Accelerated Development of Pulmonary Fibrosis via Cu,Zn-superoxide Dismutase-induced Alternative Activation of Macrophages

He, Chao; Ryan, Alan J.; Murthy, Shubha; Carter, A. Brent

doi:10.1074/jbc.m112.410720

Cited by 112 publications

(138 citation statements)

References 47 publications

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“…Additionally, deficiency of p47 phox , a scaffolding protein for the NOX complex, renders macrophages hyper-responsive to IL-4-induced M2 polarization (230). Likewise, SOD1 overexpression promotes M2 polarization of alveolar macrophages (86). Together, these ex vivo studies support the significance of attenuated ROS production in development of M2 polarization state, which favors resolution of inflammation.…”

Section: Role Of Ros and Protein-s-glutathionylation In Monocyte Recrsupporting

confidence: 55%

Protein Thiol Redox Signaling in Monocytes and Macrophages

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Tavakoli

et al. 2016

Antioxidants & Redox Signaling

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Significance: Monocyte and macrophage dysfunction plays a critical role in a wide range of inflammatory disease processes, including obesity, impaired wound healing diabetic complications, and atherosclerosis. Emerging evidence suggests that the earliest events in monocyte or macrophage dysregulation include elevated reactive oxygen species production, thiol modifications, and disruption of redox-sensitive signaling pathways. This review focuses on the current state of research in thiol redox signaling in monocytes and macrophages, including (i) the molecular mechanisms by which reversible protein-S-glutathionylation occurs, (ii) the identification of bona fide S-glutathionylated proteins that occur under physiological conditions, and (iii) how disruptions of thiol redox signaling affect monocyte and macrophage functions and contribute to atherosclerosis. Recent Advances: Recent advances in redox biochemistry and biology as well as redox proteomic techniques have led to the identification of many new thiol redox-regulated proteins and pathways. In addition, major advances have been made in expanding the list of S-glutathionylated proteins and assessing the role that protein-S-glutathionylation and S-glutathionylation-regulating enzymes play in monocyte and macrophage functions, including monocyte transmigration, macrophage polarization, foam cell formation, and macrophage cell death. Critical Issues: Protein-S-glutathionylation/deglutathionylation in monocytes and macrophages has emerged as a new and important signaling paradigm, which provides a molecular basis for the well-established relationship between metabolic disorders, oxidative stress, and cardiovascular diseases. Future Directions: The identification of specific S-glutathionylated proteins as well as the mechanisms that control this post-translational protein modification in monocytes and macrophages will facilitate the development of new preventive and therapeutic strategies to combat atherosclerosis and other metabolic diseases. Antioxid. Redox Signal. 25,[816][817][818][819][820][821][822][823][824][825][826][827][828][829][830][831][832][833][834][835]

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Section: Role Of Ros and Protein-s-glutathionylation In Monocyte Recrsupporting

confidence: 55%

Protein Thiol Redox Signaling in Monocytes and Macrophages

Short

Downs

Tavakoli

et al. 2016

Antioxidants & Redox Signaling

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“…In a recent study, we found that alveolar macrophages from asbestosis patients produce high levels of H 2 O 2 , and these cells demonstrate a predominantly pro-fibrotic M2 phenotype. Moreover, polarization to the M2 phenotype was driven, in part, by Cu,Zn-superoxide dismutase-mediated H 2 O 2 production in chrysotile-exposed cells (13). Our new observations demonstrate that chrysotile-exposed macrophages exhibit rapid and sustained increases in Ca 2ϩ release and later develop ER stress.…”

Section: Discussionmentioning

confidence: 58%

“…Similar to the pro-inflammatory state induced by ER stress in AECs (35), ER stress in macrophages has been associated with pro-inflammatory effects through activation of both a JNK-TNF␣ pathway and a CHOP-ERK-IL-6 pathway (50). When exposed to chrysotile, macrophages produce pro-fibrotic cytokines such as TGF-␤ as well as high levels of reactive oxygen species, including H 2 O 2 (13)(14)(15). In a recent study, we found that alveolar macrophages from asbestosis patients produce high levels of H 2 O 2 , and these cells demonstrate a predominantly pro-fibrotic M2 phenotype.…”

Section: Discussionmentioning

confidence: 99%

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Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages

Ryan¹,

Larson‐Casey

et al. 2014

Journal of Biological Chemistry

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Background:Macrophages are important cells in fibrotic diseases. Results: Chrysotile increases cytosolic calcium (Ca 2ϩ ) and induces endoplasmic reticulum (ER) stress in macrophages in a Ca 2ϩ -dependent manner. ER stress is found in alveolar macrophages from fibrotic lungs. Conclusion: Chrysotile triggers ER Ca 2ϩ leak and induces ER stress in macrophages. Significance: Macrophages undergo ER stress, which may contribute to pulmonary fibrosis.

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“…Similarly, macrophages issued from Sod1 -/-mice display a pro-inflammatory profile as compared with WT macrophages (134). Inversely, in Sod1-Tg mice, where Sod1 is overexpressed and H 2 O 2 generation is enhanced, macrophages exhibit an anti-inflammatory status, associated with an increased activation of STAT6 (134), which is known to trigger the expression of antiinflammatory genes in macrophages (178).…”

Section: A Myeloid Cellsmentioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

148

120

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Skeletal muscle shows high plasticity in response to external demand. Moreover, adult skeletal muscle is capable of complete regeneration after injury, due to the properties of muscle stem cells (MuSCs), the satellite cells, which follow a tightly regulated myogenic program to generate both new myofibers and new MuSCs for further needs. Although reactive oxygen species (ROS) and reactive nitrogen species (RNS) have long been associated with skeletal muscle physiology, their implication in the cell and molecular processes at work during muscle regeneration is more recent. This review focuses on redox regulation during skeletal muscle regeneration. An overview of the basics of ROS/RNS and antioxidant chemistry and biology occurring in skeletal muscle is first provided. Then, the comprehensive knowledge on redox regulation of MuSCs and their surrounding cell partners (macrophages, endothelial cells) during skeletal muscle regeneration is presented in normal muscle and in specific physiological (exercise-induced muscle damage, aging) and pathological (muscular dystrophies) contexts. Recent advances in the comprehension of these processes has led to the development of therapeutic assays using antioxidant supplementation, which result in inconsistent efficiency, underlying the need for new tools that are aimed at precisely deciphering and targeting ROS networks. This review should provide an overall insight of the redox regulation of skeletal muscle regeneration while highlighting the limits of the use of nonspecific antioxidants to improve muscle function. Antioxid. Redox Signal. 27, 276-310.

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Accelerated Development of Pulmonary Fibrosis via Cu,Zn-superoxide Dismutase-induced Alternative Activation of Macrophages

Cited by 112 publications

References 47 publications

Protein Thiol Redox Signaling in Monocytes and Macrophages

Protein Thiol Redox Signaling in Monocytes and Macrophages

Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages

Redox Control of Skeletal Muscle Regeneration

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