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TRP Channels in Oxidative Stress Signalling
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TRP Channels in Oxidative Stress Signalling

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (15 October 2022) | Viewed by 24158

Special Issue Editors

Dr. Lin-Hua Jiang

E-Mail Website
Guest Editor
School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK
Interests: ROS-sensitive calcium channels; oxidative stress calcium signalling; neuroinflammation; stroke; neurodegeneration; depression
Prof. Dr. Xiaoqiang Yao

E-Mail Website
Guest Editor
School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China
Interests: TRP channels in cardiovascular system and cancer; Ca2+ signalling; ER stress and cardiomyopathy
Dr. Bilal ÇİĞ

E-Mail Website
Guest Editor
Medicine Faculty Department of Physiology, Kirsehir Ahi Evran University, Kirsehir, Turkey
Interests: TRP channels in the brain; Kir channels; electrophysiology; neurodegeneration; ion channel recording; epilepsy; oligodendrocytes; myelin dysfunction and damage; neural–glial interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are potent in modifying biologically important macromolecules. Thus, in mammalian cells, accumulation of high levels of ROS, due to imbalance between ROS generation and the antioxidant capacity, can lead to oxidative stress. Oxidative damage has been long and well documented as a conspicuous and common feature in numerous pathological conditions. There is an increasing body of evidence to suggest that oxidative stress is a significant factor in the pathogenesis of these conditions, as well as aging.

Transient receptor potential (TRP) channels, a large family of structurally related cation channels, are widely distributed and involved in a variety of physiological and pathological processes. Several TRP channels exhibit a salient sensitivity to activation and modulation by ROS. Emerging evidence supports that these redox-sensitive TRP channels play a vital role in transducing oxidative stress signalling in many pathological conditions, including but not limited to ischemic stroke, neurodegenerative diseases, neurovascular injury, psychiatric disorders, cardiovascular diseases, diabetes, pancreatitis, chronic kidney disease, and liver damage.

This Special Issue aims to provide a platform for researchers to discuss their findings or insights into the TRP channels in oxidative stress signalling and related mechanisms in the pathogenesis of diseases induced by endogenously or externally pathological factors.

  • Mechanisms for activation and modulation by ROS;
  • ROS-generating mechanisms;
  • Alterations in ionic homeostasis;
  • Disruption of intracellular organelles such as ER, lysosome and mitochondria;
  • Cell viability and death;
  • Generation of inflammatory mediators;
  • Tissue inflammation;
  • Ageing;
  • Disease pathogenesis.

Dr. Lin-Hua Jiang
Prof. Dr. Xiaoqiang Yao
Dr. Bilal ÇİĞ
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • TRP channels
  • ageing
  • diseases

Published Papers (8 papers)

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Editorial

Jump to: Research, Review

4 pages, 210 KiB  
Editorial
TRP Channels in Oxidative Stress Signalling
by Lin-Hua Jiang, Xiaoqiang Yao and Bilal Çiğ
Cells 2023, 12(9), 1251; https://doi.org/10.3390/cells12091251 - 26 Apr 2023
Cited by 1 | Viewed by 985
Abstract
It is well established that the accumulation of high levels of reactive oxygen species (ROS), due to excessive generation of ROS and/or impaired antioxidant capacity of cells, can result in oxidative stress and cause oxidative damage to cells and their functions [...] Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)

Research

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19 pages, 3241 KiB  
Article
A TRPC3/6 Channel Inhibitor Promotes Arteriogenesis after Hind-Limb Ischemia
by Tsukasa Shimauchi, Takuro Numaga-Tomita, Yuri Kato, Hiroyuki Morimoto, Kosuke Sakata, Ryosuke Matsukane, Akiyuki Nishimura, Kazuhiro Nishiyama, Atsushi Shibuta, Yutoku Horiuchi, Hitoshi Kurose, Sang Geon Kim, Yasuteru Urano, Takashi Ohshima and Motohiro Nishida
Cells 2022, 11(13), 2041; https://doi.org/10.3390/cells11132041 - 27 Jun 2022
Cited by 2 | Viewed by 2425
Abstract
Retarded revascularization after progressive occlusion of large conductance arteries is a major cause of bad prognosis for peripheral artery disease (PAD). However, pharmacological treatment for PAD is still limited. We previously reported that suppression of transient receptor potential canonical (TRPC) 6 channel activity [...] Read more.
Retarded revascularization after progressive occlusion of large conductance arteries is a major cause of bad prognosis for peripheral artery disease (PAD). However, pharmacological treatment for PAD is still limited. We previously reported that suppression of transient receptor potential canonical (TRPC) 6 channel activity in vascular smooth muscle cells (VSMCs) facilitates VSMC differentiation without affecting proliferation and migration. In this study, we found that 1-benzilpiperadine derivative (1-BP), a selective inhibitor for TRPC3 and TRPC6 channel activities, induced VSMC differentiation. 1-BP-treated mice showed increased capillary arterialization and improvement of peripheral circulation and skeletal muscle mass after hind-limb ischemia (HLI) in mice. 1-BP had no additive effect on the facilitation of blood flow recovery after HLI in TRPC6-deficient mice, suggesting that suppression of TRPC6 underlies facilitation of the blood flow recovery by 1-BP. 1-BP also improved vascular nitric oxide bioavailability and blood flow recovery after HLI in hypercholesterolemic mice with endothelial dysfunction, suggesting the retrograde interaction from VSMCs to endothelium. These results suggest that 1-BP becomes a potential seed for PAD treatments that target vascular TRPC6 channels. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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17 pages, 6124 KiB  
Article
TRPM2 Promotes Atherosclerotic Progression in a Mouse Model of Atherosclerosis
by Yunting Zhang, Fan Ying, Xiaoyu Tian, Zhenchuan Lei, Xiao Li, Chun-Yin Lo, Jingxuan Li, Liwen Jiang and Xiaoqiang Yao
Cells 2022, 11(9), 1423; https://doi.org/10.3390/cells11091423 - 22 Apr 2022
Cited by 15 | Viewed by 3254
Abstract
Atherosclerosis is a chronic inflammatory arterial disease characterized by build-up of atheromatous plaque, which narrows the lumen of arteries. Hypercholesterolemia and excessive oxidative stress in arterial walls are among the main causative factors of atherosclerosis. Transient receptor potential channel M2 (TRPM2) is a [...] Read more.
Atherosclerosis is a chronic inflammatory arterial disease characterized by build-up of atheromatous plaque, which narrows the lumen of arteries. Hypercholesterolemia and excessive oxidative stress in arterial walls are among the main causative factors of atherosclerosis. Transient receptor potential channel M2 (TRPM2) is a Ca2+-permeable cation channel activated by oxidative stress. However, the role of TRPM2 in atherosclerosis in animal models is not well studied. In the present study, with the use of adeno-associated virus (AAV)-PCSK9 and TRPM2 knockout (TRPM2−/−) mice, we determined the role of TRPM2 in hypercholesterolemia-induced atherosclerosis. Our results demonstrated that TRPM2 knockout reduced atherosclerotic plaque area in analysis of En face Oil Red O staining of both whole aortas and aortic-root thin sections. Furthermore, TRPM2 knockout reduced the expression of CD68, α-SMA, and PCNA in the plaque region, suggesting a role of TRPM2 in promoting macrophage infiltration and smooth-muscle cell migration into the lesion area. Moreover, TRPM2 knockout reduced the expression of ICAM-1, MCP-1, and TNFα and decreased the ROS level in the plaque region, suggesting a role of TRPM2 in enhancing monocyte adhesion and promoting vascular inflammation. In bone-marrow-derived macrophages and primary cultured arterial endothelial cells, TRPM2 knockout reduced the production of inflammatory cytokines/factors and decreased ROS production. In addition, a TRPM2 antagonist N-(p-amylcinnamoyl) anthranilic acid (ACA) was able to inhibit atherosclerotic development in an ApoE−/− mouse model of atherosclerosis. Taken together, the findings of our study demonstrated that TRPM2 contributes to the progression of hypercholesterolemia-induced atherosclerosis. Mechanistically, TRPM2 channels may provide an essential link that can connect ROS to Ca2+ and inflammation, consequently promoting atherosclerotic progression. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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14 pages, 4130 KiB  
Article
Oxidative Stress-Induced TRPV2 Expression Increase Is Involved in Diabetic Cataracts and Apoptosis of Lens Epithelial Cells in a High-Glucose Environment
by Linghui Chen, Yanzhuo Chen, Wen Ding, Tao Zhan, Jie Zhu, Lesha Zhang, Han Wang, Bing Shen and Yong Wang
Cells 2022, 11(7), 1196; https://doi.org/10.3390/cells11071196 - 2 Apr 2022
Cited by 11 | Viewed by 2126
Abstract
Cataracts are a serious complication of diabetes. In long-term hyperglycemia, intracellular Ca2+ concentration ([Ca2+]i) and reactive oxygen species (ROS) are increased. The apoptosis of lens epithelial cells plays a key role in the development of cataract. We investigated [...] Read more.
Cataracts are a serious complication of diabetes. In long-term hyperglycemia, intracellular Ca2+ concentration ([Ca2+]i) and reactive oxygen species (ROS) are increased. The apoptosis of lens epithelial cells plays a key role in the development of cataract. We investigated a potential role for transient receptor potential vanilloid 2 (TRPV2) in the development of diabetic cataracts. Immunohistochemical and Western blotting analyses showed that TRPV2 expression levels were significantly increased in the lens epithelial cells of patients with diabetic cataracts as compared with senile cataract, as well as in both a human lens epithelial cell line (HLEpiC) and primary rat lens epithelial cells (RLEpiCs) cultured under high-glucose conditions. The [Ca2+]i increase evoked by a TRPV2 channel agonist was significantly enhanced in both HLEpiCs and RLEpiCs cultured in high-glucose media. This enhancement was blocked by the TRPV2 nonspecific inhibitor ruthenium red and by TRPV2-specific small interfering (si)RNA transfection. Culturing HLEpiCs or RLEpiCs for seven days in high glucose significantly increased apoptosis, which was inhibited by TRPV2-specific siRNA transfection. In addition, ROS inhibitor significantly suppressed the ROS-induced increase of TRPV2-mediated Ca2+ signal and apoptosis under high-glucose conditions. These findings suggest a mechanism underlying high-glucose–induced apoptosis of lens epithelial cells, and offer a potential target for developing new therapeutic options for diabetes-related cataracts. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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16 pages, 7047 KiB  
Article
Neuroprotective Effects of TRPM7 Deletion in Parvalbumin GABAergic vs. Glutamatergic Neurons following Ischemia
by Pengju Zhang, Wei Li, Yaan Liu, Yanqin Gao and Nashat Abumaria
Cells 2022, 11(7), 1178; https://doi.org/10.3390/cells11071178 - 31 Mar 2022
Cited by 7 | Viewed by 2629
Abstract
Oxidative stress induced by brain ischemia upregulates transient receptor potential melastatin-like-7 (TRPM7) expression and currents, which could contribute to neurotoxicity and cell death. Accordingly, suppression of TRPM7 reduces neuronal death, tissue damage and motor deficits. However, the neuroprotective effects of TRPM7 suppression in [...] Read more.
Oxidative stress induced by brain ischemia upregulates transient receptor potential melastatin-like-7 (TRPM7) expression and currents, which could contribute to neurotoxicity and cell death. Accordingly, suppression of TRPM7 reduces neuronal death, tissue damage and motor deficits. However, the neuroprotective effects of TRPM7 suppression in different cell types have not been investigated. Here, we found that induction of ischemia resulted in loss of parvalbumin (PV) gamma-aminobutyric acid (GABAergic) neurons more than Ca2+/calmodulin-kinase II (CaMKII) glutamatergic neurons in the mouse cortex. Furthermore, brain ischemia increased TRPM7 expression in PV neurons more than that in CaMKII neurons. We generated two lines of conditional knockout mice of TRPM7 in GABAergic PV neurons (PV-TRPM7−/−) and in glutamatergic neurons (CaMKII-TRPM7−/−). Following exposure to brain ischemia, we found that deleting TRPM7 reduced the infarct volume in both lines of transgenic mice. However, the volume in PV-TRPM7−/− mice was more significantly lower than that in the control group. Neuronal survival of both GABAergic and glutamatergic neurons was increased in PV-TRPM7−/− mice; meanwhile, only glutamatergic neurons were protected in CaMKII-TRPM7−/−. At the behavioral level, only PV-TRPM7−/− mice exhibited significant reductions in neurological and motor deficits. Inflammatory mediators such as GFAP, Iba1 and TNF-α were suppressed in PV-TRPM7−/− more than in CaMKII-TRPM7−/−. Mechanistically, p53 and cleaved caspase-3 were reduced in both groups, but the reduction in PV-TRPM7−/− mice was more than that in CaMKII-TRPM7−/− following ischemia. Upstream from these signaling molecules, the Akt anti-oxidative stress signaling was activated only in PV-TRPM7−/− mice. Therefore, deleting TRPM7 in GABAergic PV neurons might have stronger neuroprotective effects against ischemia pathologies than doing so in glutamatergic neurons. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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14 pages, 7578 KiB  
Article
The TRPA1 Channel Amplifies the Oxidative Stress Signal in Melanoma
by Francesco De Logu, Daniel Souza Monteiro de Araujo, Filippo Ugolini, Luigi Francesco Iannone, Margherita Vannucchi, Francesca Portelli, Lorenzo Landini, Mustafa Titiz, Vincenzo De Giorgi, Pierangelo Geppetti, Daniela Massi and Romina Nassini
Cells 2021, 10(11), 3131; https://doi.org/10.3390/cells10113131 - 11 Nov 2021
Cited by 11 | Viewed by 3198
Abstract
Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma cell lines, [...] Read more.
Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma cell lines, and oxidative stress has been associated with melanocytic transformation, their role in melanoma remains poorly known. Here, we localized MΦs, the final end-product of oxidative stress, 4-hydroxynonenal (4-HNE), and TRPA1 in tissue samples of human common dermal melanocytic nevi, dysplastic nevi, and thin (pT1) and thick (pT4) cutaneous melanomas. The number (amount) of intratumoral and peritumoral M2 MΦs and 4-HNE staining progressively increased with tumor severity, while TRPA1 expression was similar in all samples. Hydrogen peroxide (H2O2) evoked a TRPA1-dependent calcium response in two distinct melanoma cell lines (SK-MEL-28 and WM266-4). Furthermore, H2O2 induced a TRPA1-dependent H2O2 release that was prevented by the TRPA1 antagonist, A967079, or Trpa1 gene silencing (siRNA). ROS release from infiltrating M2 MΦs may target TRPA1-expressing melanoma cells to amplify the oxidative stress signal that affects tumor cell survival and proliferation. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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Review

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35 pages, 3892 KiB  
Review
An Overview of the TRP-Oxidative Stress Axis in Metabolic Syndrome: Insights for Novel Therapeutic Approaches
by Mizael C. Araújo, Suzany H. S. Soczek, Jaqueline P. Pontes, Leonardo A. C. Marques, Gabriela S. Santos, Gisele Simão, Laryssa R. Bueno, Daniele Maria-Ferreira, Marcelo N. Muscará and Elizabeth S. Fernandes
Cells 2022, 11(8), 1292; https://doi.org/10.3390/cells11081292 - 11 Apr 2022
Cited by 7 | Viewed by 4114
Abstract
Metabolic syndrome (MS) is a complex pathology characterized by visceral adiposity, insulin resistance, arterial hypertension, and dyslipidaemia. It has become a global epidemic associated with increased consumption of high-calorie, low-fibre food and sedentary habits. Some of its underlying mechanisms have been identified, with [...] Read more.
Metabolic syndrome (MS) is a complex pathology characterized by visceral adiposity, insulin resistance, arterial hypertension, and dyslipidaemia. It has become a global epidemic associated with increased consumption of high-calorie, low-fibre food and sedentary habits. Some of its underlying mechanisms have been identified, with hypoadiponectinemia, inflammation and oxidative stress as important factors for MS establishment and progression. Alterations in adipokine levels may favour glucotoxicity and lipotoxicity which, in turn, contribute to inflammation and cellular stress responses within the adipose, pancreatic and liver tissues, in addition to hepatic steatosis. The multiple mechanisms of MS make its clinical management difficult, involving both non-pharmacological and pharmacological interventions. Transient receptor potential (TRP) channels are non-selective calcium channels involved in a plethora of physiological events, including energy balance, inflammation and oxidative stress. Evidence from animal models of disease has contributed to identify their specific contributions to MS and may help to tailor clinical trials for the disease. In this context, the oxidative stress sensors TRPV1, TRPA1 and TRPC5, play major roles in regulating inflammatory responses, thermogenesis and energy expenditure. Here, the interplay between these TRP channels and oxidative stress in MS is discussed in the light of novel therapies to treat this syndrome. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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20 pages, 16600 KiB  
Review
A Systemic Review of the Integral Role of TRPM2 in Ischemic Stroke: From Upstream Risk Factors to Ultimate Neuronal Death
by Pengyu Zong, Qiaoshan Lin, Jianlin Feng and Lixia Yue
Cells 2022, 11(3), 491; https://doi.org/10.3390/cells11030491 - 31 Jan 2022
Cited by 9 | Viewed by 3794
Abstract
Ischemic stroke causes a heavy health burden worldwide, with over 10 million new cases every year. Despite the high prevalence and mortality rate of ischemic stroke, the underlying molecular mechanisms for the common etiological factors of ischemic stroke and ischemic stroke itself remain [...] Read more.
Ischemic stroke causes a heavy health burden worldwide, with over 10 million new cases every year. Despite the high prevalence and mortality rate of ischemic stroke, the underlying molecular mechanisms for the common etiological factors of ischemic stroke and ischemic stroke itself remain unclear, which results in insufficient preventive strategies and ineffective treatments for this devastating disease. In this review, we demonstrate that transient receptor potential cation channel, subfamily M, member 2 (TRPM2), a non-selective ion channel activated by oxidative stress, is actively involved in all the important steps in the etiology and pathology of ischemic stroke. TRPM2 could be a promising target in screening more effective prophylactic strategies and therapeutic medications for ischemic stroke. Full article
(This article belongs to the Special Issue TRP Channels in Oxidative Stress Signalling)
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