Cypermethrin-induced cortical neurons apoptosis via the Nrf2/ARE signaling pathway

Zhou, Liang; Zhou, Meng; Tan, Handan; Xiao, Mengxi

doi:10.1016/j.pestbp.2020.02.013

Cited by 32 publications

(21 citation statements)

References 46 publications

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“…[ 61,62 ] Another study examined the protective role of the Nrf2/ARE signaling pathway in cypermethrin‐induced apoptosis of the cortical neurons. [ 63 ] Thus, these results suggest that Nrf2 is associated with cytoprotection, cell detoxification, and pesticide stress tolerance, and therefore, Nrf2 inhibition may provide new therapeutic interventions.…”

Section: Discussionmentioning

confidence: 99%

Organophosphate‐pesticides induced survival mechanisms and APE1‐mediated Nrf2 regulation in non‐small‐cell lung cancer cells

Thakur

Sarkar

Dhiman

et al. 2020

J Biochem & Molecular Tox

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Epidemiological and molecular studies have indicated that environmental exposure to organophosphate pesticides (OPPs) is associated with increased cancer risk; however, the underlying molecular mechanisms still need to be explained. Increasing cancer incidence is linked to OPPs‐induced oxidative stress (OS). Our study evaluates monocrotophos (MCP) and chlorpyrifos (CP)‐induced OS responses and apurinic/apyrimidinic endonuclease 1 (APE1) role in human non‐small‐cell lung cancer (NSCLC) cells. Our prior study has implicated OPPs‐induced base excision repair (BER)‐pathway dysregulation and APE1‐mediated regulation of transcription factor (TF) c‐jun in A549 cells. We further investigated the effects of MCP and CP on apoptosis, proliferation, and APE1's redox‐regulation of nuclear factor‐like 2 (Nrf2). Data demonstrates that MCP and CP at subtoxic concentrations induced reactive oxygen species generation and oxidative DNA base damage 8‐oxo‐dG lesions in NCI‐H1299 cells. CP moderately upregulated the apoptosis‐inducing factor (AIF) in A549 cells, however, it did not trigger other pro‐apoptotic factors viz. caspase‐9 and caspase‐3, suggesting early caspase‐independent apoptosis. However, dose‐dependent AIF‐downregulation was observed for MCP treatment. Furthermore, CP and MCP treatments upregulated proliferating cell nuclear antigen levels. Immunofluorescent confocal imaging showed the colocalization of APE1 with Nrf2 in 10 µM CP‐ and MCP‐treated NCI‐H1299 cells. Immunoprecipitation confirmed that APE1 and Nrf2 physically interacted, indicating the role of APE1‐mediated Nrf2 activation following OPPs treatment. This study suggests that low concentration MCP and CP exposure generates OS along with DNA damage, and modulates apoptosis, and APE1‐mediated Nrf2 activation, which might be considered as the possible mechanism promoting lung cancer cell survival, suggesting that APE1 may have the potential to become a therapeutic target for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

Organophosphate‐pesticides induced survival mechanisms and APE1‐mediated Nrf2 regulation in non‐small‐cell lung cancer cells

Thakur

Sarkar

Dhiman

et al. 2020

J Biochem & Molecular Tox

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“…The Nrf2/ARE pathway is protective of central nervous system diseases [29] and is a key defense against oxidative stress and in ammation [30]. Because TET1 can demethylate Nrf2 and increase its active expression, we think that TET1 may affect DN by mediating the Nrf2/ARE pathway.…”

Section: Discussionmentioning

confidence: 97%

The Role of Transcription Factor Ap1 in The Activation of Nrf2/ARE Pathway Through TET1 in Diabetic Nephropathy

Tan

Cao

et al. 2020

Preprint

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Background: TET1 abnormal expression is related to tumorigenesis, but its role in diabetic nephropathy (DN), the most common diabetic complication, is unclear. We attempted to probe the possible mechanism of TET1 in DN.Methods: The DN rat model was established and verified by marker detection and histopathological observation. The in vitro model was established in human mesangial cells (HMCs) induced by high glucose (HG), and levels of IL-6, TNF-α, IV-C and FN were examined. The differentially expressed mRNAs were screened out by microarray analysis. The most differentially expressed mRNA (TET1) was overexpressed in DN rats and HMCs to evaluate inflammation, cell viability and apoptosis, biochemical indexes and renal injury. The upstream transcription factor of TET1 was verified, and overexpressed with/without TETE1 to access its role in inflammation and renal injury. The downstream gene and pathway were also verified.Results: TET1 was poorly expressed in DN rats and HG-HMCs. High expression of TET1 decreased biochemical indexes, and renal injury of DN rats, decreased the activity, fibrosis and inflammation of HG-HMCs. Ap1 inhibited TET1 expression, and enhanced secretion of inflammatory factors in HG-HMCs and renal injury in DN rats. TET1 overexpression inhibited the effect of Ap1 on DN. TET1 promoted the transcription of Nrf2. The Ap1/Tet1 axis mediated the Nrf2/ARE pathway activity.Conclusion: Ap1 inhibits TET1 expression and activates the Nrf2/ARE pathway in DN, thus aggravating inflammation and renal injury.

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“…The Nrf2/ARE pathway is protective of central nervous system diseases (S. Zhou et al, 2020) and is a key defense against oxidative stress and inflammation (Hassanein et al, 2020). As TET1 can demethylate Nrf2 and increase its active expression, we think that TET1 may affect DN by mediating the Nrf2/ARE pathway.…”

Section: Discussionmentioning

confidence: 99%

The role of transcription factor Ap1 in the activation of the Nrf2/ARE pathway through TET1 in diabetic nephropathy

Tan

Cao

et al. 2021

Cell Biology International

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Background: TET1 abnormal expression is related to tumorigenesis, but its role in diabetic nephropathy (DN), the most common diabetic complication, is unclear. We attempted to probe the possible mechanism of TET1 in DN. Methods: The DN rat model was established and veri ed by marker detection and histopathological observation. The in vitro model was established in human mesangial cells (HMCs) induced by high glucose (HG), and levels of IL-6, TNF-α, IV-C and FN were examined. The differentially expressed mRNAs were screened out by microarray analysis. The most differentially expressed mRNA (TET1) was overexpressed in DN rats and HMCs to evaluate in ammation, cell viability and apoptosis, biochemical indexes and renal injury. The upstream transcription factor of TET1 was veri ed, and overexpressed with/without TETE1 to access its role in in ammation and renal injury. The downstream gene and pathway were also veri ed. Results: TET1 was poorly expressed in DN rats and HG-HMCs. High expression of TET1 decreased biochemical indexes, and renal injury of DN rats, decreased the activity, brosis and in ammation of HG-HMCs. Ap1 inhibited TET1 expression, and enhanced secretion of in ammatory factors in HG-HMCs and renal injury in DN rats. TET1 overexpression inhibited the effect of Ap1 on DN. TET1 promoted the transcription of Nrf2. The Ap1/Tet1 axis mediated the Nrf2/ARE pathway activity. Conclusion: Ap1 inhibits TET1 expression and activates the Nrf2/ARE pathway in DN, thus aggravating in ammation and renal injury.

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Cypermethrin-induced cortical neurons apoptosis via the Nrf2/ARE signaling pathway

Cited by 32 publications

References 46 publications

Organophosphate‐pesticides induced survival mechanisms and APE1‐mediated Nrf2 regulation in non‐small‐cell lung cancer cells

Organophosphate‐pesticides induced survival mechanisms and APE1‐mediated Nrf2 regulation in non‐small‐cell lung cancer cells

The Role of Transcription Factor Ap1 in The Activation of Nrf2/ARE Pathway Through TET1 in Diabetic Nephropathy

The role of transcription factor Ap1 in the activation of the Nrf2/ARE pathway through TET1 in diabetic nephropathy

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