Dendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation

Araos, Patricio; Prado, Carolina; Lozano, Mauricio; Figueroa, Stefanny; Espinoza, Alexandra; Berger, Thorsten; Mak, Tak W.; Jaisser, Frédéric; Pacheco, Rodrigo; Michea, Luis; Amador, Cristián A.

doi:10.1097/hjh.0000000000002067

Cited by 26 publications

(23 citation statements)

References 43 publications

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“…We recently showed that IL4 protected mouse cardiomyocytes from H 2 O 2 -induced apoptosis (Liu et al, 2020). As discussed, induced DC depletion in CD11c + DOG mice decreased the expression of profibrotic molecules collagen and connective tissue growth factor in hypertrophic heart (Araos et al, 2019), supporting a role for DCs in cardiac fibrosis. Besides the role of DCs in promoting T-cell activation as a mechanism to activate fibroblasts (Nevers et al, 2017), DCs also promote myofibroblast proliferation, differentiation, and activation (Chia et al, 2012), providing additional mechanisms of DC activity in profibrotic protein expression.…”

Section: Mechanisms Of DC Functionmentioning

confidence: 81%

“…In CD11c + DOG mice, DT-induced depletion of DCs reduced aldosterone and high-salt diet-induced cardiac hypertrophy, perivascular fibrosis, expression of cardiac collagen, connective tissue growth factor, lipocalin, and hypertrophic marker BNP (Araos et al, 2019). CD11c + DOG mice are transgenic mice in which the DT receptor gene is expressed under the control of the CD11c promoter (Hochweller et al, 2008).…”

Section: Dcs In Pressure Overload-induced Cardiac Hypertrophy and Fibrosismentioning

confidence: 99%

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Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling

Liu

Shi

Guo

2021

Front. Cell Dev. Biol.

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Pressure overload and heart failure are among the leading causes of cardiovascular morbidity and mortality. Accumulating evidence suggests that inflammatory cell activation and release of inflammatory mediators are of vital importance during the pathogenesis of these cardiac diseases. Yet, the roles of innate immune cells and subsequent inflammatory events in these processes remain poorly understood. Here, we outline the possible underlying mechanisms of innate immune cell participation, including mast cells, macrophages, monocytes, neutrophils, dendritic cells, eosinophils, and natural killer T cells in these pathological processes. Although these cells accumulate in the atrium or ventricles at different time points after pressure overload, their cardioprotective or cardiodestructive activities differ from each other. Among them, mast cells, neutrophils, and dendritic cells exert detrimental function in experimental models, whereas eosinophils and natural killer T cells display cardioprotective activities. Depending on their subsets, macrophages and monocytes may exacerbate cardiodysfunction or negatively regulate cardiac hypertrophy and remodeling. Pressure overload stimulates the secretion of cytokines, chemokines, and growth factors from innate immune cells and even resident cardiomyocytes that together assist innate immune cell infiltration into injured heart. These infiltrates are involved in pro-hypertrophic events and cardiac fibroblast activation. Immune regulation of cardiac innate immune cells becomes a promising therapeutic approach in experimental cardiac disease treatment, highlighting the significance of their clinical evaluation in humans.

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Section: Mechanisms Of DC Functionmentioning

confidence: 81%

Section: Dcs In Pressure Overload-induced Cardiac Hypertrophy and Fibrosismentioning

confidence: 99%

Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling

Liu

Shi

Guo

2021

Front. Cell Dev. Biol.

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“…The orchestrated responses by DCs are supported by a recent study showing that the absence of DCs protects against renal dysfunction, kidney damage, and CV inflammation/fibrosis in an AngII-dependent hypertensive model [ 31 ]. The protective effect of DC depletion for AH development was also corroborated in the nephrectomy aldosterone salt (NAS) model, which involved the prevention of cardiac hypertrophy and fibrosis [ 32 ]. Finally, monocytes and macrophages have also been implicated, principally due to their increase and the phenotypic changes in vasculature, kidney, heart, and brain during AH [ 33 ], promoting fibrosis and maintaining AH through NADPH oxidase-dependent mechanisms in vascular tissue [ 34 , 35 ].…”

Section: Role Of Immune System In Hypertensionmentioning

confidence: 99%

“…In a recent study, it was shown that NGAL is necessary for the development of AH and CV fibrosis in NAS mice [ 89 ], while Buonafine et al showed that NGAL absence, particularly in myeloid cells, is sufficient to prevent the hypertensive phenotype after NAS stimulus [ 86 ]. Recently, we demonstrated that NGAL ablation prevents the overexpression of the IL-23p19 subunit, a polarizing/maintaining cytokine for the T H 17 phenotype, after aldosterone stimulation on DC cultures [ 32 ]. However, whether NGAL presents some direct regulation of the secretion of cytokines, chemokines, or ROS from neutrophils during AH remains unknown.…”

Section: Neutrophils As Contributors Of High Blood Pressurementioning

confidence: 99%

The Role of Neutrophils in Hypertension

Araos

Figueroa

Amador

2020

IJMS

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It is well accepted that the immune system and some cells from adaptive and innate immunity are necessary for the initiation/perpetuation of arterial hypertension (AH). However, whether neutrophils are part of this group remains debatable. There is evidence showing that the neutrophil/lymphocyte ratio correlates with AH and is higher in non-dipper patients. On the other hand, the experimental neutrophil depletion in mice reduces basal blood pressure. Nevertheless, their participation in AH is still controversial. Apparently, neutrophils may modulate the microenvironment in blood vessels by increasing oxidative stress, favoring endothelial disfunction. In addition, neutrophils may contribute to the tissue infiltration of immune cells, secreting chemoattractant chemokines/cytokines and promoting the proinflammatory phenotype, leading to AH development. In this work, we discuss the potential role of neutrophils in AH by analyzing different mechanisms proposed from clinical and basic studies, with a perspective on cardiovascular and renal damages relating to the hypertensive phenotype.

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“…The hypothesis for a causal role of immune cells in AH was proposed in 2007 starting with the Guzik's study [13]. In the last to evaluate how cells of the innate and adaptive immune systems participate in AH, where monocytes-macrophages [14], dendritic cells (DCs) [15,16], and lymphocytes [17][18][19] present experimental evidence that supports their participation in AH [20]. In relation to the mechanisms involved, it has been described that monocytemacrophages act by increasing damage to target tissues [21], while DCs may produce isolevuglandin (IsoLG)-adduct, forming neoantigens after the activation of Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase [22,23], promoting the activation of T-lymphocytes and the secretion of pro-inflammatory cytokines that favor to the sodium reabsorption and cardiovascular/ renal damage [24].…”

Section: Immune Cells In Hypertensionmentioning

confidence: 99%

Is the Sodium an Activator of Immune System in Hypertension?

Amador

2021

BJSTR

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The sodium plays an essential role in human homeostasis and it has been described that a 30-50% of hypertensive patients are sensible to changes in their blood pressure after dietary high sodium intake. The last 20 years have been very active in trying to answer how the immune cells participate in hypertension, where the implications of increased sodium salt intake on the activation of the immune system have not been fully clarified. Even when some described mechanisms for macrophages, dendritic cells and lymphocytes proportion great insight for this understanding, the information concerning the different sodium compartments for its storage arise a new challenge for this area. This mini review highlights recent studies in different experimental settings regarding the effect of sodium as an activator for the immune system in hypertension and the mechanisms involved. We comment also the last studies suggesting the role of sodium as a regulator of immune cells in kidney medulla and extrarenal compartments that possibly may be involved in hypertension.

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Dendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation

Cited by 26 publications

References 43 publications

Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling

Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling

The Role of Neutrophils in Hypertension

Is the Sodium an Activator of Immune System in Hypertension?

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