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Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Biochem+Biophys+Res+Commun 2017 ; 493 (1): 494-499 Nephropedia Template TP
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Activation of transient receptor potential melastatin 7 (TRPM7) channel increases basal autophagy and reduces amyloid beta-peptide #MMPMID28870815
Oh HG; Chung S
Biochem Biophys Res Commun 2017[Nov]; 493 (1): 494-499 PMID28870815show ga
Cerebral accumulation of amyloid beta-peptide (Abeta), which is produced from amyloid precursor protein (APP), is the primary cause of Alzheimer's disease (AD). Autophagy recycles cellular components and digests intracellular components including Abeta. The Ca(2+)- and Mg(2+)-permeable transient receptor potential melastatin 7 (TRPM7) channel underlies the constitutive Ca(2+) influx in some cells. Since we already reported that TRPM7 channel-mediated Ca(2+) influx regulates basal autophagy, we hypothesize that the activation of TRPM7 channel could increase basal autophagy and consequently decrease Abeta. In this study, we showed that naltriben (NTB), a specific TRPM7 channel activator, induced Ca(2+) influx and activated autophagic signaling in neuroblastoma SH-SY5Y cells. NTB also promoted co-localization of LC3 and APP, and reduced Abeta. Furthermore, we found that an early-onset familial AD-associated presenilin1 DeltaE9 (PS1 DeltaE9) mutant cells had attenuated basal autophagy. NTB was able to recover autophagy and decrease Abeta in PS1 DeltaE9 cells. Our results show that the activating TRPM7 channel may prevent AD-related Abeta neuropathology via modulating Ca(2+)-regulated basal autophagy.