Uncoupling Proteins as Therapeutic Targets for Neurodegenerative Diseases

Barnstable, Colin J.; Zhang, Mingliang; Tombran-Tink, Joyce

doi:10.3390/ijms23105672

Cited by 8 publications

(2 citation statements)

References 108 publications

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“…UCP2 not only neutralize ROS, but also prevent their formation, influencing MC degranulation indirectly through an increased concentration of Ca 2+ [113]. Therefore, UCP2 activators have the potential to reduce the production of mitochondrial ROS [114]. ROS can cause reversible post-translational changes in proteins involved in intracellular signaling.…”

Section: Reactive Oxygen Species In the Mechanisms Of Activation Of M...mentioning

confidence: 99%

Mast Cells as a Potential Target of Molecular Hydrogen in Regulating the Local Tissue Microenvironment

et al. 2023

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Knowledge of the biological effects of molecular hydrogen (H2), hydrogen gas, is constantly advancing, giving a reason for the optimism in several healthcare practitioners regarding the management of multiple diseases, including socially significant ones (malignant neoplasms, diabetes mellitus, viral hepatitis, mental and behavioral disorders). However, mechanisms underlying the biological effects of H2 are still being actively debated. In this review, we focus on mast cells as a potential target for H2 at the specific tissue microenvironment level. H2 regulates the processing of pro-inflammatory components of the mast cell secretome and their entry into the extracellular matrix; this can significantly affect the capacity of the integrated-buffer metabolism and the structure of the immune landscape of the local tissue microenvironment. The analysis performed highlights several potential mechanisms for developing the biological effects of H2 and offers great opportunities for translating the obtained findings into clinical practice.

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Section: Reactive Oxygen Species In the Mechanisms Of Activation Of M...mentioning

confidence: 99%

Mast Cells as a Potential Target of Molecular Hydrogen in Regulating the Local Tissue Microenvironment

et al. 2023

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“…Mitochondria play a crucial role in energy production through oxidative phosphorylation. Extensive literature supports the idea that mitochondria are the main source of ROS generation [ 8 , 9 , 10 ]. The proton gradient across the inner mitochondrial membrane is a key driving force for mitochondrial ROS production, and this gradient can be modulated by members of the mitochondrial uncoupling protein (UCP) family.…”

Section: Introductionmentioning

confidence: 96%

Molecular Mechanisms of Oxidative Stress Relief by CAPE in ARPE−19 Cells

Ren

Zhou

Zhang

et al. 2023

IJMS

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Caffeic acid phenylethyl ester (CAPE) is an antioxidative agent originally derived from propolis. Oxidative stress is a significant pathogenic factor in most retinal diseases. Our previous study revealed that CAPE suppresses mitochondrial ROS production in ARPE−19 cells by regulating UCP2. The present study explores the ability of CAPE to provide longer-term protection to RPE cells and the underlying signal pathways involved. ARPE−19 cells were given CAPE pretreatment followed by t-BHP stimulation. We used in situ live cell staining with CellROX and MitoSOX to measure ROS accumulation; Annexin V-FITC/PI assay to evaluate cell apoptosis; ZO−1 immunostaining to observe tight junction integrity in the cells; RNA-seq to analyze changes in gene expression; q-PCR to validate the RNA-seq data; and Western Blot to examine MAPK signal pathway activation. CAPE significantly reduced both cellular and mitochondria ROS overproduction, restored the loss of ZO−1 expression, and inhibited apoptosis induced by t-BHP stimulation. We also demonstrated that CAPE reverses the overexpression of immediate early genes (IEGs) and activation of the p38-MAPK/CREB signal pathway. Either genetic or chemical deletion of UCP2 largely abolished the protective effects of CAPE. CAPE restrained ROS generation and preserved the tight junction structure of ARPE−19 cells against oxidative stress-induced apoptosis. These effects were mediated via UCP2 regulation of p38/MAPK-CREB-IEGs pathway.

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