Plasticity‐related gene 1 is important for survival of neurons derived from rat neural stem cells

Abstract

Plasticity-related gene 1 (Prg1) is a membrane-associated lipid phosphate phosphatase. In this study, we first investigated the role of Prg1 in the survival of neurons derived from rat neural stem cells (NSCs) using small interfering RNA (siRNA). Prg1 knock-down decreased the cell number. Interestingly, Prg1 knock-down increased genomic DNA fragmentation, suggesting the possible induction of apoptosis. Exogenously expressed Prg1 rescued the cells from death and restored the loss of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) activity induced with Prg1 siRNA. However, exogenously expressed mutated-Prg1 (the 253rd amino acid, histidine253, had been changed to alanine) did not rescue the cell death or restore the MTT activity. Histidine253 of Prg1 has been reported to be important for lipid phosphate phosphatase activity. These results suggest that Prg1 is important for survival of neurons through its dephosphorylation activity.

PRG-1 relieves pain and depressive-like behaviors in rats of bone cancer pain by regulation of dendritic spine in hippocampus

“…In study on human tissue, PRG-1 was found differentially regulated in the substantia nigra of clinically and histologically confirmed epileptic seizures and Parkinson' s disease patients [37]. At present, studies on PRGs family mainly focus on neuropsychiatric diseases and nerve injuries such as epilepsy [34,38,39], schizophrenia [40,41], memory disorders [35], nerve trauma [42,43], sensory discrimination deficit [44,45], etc. Besides, PRG-1 may be involved in cancerogenesis because the target role of LPA in cancer [33,46].…”

Plasma membrane phospholipid phosphatase-related proteins as pleiotropic regulators of neuron growth and excitability

“…Although there have been no conclusive studies on PLPPR-dependent neuronal survival or apoptosis, it has been reported that knockdown of PLPPR4 in neural stem cells decreases neuron viability in vitro , supposedly via induction of apoptotic death ( Hashimoto et al, 2013 ). It is noteworthy that the H253A mutant of PLPPR4, which disables the conserved LPA binding motif of PLPPRs and PLPPs ( Figure 1B ) and prevents PLPPRs from plasma membrane localization, cannot support PLPPR4-dependent neuronal survival ( Hashimoto et al, 2013 ). Whether this function is unique for PLPPR4 and whether it depends on LPA and LPARs remains to be studied.…”

PRG-1 prevents neonatal stimuli-induced persistent hyperalgesia and memory dysfunction via NSF/Glu/GluR2 signaling

“…To date, studies on PRGs family have mainly focused on neuropsychiatric diseases and nerve injuries such as epilepsy (Ni et al, 2009;Trimbuch et al, 2009;Vogt et al, 2017), schizophrenia (Thalman et al, 2018;Vogt et al, 2016), memory disorders (Liu et al, 2016), nerve trauma (Hashimoto et al, 2013;Peeva et al, 2006), and sensory discrimination deficit (Cheng et al, 2016;Unichenko et al, 2016). We recently delineated a new physiological role for PRG-1 in chronic pain where we found that hippocampal PRG-1 relieves pain and depressive-like behaviors caused by bone cancer pain via P2X 7 R/PRG-1/PP2A pathway regulation of dendritic spine density in a cell-autonomous fashion (Liu et al, 2021a).…”