The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells

Objectives The study aimed to investigate the signalling mechanism for TRPM2 channel activation by non-cytolytic oxidative stress in microglia.Methods Microglia from wild-type (WT) and TRPM2-knockout (KO) mice were exposed to 10-30 mM H2O2 for up to 24 hours. Morphological changes characteristic of...

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Main Authors: Sharifah Alawieyah Syed Mortadza, Nur Zulaikha Mohamad Zahir, Chew Tze Wei, Lin-Hua Jiang
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Redox Report
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Online Access:https://www.tandfonline.com/doi/10.1080/13510002.2025.2503131
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author Sharifah Alawieyah Syed Mortadza
Nur Zulaikha Mohamad Zahir
Chew Tze Wei
Lin-Hua Jiang
author_facet Sharifah Alawieyah Syed Mortadza
Nur Zulaikha Mohamad Zahir
Chew Tze Wei
Lin-Hua Jiang
author_sort Sharifah Alawieyah Syed Mortadza
collection DOAJ
description Objectives The study aimed to investigate the signalling mechanism for TRPM2 channel activation by non-cytolytic oxidative stress in microglia.Methods Microglia from wild-type (WT) and TRPM2-knockout (KO) mice were exposed to 10-30 mM H2O2 for up to 24 hours. Morphological changes characteristic of microglial activation, [Ca2+]c, ROS generation and the effects of inhibiting particular signalling pathways were examined.Results Exposure of WT microglia to H2O2 for 24 hours caused no cell death but induced salient morphological changes, which was prevented by TRPM2-KO. Exposure of WT microglia to H2O2 to 2 hours failed, and extension to 8 hours was required, to induce an increase in [Ca2+]c, which was abolished by TRPM2-KO. Exposure of microglia to H2O2 for 8 hours induced ROS generation, which was suppressed by inhibition of PKC and NADPH oxidases (NOX). H2O2-induced PARP activation in TRPM2-KO cells was lower than that in WT cells. Furthermore, H2O2-induced activation of PARP and TRPM2 and morphological changes were attenuated by inhibition of PCK and NOX as well as PYK2 and MEK/ERK.Conclusion Our results support that PKC/NOX-mediated ROS generation and TRPM2-mediated Ca2+-induced activation of the PYK2/MEK/ERK pathway form a positive feedback mechanism to drive TRPM2 channel activation by non-cytolytic oxidative stress.
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spelling doaj-art-a2e5d1642c1d4a2b9cfda170dad4740d2025-08-20T03:09:42ZengTaylor & Francis GroupRedox Report1351-00021743-29282025-12-0130110.1080/13510002.2025.2503131The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cellsSharifah Alawieyah Syed Mortadza0Nur Zulaikha Mohamad Zahir1Chew Tze Wei2Lin-Hua Jiang3Sino-UK Joint Laboratory of Brain Function and Injury of Henan Province, Department of Physiology and Pathophysiology, Xinxiang Medical University, Xinxiang, People's Republic of ChinaDepartment of Biochemistry, Faculty of Biotechnology and Biomolecular Sciences, Universiti Putra Malaysia, Serdang, MalaysiaDepartment of Biochemistry, Faculty of Biotechnology and Biomolecular Sciences, Universiti Putra Malaysia, Serdang, MalaysiaSino-UK Joint Laboratory of Brain Function and Injury of Henan Province, Department of Physiology and Pathophysiology, Xinxiang Medical University, Xinxiang, People's Republic of ChinaObjectives The study aimed to investigate the signalling mechanism for TRPM2 channel activation by non-cytolytic oxidative stress in microglia.Methods Microglia from wild-type (WT) and TRPM2-knockout (KO) mice were exposed to 10-30 mM H2O2 for up to 24 hours. Morphological changes characteristic of microglial activation, [Ca2+]c, ROS generation and the effects of inhibiting particular signalling pathways were examined.Results Exposure of WT microglia to H2O2 for 24 hours caused no cell death but induced salient morphological changes, which was prevented by TRPM2-KO. Exposure of WT microglia to H2O2 to 2 hours failed, and extension to 8 hours was required, to induce an increase in [Ca2+]c, which was abolished by TRPM2-KO. Exposure of microglia to H2O2 for 8 hours induced ROS generation, which was suppressed by inhibition of PKC and NADPH oxidases (NOX). H2O2-induced PARP activation in TRPM2-KO cells was lower than that in WT cells. Furthermore, H2O2-induced activation of PARP and TRPM2 and morphological changes were attenuated by inhibition of PCK and NOX as well as PYK2 and MEK/ERK.Conclusion Our results support that PKC/NOX-mediated ROS generation and TRPM2-mediated Ca2+-induced activation of the PYK2/MEK/ERK pathway form a positive feedback mechanism to drive TRPM2 channel activation by non-cytolytic oxidative stress.https://www.tandfonline.com/doi/10.1080/13510002.2025.2503131Oxidative stressTRPM2PKCNOXPYK2ERK
spellingShingle Sharifah Alawieyah Syed Mortadza
Nur Zulaikha Mohamad Zahir
Chew Tze Wei
Lin-Hua Jiang
The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells
Redox Report
Oxidative stress
TRPM2
PKC
NOX
PYK2
ERK
title The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells
title_full The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells
title_fullStr The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells
title_full_unstemmed The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells
title_short The PKC/NOX/ROS and PYK2/MEK/ERK/PARP signalling pathways drive TRPM2 channel activation induced by non-cytolytic oxidative stress in microglial cells
title_sort pkc nox ros and pyk2 mek erk parp signalling pathways drive trpm2 channel activation induced by non cytolytic oxidative stress in microglial cells
topic Oxidative stress
TRPM2
PKC
NOX
PYK2
ERK
url https://www.tandfonline.com/doi/10.1080/13510002.2025.2503131
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