The crosstalk between the cardiovascular and the immune system

Lin, Carlo Dal; Tona, Francesco; Osto, Elena

doi:10.1530/vb-19-0023

Cited by 24 publications

(19 citation statements)

References 48 publications

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“…For analysis of vascular reactivity, individual concentrationeffect curves were plotted on a sigmoidal curve, by non-linear regression analysis. These curves, in turn, provide the maximum response value (Emax) and pEC 50…”

Section: Discussionmentioning

confidence: 99%

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Supraphysiological Levels of Testosterone Induce Vascular Dysfunction via Activation of the NLRP3 Inflammasome

et al. 2020

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Background: Both supraphysiological and subphysiological testosterone levels are associated with increased cardiovascular risk. Testosterone consumption at supraphysiological doses has been linked to increased blood pressure, left ventricular hypertrophy, vascular dysfunction, and increased levels of inflammatory markers. Activation of the NLRP3 inflammasome contributes to the production of proinflammatory cytokines, leading to cardiovascular dysfunction. We hypothesized that supraphysiological levels of testosterone, via generation of mitochondrial reactive oxygen species (mROS), activates the NLRP3 inflammasome and promotes vascular dysfunction. Methods: Male, 12 week-old C57Bl/6J (WT) and NLRP3 knockout (NLRP3 −/−) mice were used. Mice were treated with testosterone propionate [TP (10 mg/kg) in vivo] or vehicle for 30 days. In addition, vessels were incubated with testosterone [Testo (10 −6 M, 2 h) in vitro]. Testosterone levels, blood pressure, vascular function (thoracic aortic rings), pro-caspase-1/caspase-1 and interleukin-1β (IL-1β) expression, and generation of reactive oxygen species were determined. Results: Testosterone increased contractile responses and reduced endothelium-dependent vasodilation, both in vivo and in vitro. These effects were not observed in arteries from NLRP3 −/− mice. Aortas of TP-treated WT mice (in vivo), as well as aortas from WT mice incubated with testo (in vitro), exhibited increased mROS levels and increased caspase-1 and IL-1β expression. These effects were not observed in arteries from NLRP3 −/− mice. Flutamide [Flu, 10 −5 M, androgen receptor (AR) antagonist], carbonyl cyanide m-chlorophenyl hydrazone (CCCP, 10 −6 M, mitochondrial uncoupler) and MCC950 (MCC950, 10 −6 M, a NLRP3 receptor inhibitor) prevented testosterone-induced mROS generation. Conclusion: Supraphysiological levels of testosterone induce vascular dysfunction via mROS generation and NLRP3 inflammasome activation. These events may contribute to increased cardiovascular risk.

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Section: Discussionmentioning

confidence: 99%

“…In the present study, we addressed direct and long-term effects of testosterone on NLRP3 inflammasome-mediated vascular dysfunction. The innate and adaptive immune responses significantly influence both acute and chronic changes in cardiovascular phenotype that lead to clinical cardiovascular abnormalities ( 47 – 50 ).…”

Section: Discussionmentioning

confidence: 99%

Supraphysiological Levels of Testosterone Induce Vascular Dysfunction via Activation of the NLRP3 Inflammasome

et al. 2020

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“…At 80% of confluence, HL1 cells were exposed to 20 min of sound sequences. We used this specific time period because we wanted to begin to study in vitro any possible direct effect of sound that could help to explain the results that we are obtaining in vivo in our research protocols [ 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 ].…”

Section: Methodsmentioning

confidence: 99%

“…The possible biophysical and molecular mechanisms underlying the heart–brain correlation have been discussed [ 12 ] and it has been shown [ 13 , 14 , 15 , 16 , 17 , 18 ] how the practice of relaxation response (RR) improves coronary blood flow, the heart contractility, and determines a favourable variation of inflammation molecules, stress hormones, neurotransmitters, aging markers, and circulating microRNAs, inducing an attenuation of the expression of some inflammatory genes in white blood cell precursors. Remarkably, the physical appearance of the subjects’ serum changes during RR [ 14 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Sounds Stimulation on In Vitro HL1 Cells: A Pilot Study and a Theoretical Physical Model

Lin

Radu

Vitiello

et al. 2020

IJMS

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Mechanical vibrations seem to affect the behaviour of different cell types and the functions of different organs. Pressure waves, including acoustic waves (sounds), could affect cytoskeletal molecules via coherent changes in their spatial organization and mechano-transduction signalling. We analyzed the sounds spectra and their fractal features. Cardiac muscle HL1 cells were exposed to different sounds, were stained for cytoskeletal markers (phalloidin, beta-actin, alpha-tubulin, alpha-actinin-1), and studied with multifractal analysis (using FracLac for ImageJ). A single cell was live-imaged and its dynamic contractility changes in response to each different sound were analysed (using Musclemotion for ImageJ). Different sound stimuli seem to influence the contractility and the spatial organization of HL1 cells, resulting in a different localization and fluorescence emission of cytoskeletal proteins. Since the cellular behaviour seems to correlate with the fractal structure of the sound used, we speculate that it can influence the cells by virtue of the different sound waves’ geometric properties that we have photographed and filmed. A theoretical physical model is proposed to explain our results, based on the coherent molecular dynamics. We stress the role of the systemic view in the understanding of the biological activity.

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“…Los mecanismos moleculares que subyacen a la alteración de la homeostasis endotelial siguen sin estar claros (36). La disfunción de las células endoteliales se considera un evento temprano Figura 1.…”

Section: Disfunción Endotelialunclassified

Interferon-stimulated gene 15, a common link of vascular damage in hypertension, obesity and aortic aneurysms

Amor

Redondo

2022

an.ranf

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Hypertension and obesity are major health problems worldwide with significant consequences on morbidity and mortality. In fact, both hypertension and obesity are important risk factors for the development of cardiovascular diseases. Endothelial dysfunction, vascular remodeling, and alterations in vascular mechanics are common aspects of vascular damage in hypertension, obesity, and aneurysms. During the last decades, the importance of low-grade inflammation in vascular damage associated with cardiovascular diseases has been demonstrated. This inflammation is characterized by the accumulation of inflammatory cells in the vasculature, as well as by the increase of local and circulating pro-inflammatory cytokines. Therefore, the identification of new inflammatory mediators involved in this damage has become a very important area of research. Interferón-γ (IFNγ) or tumor necrosis tumoral-α (TNFα) are important cytokines involved in the vascular damage associated with hypertension. Furthermore, it is accepted that TNFα is a key mediator involved in insulin resistance and vascular damage observed in obesity. Both cytokines induce the expression of interferon-stimulated gene 15 (ISG15), a protein similar to ubiquitin that induces a reversible post-translational modification (ISGylation) and that can also be secreted as a free form. The functions of ISG15 are mainly related to the immune response against infections, however, it could also be an interesting new target for cardiovascular damage.

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The crosstalk between the cardiovascular and the immune system

Cited by 24 publications

References 48 publications

Supraphysiological Levels of Testosterone Induce Vascular Dysfunction via Activation of the NLRP3 Inflammasome

Supraphysiological Levels of Testosterone Induce Vascular Dysfunction via Activation of the NLRP3 Inflammasome

Sounds Stimulation on In Vitro HL1 Cells: A Pilot Study and a Theoretical Physical Model

Interferon-stimulated gene 15, a common link of vascular damage in hypertension, obesity and aortic aneurysms

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