TNF-α and Shear Stress-Induced Large Artery Adaptations

Ozaki, C. Keith; Jiang, Zhihua; Berceli, Scott A.

doi:10.1016/j.jss.2006.12.563

Cited by 4 publications

(2 citation statements)

References 52 publications

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“…Shear stress differentially regulates TNF-␣ expression in remodeling large arteries. Indeed, while low shear acutely upregulates large artery TNF-␣, high shear evokes a delayed and sustained expression associated with an outward remodeling (310). TNF-␣ has been shown to reduce NO bioavailability by decreasing eNOS expression or by increasing NO inactivation through stimulation of NADPH oxidase.…”

Section: E Role Of No In the Phenotypic Adaptation Of Endothelial Cementioning

confidence: 99%

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand¹,

Feron²,

Dessy³

2009

Physiological Reviews

388

328

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Nitric oxide production in response to flow-dependent shear forces applied on the surface of endothelial cells is a fundamental mechanism of regulation of vascular tone, peripheral resistance, and tissue perfusion. This implicates the concerted action of multiple upstream "mechanosensing" molecules reversibly assembled in signalosomes recruiting endothelial nitric oxide synthase (eNOS) in specific subcellular locales, e.g., plasmalemmal caveolae. Subsequent short- and long-term increases in activity and expression of eNOS translate this mechanical stimulus into enhanced NO production and bioactivity through a complex transcriptional and posttranslational regulation of the enzyme, including by shear-stress responsive transcription factors, oxidant stress-dependent regulation of transcript stability, eNOS regulatory phosphorylations, and protein-protein interactions. Notably, eNOS expressed in cardiac myocytes is amenable to a similar regulation in response to stretching of cardiac muscle cells and in part mediates the length-dependent increase in cardiac contraction force. In addition to short-term regulation of contractile tone, eNOS mediates key aspects of cardiac and vascular remodeling, e.g., by orchestrating the mobilization, recruitment, migration, and differentiation of cardiac and vascular progenitor cells, in part by regulating the stabilization and transcriptional activity of hypoxia inducible factor in normoxia and hypoxia. The continuum of the influence of eNOS in cardiovascular biology explains its growing implication in mechanosensitive aspects of integrated physiology, such as the control of blood pressure variability or the modulation of cardiac remodeling in situations of hemodynamic overload.

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Section: E Role Of No In the Phenotypic Adaptation Of Endothelial Cementioning

confidence: 99%

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand¹,

Feron²,

Dessy³

2009

Physiological Reviews

388

328

View full text Add to dashboard Cite

show abstract

“…2). One subcutaneous injection of sTNFR1 [15 mg/kg body wt (22)] diluted in PBS or daily injections of PTX [10 mg/100 g body wt (9)] were administered. Each TNF inhibitor-treated rat, as well as respective controls, was exposed to the same number of days in a cachectic state as rats given MCT alone.…”

Section: Animals the Investigation Conforms To The Guide For The Carmentioning

confidence: 99%

Anti-TNF treatment reduces rat skeletal muscle wasting in monocrotaline-induced cardiac cachexia

Steffen¹,

Lees²,

Booth³

2008

Journal of Applied Physiology

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Steffen BT, Lees SJ, Booth FW. Anti-TNF treatment reduces rat skeletal muscle wasting in monocrotaline-induced cardiac cachexia. J Appl Physiol 105: 1950 -1958, 2008. First published September 18, 2008 doi:10.1152/japplphysiol.90884.2008The aim was to explore efficacy of tumor necrosis factor (TNF) inhibitors in attenuating increases in anorexia and ubiquitin proteasome pathway transcripts in cardiac cachexia, a potentially lethal condition that responds poorly to current treatments. Cardiac cachexia was rapidly induced with monocrotaline in Sprague-Dawley rats. Either soluble TNF receptor-1 or the general inhibitor of TNF production, pentoxifylline, was given to diminish TNF action on the first indication of cachexia. Animals were anesthetized with a ketamine-xylazine-acepromazine cocktail, and then skeletal muscles were removed for subsequent measurements including ubiquitin proteasome pathway transcripts and Western blots. Both soluble TNF receptor-1 and pentoxifylline attenuated losses in both body and skeletal muscle masses and also reduced increases in selected ubiquitin proteasome pathway transcripts. The action of soluble TNF receptor-1 was partly through reversal of reduced food consumption, while the effects of pentoxifylline were independent of food intake. Here we demonstrate, for the first time, that attenuation of anorexia by soluble TNF receptor-1 treatment in monocrotaline-induced cardiac cachexia is responsible for attenuating increases in some ubiquitin proteasome pathway transcripts as well as preserving body mass and attenuating loss of skeletal muscle mass. atrophy; nutrition; proinflammatory cytokine CACHEXIA is a highly complex metabolic disorder characterized by inflammation, anorexia, and severe muscle loss in the presence of an underlying illness. Both inflammation and anorexia can independently contribute to skeletal muscle wasting. Cachexia associated with congestive heart failure (CHF), or cardiac cachexia, has a 50% mortality rate at 18 mo for the 10 -16% of CHF patients diagnosed as cachectic (2).Increased protein degradation by the ubiquitin-proteasome pathway (UPP) is implicated in skeletal muscle wasting in cachectic conditions (15,29). In those cachectic states investigated to date, UPP activity is upregulated in skeletal muscle; transcript levels for UPP members are also upregulated 8-, 2-, 40-, and 8-fold for ubiquitin, E2 ubiquitin conjugating enzymes, E3 ubiquitin ligases, and subunits of the 26S proteasome, respectively (4, 6, 15). Collectively, these mRNAs in skeletal muscle form a subpopulation of ϳ120 genes coordinately induced or suppressed in different catabolic states and are termed "atrogenes" (25). However, insufficient information exists on whether atrogene mRNA levels in skeletal muscle increase in cardiac cachexia and on whether inflammation and anorexia each play some role. One purpose of the present study is to test the hypothesis that monocrotaline (MCT)-induced cachexia increases atrogene mRNAs.Although there is no intervention that exhibits 100% therapeuti...

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Coronary artery plaque rupture and erosion: Role of wall shear stress profiling and biological patterns in acute coronary syndromes

Russo¹,

Pedicino²,

Chiastra³

et al. 2023

International Journal of Cardiology

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TNF-α and Shear Stress-Induced Large Artery Adaptations

Cited by 4 publications

References 52 publications

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Anti-TNF treatment reduces rat skeletal muscle wasting in monocrotaline-induced cardiac cachexia

Coronary artery plaque rupture and erosion: Role of wall shear stress profiling and biological patterns in acute coronary syndromes

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