Extracellular SOD modulates canonical TNFα signaling and α5β1 integrin transactivation in vascular smooth muscle cells

Choi, Hyehun; Miller, Michael R.; Nguyen, Hong-Ngan; Surratt, Victoria E.; Koch, Stephen R.; Stark, Ryan J.; Lamb, Fred S.

doi:10.1016/j.freeradbiomed.2023.10.397

Free Radical Biology and Medicine

2023

DOI: 10.1016/j.freeradbiomed.2023.10.397

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Extracellular SOD modulates canonical TNFα signaling and α5β1 integrin transactivation in vascular smooth muscle cells

Hyehun Choi,

Michael R. Miller,

Hong-Ngan Nguyen

et al.

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2024

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Cited by 2 publications

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“…•− exposure, while creating higher local H 2 O 2 concentrations. In the extracellular space, SOD3 modulates canonical TNF-α signaling, as well as transactivation of integrins, 111 and exerts a protective effect. 112 H 2 O 2 is a polar, hydrophilic molecule with limited membrane permeability 113 but readily crosses membranes via aquaporins 114 and has its own signaling properties.…”

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confidence: 99%

Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels

Lamb,

Choi,

Miller

et al. 2024

Hypertension

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Vascular inflammation underlies the development of hypertension, and the mechanisms by which it increases blood pressure remain the topic of intense investigation. Proinflammatory factors including glucose, salt, vasoconstrictors, cytokines, wall stress, and growth factors enhance contractility and impair relaxation of vascular smooth muscle cells. These pathways share a dependence upon redox signaling, and excessive activation promotes oxidative stress that promotes vascular aging. vascular smooth muscle cell phenotypic switching and migration into the intima contribute to atherosclerosis, while hypercontractility increases systemic vascular resistance and vasospasm that can trigger ischemia. Here, we briefly review factors that drive the initiation and progression of this vasculopathy in vascular smooth muscle cells. Emphasis is placed on the contribution of reactive oxygen species generated by the Nox1 NADPH oxidase which produces extracellular superoxide (O 2 •− ). The mechanisms of O 2 •− signaling remain poorly defined, but recent evidence demonstrates physical association of Nox1 with leucine-rich repeat containing 8 family volume-sensitive anion channels . These may provide a pathway for influx of O 2 •− to the cytoplasm, creating an oxidized cytoplasmic nanodomain where redox-based signals can affect both cytoskeletal structure and vasomotor function. Understanding the mechanistic links between inflammation, O 2 •− and vascular smooth muscle cell contractility may facilitate targeting of anti-inflammatory therapy in hypertension.

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confidence: 99%

Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels

Lamb,

Choi,

Miller

et al. 2024

Hypertension

Self Cite

View full text Add to dashboard Cite

show abstract

Vascular smooth muscle cell phenotypic switching in atherosclerosis

Yu,

Cai,

Yang

et al. 2024

Heliyon

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Extracellular SOD modulates canonical TNFα signaling and α5β1 integrin transactivation in vascular smooth muscle cells

Cited by 2 publications

References 51 publications

Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels

Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels

Vascular smooth muscle cell phenotypic switching in atherosclerosis

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