Neuropathy target esterase: An essential enzyme for neural development and axonal maintenance

Chang, Ping‐An; Wu, Yi‐Jun

doi:10.1016/j.biocel.2009.12.007

Cited by 31 publications

(27 citation statements)

References 27 publications

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“…2,38 Furthermore, a prominent target for OPs that induce OPIDN, is neuropathy target esterase (NTE), a member of the patatin-like phospholipase (PNPLA) family whose functions include regulation of lipid metabolism and cell signalling. [40][41] Although NTE (PNPLA6) has been detected in nonneuronal tissues including human heart, 42 it is not known if mitotic or differentiated H9c2 cells express NTE. Although beyond the scope of the present study, it would be of interest to investigate NTE expression and the effect of PSP on NTE activity in H9c2 cells.…”

Section: Identification Of Psp Binding Proteinsmentioning

confidence: 99%

Phenyl Saligenin Phosphate Induced Caspase-3 and c-Jun N-Terminal Kinase Activation in Cardiomyocyte-Like Cells

Felemban

Garner

Smida

et al. 2015

Chem. Res. Toxicol.

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At present, little is known about the effect(s) of organophosphorous compounds (OPs) on cardiomyocytes. In this study we have investigated the effects of phenyl saligenin phosphate (PSP), two organophosphorothioate insecticides (diazinon and chlorpyrifos) and their acutely toxic metabolites (diazoxon and chlorpyrifos oxon) on mitotic and differentiated H9c2 cardiomyoblasts. OP-induced cytotoxicity was assessed by monitoring MTT reduction, LDH release and caspase-3 activity. Cytotoxicity was not observed with diazinon, diazoxon or chlorpyrifos oxon (48 h exposure; 200 µM).Chlorpyrifos-induced cytotoxicity was only evident at concentrations >100 µM. In

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Section: Identification Of Psp Binding Proteinsmentioning

confidence: 99%

Phenyl Saligenin Phosphate Induced Caspase-3 and c-Jun N-Terminal Kinase Activation in Cardiomyocyte-Like Cells

Felemban

Garner

Smida

et al. 2015

Chem. Res. Toxicol.

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“…In the adult, NTE is observed throughout the brain, particularly in the hippocampus and cortex [11, 12]. Additionally, NTE is also expressed in non-neural tissues, such as spleen, liver and placenta [7, 13, 14]. Gurba et al showed that human placental NTE is similar to forms found in avian and human brain [14].…”

Section: Introductionmentioning

confidence: 97%

“…This syndrome is characterized by delayed paralysis of the lower limbs due to degeneration of nerve axons in the spinal cord and peripheral nerves [7, 8]. However, the human NTE gene was cloned only 10 years ago [9, 10].…”

Section: Introductionmentioning

confidence: 99%

“…Neuropathy target esterase (NTE), also named neurotoxic target esterase, was originally discovered 40 years ago as the primary target of organophosphorus (OP) compounds that cause delayed neuropathy [7]. This syndrome is characterized by delayed paralysis of the lower limbs due to degeneration of nerve axons in the spinal cord and peripheral nerves [7, 8].…”

Section: Introductionmentioning

confidence: 99%

“…Histological analysis indicated that NTE is essential for the formation of labyrinth layer and survival and differentiation of secondary giant cells [14, 15]. In addition, NTE has been demonstrated to have potential lysophospholipase activity and deacylate phosphatidylcholine (PC) to glycerophosphocholine (GPC) as a phospholipase B in Drosophila and mammalian cells [7, 16-18]. Furthermore, Omatsu et al found that phosphatidylserine (PS) /PC microvesicles can induce preeclampsia-like changes in pregnant mice [19].…”

Section: Introductionmentioning

confidence: 99%

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Down-Regulation of Neuropathy Target Esterase in Preeclampsia Placenta Inhibits Human Trophoblast Cell Invasion via Modulating MMP-9 Levels

Zhong

Chen

Ling

et al. 2018

Cell Physiol Biochem

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Background/Aims: Neuropathy target esterase (NTE, also known as neurotoxic esterase) is proven to deacylate phosphatidylcholine (PC) to glycerophosphocholine as a phospholipase B. Recently; studies showed that artificial phosphatidylserine/PC microvesicles can induce preeclampsia (PE)-like changes in pregnant mice. However, it is unclear whether NTE plays a key role in the pathology of PE, a pregnancy-related disease, which was characterized by deficient trophoblast invasion and reduced trophoblast-mediated remodeling of spiral arteries. The aim of this study was to investigate the expression pattern of NTE in the placenta from women with PE and normal pregnancy, and the molecular mechanism of NTE involved in the development of PE. Methods: NTE expression levels in placentas from 20 pregnant women with PE and 20 healthy pregnant women were detected using quantitative PCR and immunohistochemistry staining. The effect of NTE on trophoblast migration and invasion and the underlying mechanisms were examined in HTR-8/SVneo cell lines by transfection method. Results: NTE mRNA and protein expression levels were significantly decreased in preeclamptic placentas than normal control. Over-expression of NTE in HTR-8/SVneo cells significantly promoted trophoblast cells migration and invasion and was associated with increased MMP-9 levels. Conversely, shRNA-mediated down-regulation of NTE markedly inhibited the cell migration and invasion. In addition, silencing NTE reduced the MMP-9 activity and phosphorylated Erk1/2 and AKT levels. Conclusions: Our results suggest that the decreased NTE may contribute to the development of PE through impairing trophoblast invasion by down-regulating MMP-9 via the Erk1/2 and AKT signaling pathway.

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Reduced neuropathy target esterase in pre‐eclampsia suppresses tube formation of HUVECs via dysregulation of phospholipid metabolism

Shen

Liu

et al. 2020

Journal Cellular Physiology

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Recently, studies have shown that neuropathy target esterase (NTE) is essential to placental and normal blood vessel development. However, whether it is involved in abnormal placenta angiogenesis of pre-eclampsia remains unknown. Thus, our aim was to observe the expression of NTE in pre-eclamptic placentas and its effects and mechanism of NTE on the migration and the tube formation of human umbilical vein endothelial cells (HUVECs). Immunohistochemical staining showed that the NTE protein was intensely located in blood vessels of the normal pregnant placenta. However, western blot revealed that the expression level of NTE protein was significantly reduced in pre-eclamptic placenta. The results indicated that overexpression of NTE significantly promoted the migration and the tube formation of HUVECs compared with those of the control and scramble short hairpin RNA (shRNA) group. Conversely, NTE shRNA obviously inhibited the migration and the tube formation of HUVECs. Additionally, chromatography assay evidenced that NTE overexpression significantly reduced the level of phosphatidylcholine (PC) of HUVECs, but NTE shRNA obviously increased the level of PC of HUVECs. Furthermore, exogenous PC and lysophosphatidylcholine (LPC) significantly inhibited the tube formation of HUVECs in a dose-dependent manner. Collectively, our results suggest that reduced NTE in placenta may contribute to abnormal placenta angiogenesis of pre-eclampsia via the dysregulation of PC and LPC metabolism.

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Neuropathy target esterase: An essential enzyme for neural development and axonal maintenance

Cited by 31 publications

References 27 publications

Phenyl Saligenin Phosphate Induced Caspase-3 and c-Jun N-Terminal Kinase Activation in Cardiomyocyte-Like Cells

Phenyl Saligenin Phosphate Induced Caspase-3 and c-Jun N-Terminal Kinase Activation in Cardiomyocyte-Like Cells

Down-Regulation of Neuropathy Target Esterase in Preeclampsia Placenta Inhibits Human Trophoblast Cell Invasion via Modulating MMP-9 Levels

Reduced neuropathy target esterase in pre‐eclampsia suppresses tube formation of HUVECs via dysregulation of phospholipid metabolism

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