High-throughput screening of cellular redox sensors using modern redox proteomics approaches

Jiang, Jingwen; Wang, Kui; Nice, Edouard C.; Zhang, Tao; Huang, Canhua

doi:10.1586/14789450.2015.1069189

Cited by 10 publications

(7 citation statements)

References 121 publications

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“…Redox sensor proteins are involved in detecting the dynamic balance between oxidants and antioxidants in the cell and driving the intracellular feedback mechanisms to increase the synthesis of important endogenous antioxidant systems or to regulate intracellular ROS signalling (Brigelius‐Flohe & Flohe, ). High‐throughput screening of cellular redox sensors using modern redox proteomics revealed that redox‐related transcription factors NRF2 and HIF are promising targets for modulation, especially on the antioxidant side of the balance (Jiang, Wang, Nice, Zhang, & Huang, ; Figure b).…”

Section: Molecular Targets For Tissue Engineersmentioning

confidence: 99%

Redox regulation in regenerative medicine and tissue engineering: The paradox of oxygen

Sthijns

Blitterswijk

LaPointe

2018

J Tissue Eng Regen Med

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One of the biggest challenges in tissue engineering and regenerative medicine is to incorporate a functioning vasculature to overcome the consequences of a lack of oxygen and nutrients in the tissue construct. Otherwise, decreased oxygen tension leads to incomplete metabolism and the formation of the so‐called reactive oxygen species (ROS). Cells have many endogenous antioxidant systems to ensure a balance between ROS and antioxidants, but if this balance is disrupted by factors such as high levels of ROS due to long‐term hypoxia, there will be tissue damage and dysfunction. Current attempts to solve the oxygen problem in the field rarely take into account the importance of the redox balance and are instead centred on releasing or generating oxygen. The first problem with this approach is that although oxygen is necessary for life, it is paradoxically also a highly toxic molecule. Furthermore, although some oxygen‐generating biomaterials produce oxygen, they also generate hydrogen peroxide, a ROS, as an intermediate product. In this review, we discuss why it would be a superior strategy to supplement oxygen delivery with molecules to safeguard the important redox balance. Redox sensor proteins that can stimulate the anaerobic metabolism, angiogenesis, and enhancement of endogenous antioxidant systems are discussed as promising targets. We propose that redox regulating biomaterials have the potential to tackle some of the challenges related to angiogenesis and that the knowledge in this review will help scientists in tissue engineering and regenerative medicine realize this aim.

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Section: Molecular Targets For Tissue Engineersmentioning

confidence: 99%

Redox regulation in regenerative medicine and tissue engineering: The paradox of oxygen

Sthijns

Blitterswijk

LaPointe

2018

J Tissue Eng Regen Med

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“…Several patterns of oxidative modifications have been reported, including sulfenylation (-SOH), sulfinylation (-SO 2 H), sulfonylation (-SO 3 H), S-glutathionylation (PrS-SG) and disulfide bonds (intramolecular, intermolecular and mixed types). 22 Through these redox modifications, ROS can alter the biological functions of redox-sensitive proteins involved in ECM remodeling (for example, integrin, Hu antigen R), cytoskeleton remodeling (for example, actin, cofilin), cell–cell junctions (for example, NF-κB, HIF-1α, TGF-β) and cell mobility (for example, Src, FAK, PTEN), thereby regulating EMT initiation and cancer cell progression. 9 …”

Section: Introductionmentioning

confidence: 99%

Redox regulation in tumor cell epithelial–mesenchymal transition: molecular basis and therapeutic strategy

Jiang

Wang

Chen

et al. 2017

Sig Transduct Target Ther

Self Cite

164

133

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Epithelial–mesenchymal transition (EMT) is recognized as a driving force of cancer cell metastasis and drug resistance, two leading causes of cancer recurrence and cancer-related death. It is, therefore, logical in cancer therapy to target the EMT switch to prevent such cancer metastasis and recurrence. Previous reports have indicated that growth factors (such as epidermal growth factor and fibroblast growth factor) and cytokines (such as the transforming growth factor beta (TGF-β) family) are major stimulators of EMT. However, the mechanisms underlying EMT initiation and progression remain unclear. Recently, emerging evidence has suggested that reactive oxygen species (ROS), important cellular secondary messengers involved in diverse biological events in cancer cells, play essential roles in the EMT process in cancer cells by regulating extracellular matrix (ECM) remodeling, cytoskeleton remodeling, cell–cell junctions, and cell mobility. Thus, targeting EMT by manipulating the intracellular redox status may hold promise for cancer therapy. Herein, we will address recent advances in redox biology involved in the EMT process in cancer cells, which will contribute to the development of novel therapeutic strategies by targeting redox-regulated EMT for cancer treatment.

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“…Establishing a 3D niche at the specific ratio of 50:50 INS1E:alphaTC1 cells was essential for protecting both cell types against oxidative stress. As a future outlook, it would be interesting to validate this finding in the context of beta cell replacement strategies, where the cells are known to experience high levels of oxidative stress [31,32,[43][44][45]. Engineered islets could be transplanted in the ratio of 50:50 beta:alpha cells to protect them against the oxidative stress they experience during transplantation and from biomaterials used for encapsulation [46].…”

Section: Discussionmentioning

confidence: 96%

The response of three-dimensional pancreatic alpha and beta cell co-cultures to oxidative stress

Sthijns

Rademakers

Oosterveer

et al. 2021

Preprint

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The pancreatic islets of Langerhans have low endogenous antioxidant levels and are thus especially sensitive to oxidative stress, which is known to influence cell survival and behaviour. As bioengineered islets are gaining interest for therapeutic purposes, it is important to understand how their composition can be optimized to diminish oxidative stress. We investigated how the ratio of the two main islet cell types (alpha and beta cells) and their culture in three-dimensional aggregates could protect against oxidative stress. Monolayer and aggregate cultures were established by seeding the alphaTC1 (alpha) and INS1E (beta) cell lines in varying ratios, and hydrogen peroxide was applied to induce oxidative stress. Viability, oxidative stress, and the level of the antioxidant glutathione were measured. Both aggregation and an increasing prevalence of INS1E cells in the co-cultures conferred greater resistance to cell death induced by oxidative stress. Increasing the prevalence of INS1E cells also decreased the number of alphaTC1 cells experiencing oxidative stress in the monolayer culture. In 3D aggregates, culturing the alphaTC1 and INS1E cells in a ratio of 50:50 prevented oxidative stress in both cell types. Together, the results of this study lead to new insight into how modulating the composition and dimensionality of a co-culture can influence the oxidative stress levels experienced by the cells.

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High-throughput screening of cellular redox sensors using modern redox proteomics approaches

Cited by 10 publications

References 121 publications

Redox regulation in regenerative medicine and tissue engineering: The paradox of oxygen

Redox regulation in regenerative medicine and tissue engineering: The paradox of oxygen

Redox regulation in tumor cell epithelial–mesenchymal transition: molecular basis and therapeutic strategy

The response of three-dimensional pancreatic alpha and beta cell co-cultures to oxidative stress

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