Direct reciprocal effects of resistin and adiponectin on vascular endothelial cells: a new insight into adipocytokine–endothelial cell interactions

Kawanami, Daiji; Maemura, Koji; Takeda, Norihiko; Harada, Tomohiro; Nojiri, Takefumi; Imai, Yasushi; Manabe, Ichiro; Utsunomiya, Kazunori; Nagai, Ryozo

doi:10.1016/j.bbrc.2003.12.104

Cited by 406 publications

(301 citation statements)

References 21 publications

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“…28 Although in vivo studies for the effects of Res on the vasculature are rather scarce, 29 the lack of Adp in knockout mice heightens the neointimal thickening and proliferation of vascular smooth muscle cells in mechanically injured arteries, 30 whereas display impaired endotheliumdependent vasodilation and nitric oxide production. 31,32 Finally, there is growing evidence that Adp antagonizes renin-angiotensin system activation 33,34 and that the centrally-mediated sympathetic nervous system activation may be at least partially modulated by a 'hidden interplay' between leptin and Adp.…”

Section: Discussionmentioning

confidence: 99%

Association of resistin and adiponectin with different clinical blood pressure phenotypes

et al. 2010

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We investigated whether the resistin (Res) and adiponectin (Adp) levels are associated with different clinical blood pressure (BP) phenotypes. Among 465 consecutive never-treated white subjects, we excluded those with diabetes mellitus; impaired glucose metabolism; history of any cardiovascular disease or other concurrent medical condition; secondary hypertension; ongoing vasoactive treatment. Three separate clinic BP measurements and ambulatory BP monitoring were implemented to divide 328 subjects (aged 48±6 years; 172 males) into hypertensives (n ¼ 105), masked hypertensives (n ¼ 41), white-coat hypertensives (n ¼ 52) and normotensives (n ¼ 130). Participants underwent echocardiography and oral glucose tolerance testing, whereas, from fasting venous blood samples metabolic profile, plasma Res and Adp levels were assessed. Hypertensives and masked hypertensives showed higher log(10)(Res) and lower log(10)(Adp) levels compared with normotensives, whereas white-coat hypertensives had similar levels of these adipokines compared with normotensives. Common correlates for both of the adipokines were 24-h systolic BP, standing/sitting difference of both diastolic BP and heart rate, and waist circumference. Hypertensive and masked hypertensive compared with normotensive phenotype were independently associated with log(10)(Res) with odds ratios of 1.24 (1.08-1.44), and 1.16 (1.09-1.34) and log(10)(Adp) with 0.74 (0.65-0.87), and 0.81 (0.67-0.95), respectively. Increased Res and decreased Adp plasma levels are associated with out-of-clinic hypertension, whereas they did not determine whitecoat hypertension.

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Section: Discussionmentioning

confidence: 99%

Association of resistin and adiponectin with different clinical blood pressure phenotypes

et al. 2010

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“…Our study, in agreement with recent data, showed that resistin was correlated with C-reactive protein. Furthermore, resistin can strongly upregulate the expression of pentraxin 3, a close homolog of C-reactive protein, probably via nuclear factor-kappa B (Kawanami et al, 2004). Thus, it was suggested that resistin was involved in the inflammatory process of hemorrhagic stroke.…”

Section: Discussionmentioning

confidence: 99%

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage

Dong¹,

Du²,

Yu³

et al. 2012

Genet. Mol. Res.

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ABSTRACT.We examined a possible relationship -420C>G SNP of the resistin gene with plasma resistin and C-reactive protein concentrations in intracerebral hemorrhage. Three hundred and fortyfour Chinese Han patients with intracerebral hemorrhage and 344 age-and gender-matched healthy controls were included in our study. Plasma resistin and C-reactive concentrations were measured and SNP -420C>G was genotyped. The genotype frequencies in controls and patients were not significantly different (P = 0.672). Plasma resistin and C-reactive protein levels were significantly different between the SNP -420C>G genotypes, even after adjustment for age, gender and body mass index. The common homozygote (C-C) had the lowest resistin and C-reactive protein plasma concentrations; the plasma resistin and C-reactive protein concentrations in the heterozygote (C-G) and the rare allele homozygote (G-G) did not differ significantly. Plasma resistin levels were significantly associated with plasma C-reactive protein level. We conclude that SNP -420C>G of the resistin gene could be involved in the inflammatory component of intracerebral hemorrhage through enhanced production of resistin.

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“…In addition, resistin-treated cells have been reported to express lower TNFa receptor-associated factor, a potent inhibitor of CD40 ligand-mediated endothelial cell activation (Lau et al 2005). Interestingly, the resistin-induced up-regulation of adhesion molecules is antagonised by adiponectin (Kawanami et al 2004). The involvement of resistin in endothelial dysfunction in patients who are insulin resistant has been attributed to its direct effect on endothelial cells by promoting the release of endothelin-1 (Gómez-Ambrosi .…”

Section: Resistinmentioning

confidence: 99%

“…The cardio-protective characteristics of adiponectin have been attributed to its involvement in the prevention of atherosclerotic plaque formation through the inhibition of monocyte adhesion to endothelial cells, by decreasing NFkB signalling via a cAMP-dependent pathway (Ouchi et al 2000;Kawanami et al 2004). Interestingly, in rodent models of atherosclerosis, such as ob/ob and apoEdeficient mice, adiponectin reportedly exerts a protective effect on the development of both atherosclerosis and type 2 diabetes mellitus (Frühbeck, 2004a;Lau et al 2005).…”

Section: Adiponectinmentioning

confidence: 99%

The Sir David Cuthbertson Medal Lecture Hunting for new pieces to the complex puzzle of obesity

Frühbeck

2006

Proc. Nutr. Soc.

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Disentangling the neuroendocrine systems that regulate energy homeostasis and adiposity has been a long-standing challenge in pathophysiology, with obesity being an increasingly important public health problem. Adipose tissue is no longer considered a passive bystander in bodyweight regulation. It actively secretes a large number of hormones, growth factors, enzymes, cytokines, complement factors and matrix proteins, at the same time as expressing receptors for most of these elements, which influence fuel storage, mobilisation and utilisation at both central and peripheral sites. Thus, an extensive cross talk at a local and systemic level in response to specific external stimuli or metabolic changes underpins the multifunctional characteristics of adipose tissue. In addition to the already-known adipokines, such as IL, TNFa, leptin, resistin and adiponectin, more recently attention has been devoted to 'newcomers' to the 'adipose tissue arena', which include aquaporin, caveolin, visfatin, serum amyloid A and vascular endothelial growth factor. While in vitro and in vivo experiments have provided extremely valuable information, the advances in genomics, proteomics and metabolomics are offering a level of information not previously attainable to help unlock the molecular basis of obesity. The potential and power of combining pathophysiological observations with the wealth of information provided by the human genome, knock-out models, transgenesis, DNA microarrays, RNA silencing and other emerging technologies offer a new and unprecedented view of a complex disease, conferring novel insights into old questions by identifying new pieces to the unfinished jigsaw puzzle of obesity.

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Direct reciprocal effects of resistin and adiponectin on vascular endothelial cells: a new insight into adipocytokine–endothelial cell interactions

Cited by 406 publications

References 21 publications

Association of resistin and adiponectin with different clinical blood pressure phenotypes

Association of resistin and adiponectin with different clinical blood pressure phenotypes

Plasma resistin, associated with single nucleotide polymorphism -420, is correlated with C-reactive protein in Chinese Han patients with spontaneous basal ganglia hemorrhage

The Sir David Cuthbertson Medal Lecture Hunting for new pieces to the complex puzzle of obesity

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