Journal of Neurochemistry
© International Society for Neurochemistry
Edited By: Jörg Schulz
Impact Factor: 4.244
ISI Journal Citation Reports © Ranking: 2013: 63/252 (Neurosciences); 74/291 (Biochemistry & Molecular Biology)
Online ISSN: 1471-4159
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Recently Published Articles
- Caveolin-1 mediates tissue plasminogen activator-induced MMP-9 up-regulation in cultured brain microvascular endothelial cells
Xinchun Jin, Yanyun Sun, Ji Xu and Wenlan Liu
Article first published online: 4 MAR 2015 | DOI: 10.1111/jnc.13065
Thrombolysis with tissue plasminogen activator (tPA) increases matrix metalloproteinase-9 (MMP-9) activity in the ischemic brain, which exacerbates ischemic blood brain barrier (BBB) injury and increases the risk of symptomatic cerebral hemorrhage. Our results suggest a novel mechanism underlying this tPA-MMP 9 axis. In response to tPA treatment, caveolin-1 protein levels increased in endothelial cells, which mediate MMP-9 mRNA up-regulation and its secretion into extracellular space. Caveolin-1 may, however, not facilitate MMP-9 secretion in endothelial cells. Our data suggest caveolin-1 as a novel therapeutic target for protecting the BBB against ischemic damage. The schematic outlines tPA-induced MMP-9 upreguation.
- Protein kinase A directly phosphorylates metabotropic glutamate receptor 5 to modulate its function
Ken Uematsu, Myriam Heiman, Marina Zelenina, Júlio Padovan, Brian T. Chait, Anita Aperia, Akinori Nishi and Paul Greengard
Article first published online: 4 MAR 2015 | DOI: 10.1111/jnc.13038
We identified serine residue 870 (S870) in metabotropic glutamate receptor 5 (mGluR5) as a direct substrate for protein kinase A (PKA). The phosphorylation of this site regulates the ability of mGluR5 to induce extracellular signal-regulated kinase (ERK) phosphorylation and intracellular Ca2+ oscillations. This study provides a direct molecular mechanism by which PKA signaling interacts with glutamate neurotransmission.
- Regulation of RAGE splicing by hnRNP A1 and Tra2β-1 and its potential role in AD pathogenesis
Xiao-Yan Liu, Hong-Lei Li, Jia-Bin Su, Fei-Hong Ding, Jing-Jing Zhao, Fang Chai, Yuan-Xin Li, Shi-Cao Cui, Feng-Yan Sun, Zhi-Ying Wu, Ping Xu and Xian-Hua Chen
Article first published online: 2 MAR 2015 | DOI: 10.1111/jnc.13069
The receptor for advanced glycation end products (RAGE) gene expresses two major alternative splicing isoforms, membrane-bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis. Mechanism for imbalanced expression of these two isoforms in AD brain remains elusive. We proposed here a hypothetic model to illustrate that impaired glucose metabolism in AD brain may increase the expression of splicing protein hnRNP A1 and reduce Tra2β-1, which cause the imbalanced expression of mRAGE and esRAGE.
- Schwann cells contribute to neurodegeneration in transthyretin amyloidosis
Tatsufumi Murakami, Kazunori Sango, Kazuhiko Watabe, Naoko Niimi, Shizuka Takaku, Zhenghua Li, Ken-ichi Yamamura and Yoshihide Sunada
Article first published online: 2 MAR 2015 | DOI: 10.1111/jnc.13068
We established a spontaneously immortalized Schwann cell line derived from familial amyloidotic polyneuropathy transgenic mice. Conditioned medium from the cells contained variant transthyretin (TTR), and inhibited neurite outgrowth of neurons. TTR aggregates were observed in the Schwann cells and satellite cells of aged mice. Proteasome inhibition induced TTR aggregates as aggresomes in the cultured cells. These results support the hypothesis that Schwann cells contribute to neurodegeneration in familial amyloidotic polyneuropathy (FAP).
- Dynamic increases in AMPA receptor phosphorylation in the rat hippocampus in response to amphetamine
Li-Min Mao, Bing Xue, Dao-Zhong Jin and John Q. Wang
Article first published online: 2 MAR 2015 | DOI: 10.1111/jnc.13067
Acute injection of amphetamine increased phosphorylation of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 subunits at a protein kinase A (PKA)-sensitive site (S845) in the rat hippocampus. This increase was dose- and time-dependent and correlated with an increase in surface GluA1 expression. Thus, amphetamine can upregulate GluA1 phosphorylation and surface trafficking of GluA1 in hippocampal neurons in vivo.