Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor

Barp, Clarissa Germano; Benedet, Patricia Oliveira; Assreuy, Jamil

doi:10.1016/j.lfs.2020.117819

Cited by 11 publications

(3 citation statements)

References 42 publications

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“…Firstly, as mentioned above, β 3 -AR overstimulation by exogenous agonists may potentiate its negative inotropic actions, deteriorate cardiac dysfunction, and reduce survival rate in sepsis. Secondly, more recent studies showed that CLP increased β 3 -AR expression in the perivascular adipose tissue, which contribute to the vascular dysfunction in sepsis via β 3 -AR activation and constitutive NOS signal pathway (36). Thus, β 3 -AR overstimulation by exogenous agonists may aggravate vascular dysfunction in sepsis via acting on the perivascular adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

Endogenous β3-adrenergic receptor activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway

Xing,

Tian,

Zhang

et al. 2024

Shock

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β3-adrenergic receptor (β3-AR) has been proposed as a new therapy for several myocardial diseases. However, the effect of β3-AR activation on sepsis-induced myocardial apoptosis is unclear. Here, we investigated the effect of β3-AR activation on the cardiomyocyte apoptosis and cardiac dysfunction in cecal ligation and puncture (CLP)-operated rats and lipopolysaccharide (LPS)-treated cardiomyocytes. We found that β3-AR existed both in adult rat ventricular myocytes (ARVMs) and H9c2 cells. The expression of β3-AR was upregulated in LPS-treated ARVMs and the heart of CLP rats. Pretreatment with β3-AR agonist, BRL37344, inhibited LPS-induced cardiomyocyte apoptosis and caspase-3, -8 and -9 activation in ARVMs. BRL37344 also reduced apoptosis and increased the protein levels of PI3K, p-AktSer473 and p-eNOSSer1177 in LPS-treated H9c2 cells. Inhibition of PI3K using LY294002 abolished the inhibitory effect of BRL37344 on LPS-induced caspase-3, -8, and -9 activation in H9c2 cells. Furthermore, administration of β3-AR antagonist, SR59230A (5 mg/kg), significantly decreased the maximum rate of left ventricular pressure rise (+dP/dt) in CLP-induced septic rats. SR59230A not only increased myocardial apoptosis, reduced p-AktSer473 and Bcl-2 contents, but also increased mitochondrial Bax, cytoplasm cytochrome c, cleaved caspase-9 and cleaved caspase-3 levels of the myocardium in septic rats. These results suggest that endogenous β3-AR activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway and maintains intrinsic myocardial systolic function in sepsis.

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Section: Discussionmentioning

confidence: 99%

Endogenous β3-adrenergic receptor activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway

Xing,

Tian,

Zhang

et al. 2024

Shock

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“…Additionally, NO may alter the cellular methylation, acetylation, phosphorylation, ubiquitylation, or sumoylation profiles of proteins and histones by modifying these enzymes [ 101 ]. Recent evidence has revealed the presence of S-nitrosylated (SNO) proteins in abdominal aortic PVAT [ 102 ]. For example, a reduced NO level results in the activation and cellular release of tissue transglutaminase (TG2), which is involved in vascular fibrosis and remodeling [ 103 , 104 ].…”

Section: What Are the Functions Of Enos In Pvat?mentioning

confidence: 99%

Endothelial Nitric Oxide Synthase in the Perivascular Adipose Tissue

et al. 2022

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Perivascular adipose tissue (PVAT) is a special type of ectopic fat depot that adheres to most vasculatures. PVAT has been shown to exert anticontractile effects on the blood vessels and confers protective effects against metabolic and cardiovascular diseases. PVAT plays a critical role in vascular homeostasis via secreting adipokine, hormones, and growth factors. Endothelial nitric oxide synthase (eNOS; also known as NOS3 or NOSIII) is well-known for its role in the generation of vasoprotective nitric oxide (NO). eNOS is primarily expressed, but not exclusively, in endothelial cells, while recent studies have identified its expression in both adipocytes and endothelial cells of PVAT. PVAT eNOS is an important player in the protective role of PVAT. Different studies have demonstrated that, under obesity-linked metabolic diseases, PVAT eNOS may be even more important than endothelium eNOS in obesity-induced vascular dysfunction, which may be attributed to certain PVAT eNOS-specific functions. In this review, we summarized the current understanding of eNOS expression in PVAT, its function under both physiological and pathological conditions and listed out a few pharmacological interventions of interest that target eNOS in PVAT.

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“…Depending on the vessel type and region, PVAT may have different compositional, phenotypic, and functional aspects throughout the vascular system [ 9 , 10 ]. The phenotype of PVAT has been extensively reviewed [ 11 , 12 , 13 , 14 , 15 ]. In recent decades, revealing the crosstalk between blood vessels and PVAT has become a particular interest in the field of vascular biology.…”

Section: Introductionmentioning

confidence: 99%

Perivascular Adipose Tissue Oxidative Stress in Obesity

et al. 2023

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Perivascular adipose tissue (PVAT) adheres to most systemic blood vessels in the body. Healthy PVAT exerts anticontractile effects on blood vessels and further protects against cardiovascular and metabolic diseases. Healthy PVAT regulates vascular homeostasis via secreting an array of adipokine, hormones, and growth factors. Normally, homeostatic reactive oxygen species (ROS) in PVAT act as secondary messengers in various signalling pathways and contribute to vascular tone regulation. Excessive ROS are eliminated by the antioxidant defence system in PVAT. Oxidative stress occurs when the production of ROS exceeds the endogenous antioxidant defence, leading to a redox imbalance. Oxidative stress is a pivotal pathophysiological process in cardiovascular and metabolic complications. In obesity, PVAT becomes dysfunctional and exerts detrimental effects on the blood vessels. Therefore, redox balance in PVAT emerges as a potential pathophysiological mechanism underlying obesity-induced cardiovascular diseases. In this review, we summarise new findings describing different ROS, the major sources of ROS and antioxidant defence in PVAT, as well as potential pharmacological intervention of PVAT oxidative stress in obesity.

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Perivascular adipose tissue phenotype and sepsis vascular dysfunction: Differential contribution of NO, ROS and beta 3-adrenergic receptor

Cited by 11 publications

References 42 publications

Endogenous β3-adrenergic receptor activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway

Endogenous β3-adrenergic receptor activation alleviates sepsis-induced cardiomyocyte apoptosis via PI3K/Akt signaling pathway

Endothelial Nitric Oxide Synthase in the Perivascular Adipose Tissue

Perivascular Adipose Tissue Oxidative Stress in Obesity

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