrix activated the pathway of ECM, and brought about the overexpression of beta 1 integrin on cytomembrane surface and the phosphorylation of focal adhesion kinase (FAK). The formation of high concentration of FA units on the cell microfilaments further induced overexpression of paxillin, and then inhibited cytoskeleton polymerization. This phenomenon turned to cause serious cell microfilaments distortion and ultimately cytoskeleton collapse. We also conducted qRT-PCR verification on RNA-sequence data using 8 randomly chosen genes of pathway enrichment, and confirmed that the data was statistically reliable. For the first time, we proposed a relatively complete signal pathway to neurolathyrism. This work would help open a new window to cure neurolathyrism, and fully utilize grass pea germplasm resource under climate change.
Keywords
LATHYRUS-SATIVUS NEUROTOXIN, FIBRILLAR AMYLOID-BETA, BETA-N-OXALYL-L-ALPHA, BETA-DIAMINOPROPIONIC ACID, SURFACE EXPRESSION, NEURONAL DYSTROPHY, IN-VITRO, TRANSCRIPTOME, RECEPTORS, DISEASE, CELLS

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Chicago
Tan, Rui-Yue, Geng-Yan Xing, Guang-Ming Zhou, Feng-Min Li, Wen-Tao Hu, Fernand Lambein, Jun-Lan Xiong, et al. 2017. “Plant Toxin β-ODAP Activates Integrin Β1 and Focal Adhesion : a Critical Pathway to Cause Neurolathyrism.” Scientific Reports 7.
APA
Tan, R.-Y., Xing, G.-Y., Zhou, G.-M., Li, F.-M., Hu, W.-T., Lambein, F., Xiong, J.-L., et al. (2017). Plant toxin β-ODAP activates integrin β1 and focal adhesion : a critical pathway to cause neurolathyrism. SCIENTIFIC REPORTS, 7.
Vancouver
1.
Tan R-Y, Xing G-Y, Zhou G-M, Li F-M, Hu W-T, Lambein F, et al. Plant toxin β-ODAP activates integrin β1 and focal adhesion : a critical pathway to cause neurolathyrism. SCIENTIFIC REPORTS. 2017;7.
MLA
Tan, Rui-Yue, Geng-Yan Xing, Guang-Ming Zhou, et al. “Plant Toxin β-ODAP Activates Integrin Β1 and Focal Adhesion : a Critical Pathway to Cause Neurolathyrism.” SCIENTIFIC REPORTS 7 (2017): n. pag. Print.
@article{8504606,
  abstract     = {Neurolathyrism is a unique neurodegeneration disease caused by beta-N-oxalyl-L-alpha, beta-diaminopropionic (beta-ODAP) present in grass pea seed (Lathyrus stativus L.) and its pathogenetic mechanism is unclear. This issue has become a critical restriction to take full advantage of drought-tolerant grass pea as an elite germplasm resource under climate change. We found that, in a human glioma cell line, beta-ODAP treatment decreased mitochondrial membrane potential, leading to outside release and overfall of Ca2+ from mitochondria to cellular matrix. Increased Ca2+ in cellular matrix activated the pathway of ECM, and brought about the overexpression of beta 1 integrin on cytomembrane surface and the phosphorylation of focal adhesion kinase (FAK). The formation of high concentration of FA units on the cell microfilaments further induced overexpression of paxillin, and then inhibited cytoskeleton polymerization. This phenomenon turned to cause serious cell microfilaments distortion and ultimately cytoskeleton collapse. We also conducted qRT-PCR verification on RNA-sequence data using 8 randomly chosen genes of pathway enrichment, and confirmed that the data was statistically reliable. For the first time, we proposed a relatively complete signal pathway to neurolathyrism. This work would help open a new window to cure neurolathyrism, and fully utilize grass pea germplasm resource under climate change.},
  articleno    = {40677},
  author       = {Tan, Rui-Yue and Xing, Geng-Yan and Zhou, Guang-Ming and Li, Feng-Min and Hu, Wen-Tao and Lambein, Fernand and Xiong, Jun-Lan and Zhang, Sheng-Xiang and Kong, Hai-Yan and Zhu, Hao and Li, Zhi-Xiao and Xiong, You-Cai},
  issn         = {2045-2322},
  journal      = {SCIENTIFIC REPORTS},
  keyword      = {LATHYRUS-SATIVUS NEUROTOXIN,FIBRILLAR AMYLOID-BETA,BETA-N-OXALYL-L-ALPHA,BETA-DIAMINOPROPIONIC ACID,SURFACE EXPRESSION,NEURONAL DYSTROPHY,IN-VITRO,TRANSCRIPTOME,RECEPTORS,DISEASE,CELLS},
  language     = {eng},
  pages        = {11},
  title        = {Plant toxin \ensuremath{\beta}-ODAP activates integrin \ensuremath{\beta}1 and focal adhesion : a critical pathway to cause neurolathyrism},
  url          = {http://dx.doi.org/10.1038/srep40677},
  volume       = {7},
  year         = {2017},
}

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