Cooperation of Adipocytes and Endothelial Cells Required for Catecholamine Stimulation of PGI2 Production by Rat Adipose Tissue

Parker, J. Anthony; Lane, John; Axelrod, Lloyd

doi:10.2337/diab.38.9.1123

Cited by 17 publications

(6 citation statements)

References 50 publications

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“…In fact, it can be the largest organ in the body. This is physiologically and pathophysiologically important because the total amount of secreted adipokines are enormous and may affect the whole body economy, especially considering that every adipocyte is connected to the vascular network [69]. It is well known that dysregulation of the production and secretion of adipokines is involved in the development of metabolic and cardiovascular diseases.…”

Section: Role Of Adipokinesmentioning

confidence: 99%

“…Antilipolytic stimuli, insulin, for example, reduce the release of prostaglandins [100] such as prostacyclin (PGI 2 ). On the basis that insulin decreases the production of this strong vasodilator, Parker and coworkers suggested that hypertension associated with insulin resistance and hyperinsulinemia (i.e., metabolic syndrome) would be due partly caused by the lack of proper PGI 2 release [69]. It appears that PGI 2 production by the adipocytes results from the cooperation of adipocytes and vascular endothelial cells.…”

Section: Role Of Adipokinesmentioning

confidence: 99%

“…Parker and coworkers proved that adipocytes are a source of the original fatty acid component of prostaglandins, arachidonic acid, that is converted into prostaglandins by the closely located vascular endothelial cells. Adipocytes provide arachidonic acid but lack the required cyclooxygenase which is provided by adjacent endothelial cells [69]. However, adipocytes do express cyclooxygenase [101], and according to Richelsen et al, adipocytes can synthesize prostaglandins, but still provide endothelial cells with adipocyte-derived arachidonic acid to further generate prostaglandins [100].…”

Section: Role Of Adipokinesmentioning

confidence: 99%

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Hypertension in Metabolic Syndrome: Vascular Pathophysiology

Mendizábal

Lloréns

Nava

2013

International Journal of Hypertension

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Metabolic syndrome is a cluster of metabolic and cardiovascular symptoms: insulin resistance (IR), obesity, dyslipemia. Hypertension and vascular disorders are central to this syndrome. After a brief historical review, we discuss the role of sympathetic tone. Subsequently, we examine the link between endothelial dysfunction and IR. NO is involved in the insulin-elicited capillary vasodilatation. The insulin-signaling pathways causing NO release are different to the classical. There is a vasodilatory pathway with activation of NO synthase through Akt, and a vasoconstrictor pathway that involves the release of endothelin-1 via MAPK. IR is associated with an imbalance between both pathways in favour of the vasoconstrictor one. We also consider the link between hypertension and IR: the insulin hypothesis of hypertension. Next we discuss the importance of perivascular adipose tissue and the role of adipokines that possess vasoactive properties. Finally, animal models used in the study of vascular function of metabolic syndrome are reviewed. In particular, the Zucker fatty rat and the spontaneously hypertensive obese rat (SHROB). This one suffers macro- and microvascular malfunction due to a failure in the NO system and an abnormally high release of vasoconstrictor prostaglandins, all this alleviated with glitazones used for metabolic syndrome therapy.

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Section: Role Of Adipokinesmentioning

confidence: 99%

Section: Role Of Adipokinesmentioning

confidence: 99%

Section: Role Of Adipokinesmentioning

confidence: 99%

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Hypertension in Metabolic Syndrome: Vascular Pathophysiology

Mendizábal

Lloréns

Nava

2013

International Journal of Hypertension

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“…In AT, prostaglandin I2 (PGI 2 ) and E2 (PGE 2 ) are the two most abundant members of the family present ( 188 ). Studies have proposed the importance of the presence of both non-fat cells, predominantly endothelial cells, and adipocytes for optimal AT prostaglandin production and secretion ( 189 , 190 ). Experiments using isolated endothelial cells from human adipose capillaries presented evidences that human AT endothelial cells are capable to secrete both PGI 2 and PGE 2 ( 191 ).…”

Section: Small Moleculesmentioning

confidence: 99%

Paracrine Role of the Endothelium in Metabolic Homeostasis in Health and Nutrient Excess

Luk

Haywood

Bridge

et al. 2022

Front. Cardiovasc. Med.

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The vascular endothelium traditionally viewed as a simple physical barrier between the circulation and tissue is now well-established as a key organ mediating whole organism homeostasis by release of a portfolio of anti-inflammatory and pro-inflammatory vasoactive molecules. Healthy endothelium releases anti-inflammatory signaling molecules such as nitric oxide and prostacyclin; in contrast, diseased endothelium secretes pro-inflammatory signals such as reactive oxygen species, endothelin-1 and tumor necrosis factor-alpha (TNFα). Endothelial dysfunction, which has now been identified as a hallmark of different components of the cardiometabolic syndrome including obesity, type 2 diabetes and hypertension, initiates and drives the progression of tissue damage in these disorders. Recently it has become apparent that, in addition to vasoactive molecules, the vascular endothelium has the potential to secrete a diverse range of small molecules and proteins mediating metabolic processes in adipose tissue (AT), liver, skeletal muscle and the pancreas. AT plays a pivotal role in orchestrating whole-body energy homeostasis and AT dysfunction, characterized by local and systemic inflammation, is central to the metabolic complications of obesity. Thus, understanding and targeting the crosstalk between the endothelium and AT may generate novel therapeutic opportunities for the cardiometabolic syndrome. Here, we provide an overview of the role of the endothelial secretome in controlling the function of AT. The endothelial-derived metabolic regulatory factors are grouped and discussed based on their physical properties and their downstream signaling effects. In addition, we focus on the therapeutic potential of these regulatory factors in treating cardiometabolic syndrome, and discuss areas of future study of potential translatable and clinical significance. The vascular endothelium is emerging as an important paracrine/endocrine organ that secretes regulatory factors in response to nutritional and environmental cues. Endothelial dysfunction may result in imbalanced secretion of these regulatory factors and contribute to the progression of AT and whole body metabolic dysfunction. As the vascular endothelium is the first responder to local nutritional changes and adipocyte-derived signals, future work elucidating the changes in the endothelial secretome is crucial to improve our understanding of the pathophysiology of cardiometabolic disease, and in aiding our development of new therapeutic strategies to treat and prevent cardiometabolic syndrome.

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“…The advent of the always overlooked PVAT, turned over the whole concept into an inward signaling. It is worth to remember that an interaction of endothelial cells and adipocytes was proposed in the late eighties, before PVAT was known as such (Parker et al, 1989) and Richelsen published a review supporting the concept that adipocytes provide the endothelial cell with arachidonic acid for the synthesis of prostaglandins and that the release of these substances requires the action of both kind of cells (Richelsen, 1992). Since these initial proposals our understanding of the cross-talk between the different cells of the vascular milieu has experimented a remarkable growth.…”

Section: New Pathways In the Regulation Of Vascular Motionmentioning

confidence: 99%

The Local Regulation of Vascular Function: From an Inside-Outside to an Outside-Inside Model

Nava

Lloréns

2019

Front. Physiol.

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Our understanding of the regulation of vascular function, specifically that of vasomotion, has evolved dramatically over the past few decades. The classic conception of a vascular system solely regulated by circulating hormones and sympathetic innervation gave way to a vision of a local regulation. Initially by the so-called, autacoids like prostacyclin, which represented the first endothelium-derived paracrine regulator of smooth muscle. This was the prelude of the EDRF-nitric oxide age that has occupied vascular scientists for nearly 30 years. Endothelial cells revealed to have the ability to generate numerous mediators besides prostacyclin and nitric oxide (NO). The need to classify these substances led to the coining of the terms: endothelium-derived relaxing, hyperpolarizing and contracting factors, which included various prostaglandins, thromboxane A2, endothelin, as well numerous candidates for the hyperpolarizing factor. The opposite layer of the vascular wall, the adventitia, eventually and for a quite short period of time, enjoyed the attention of some vascular physiologists. Adventitial fibroblasts were recognized as paracrine cells to the smooth muscle because of their ability to produce some substances such as superoxide. Remarkably, this took place before our awareness of the functional potential of another adventitial cell, the adipocyte. Possibly, because the perivascular adipose tissue (PVAT) was systematically removed during the experiments as considered a non-vascular artifact tissue, it took quite long to be considered a major source of paracrine substances. These are now being integrated in the vast pool of mediators synthesized by adipocytes, known as adipokines. They include hormones involved in metabolic regulation, like leptin or adiponectin; classic vascular mediators like NO, angiotensin II or catecholamines; and inflammatory mediators or adipocytokines. The first substance studied was an anti-contractile factor named adipose-derived relaxing factor of uncertain chemical nature but possibly, some of the relaxing mediators mentioned above are behind this factor. This manuscript intends to review the vascular regulation from the point of view of the paracrine control exerted by the cells present in the vascular environment, namely, endothelial, adventitial, adipocyte and vascular stromal cells.

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Cooperation of Adipocytes and Endothelial Cells Required for Catecholamine Stimulation of PGI2 Production by Rat Adipose Tissue

Cited by 17 publications

References 50 publications

Hypertension in Metabolic Syndrome: Vascular Pathophysiology

Hypertension in Metabolic Syndrome: Vascular Pathophysiology

Paracrine Role of the Endothelium in Metabolic Homeostasis in Health and Nutrient Excess

The Local Regulation of Vascular Function: From an Inside-Outside to an Outside-Inside Model

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