Association of F11 receptor gene polymorphisms with central obesity and blood pressure

Leung, R; Wong, LC; Cherny, Stacey S.; Sham, Pak-Chung; Lam, TH; Lam, Karen S.L.; Cheung, Bernard M Y

doi:10.1111/j.1365-2796.2007.01886.x

Cited by 20 publications

(23 citation statements)

References 41 publications

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“…Other clinical characteristics and physical examinations had been described earlier. 7,11 Blood sampling. Subjects were studied in the morning after overnight fasting.…”

Section: Methodsmentioning

confidence: 99%

“…These seven SNPs captured all the 26 SNPs in the F11R gene with r 2 ≥ 0.9 and minor allele frequency ≥ 0.10 in the HapMap Han Chinese population (Phase II data, release 22), from the 3kb region upstream to 1kb downstream of the gene (position 159, 231, 608-159, 278, 358, GenBank accession number NC_000001). 7 The study protocol was approved by the University of Hong Kong Faculty of Medicine Ethics Committee, and written informed consent was obtained from all participants. Hypertension was defined as blood pressure ≥140/90 mm Hg or taking antihypertensive medication.…”

Section: Methodsmentioning

confidence: 99%

“…5 We previously reported the significant association of genetic variants (rs790056 and rs2774276) in the F11R gene with systolic blood pressure. 7 Salifu et al recently reported that circulating levels of a soluble, released form of F11R (sF11R) were elevated in hemodialysis patients and correlated positively with inflammatory markers known to be elevated in cardiovascular diseases, including tumor necrosis factor-α, interleukin-6, and interleukin-10. 8 Plasma sF11R levels were also elevated in CAD patients.…”

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confidence: 98%

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Elevated Plasma Level of Soluble F11 Receptor/Junctional Adhesion Molecule-A (F11R/JAM-A) in Hypertension

Ong

Leung

Babińska

et al. 2009

American Journal of Hypertension

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“…Other clinical characteristics and physical examinations had been described earlier. 7,11 Blood sampling. Subjects were studied in the morning after overnight fasting.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 98%

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Elevated Plasma Level of Soluble F11 Receptor/Junctional Adhesion Molecule-A (F11R/JAM-A) in Hypertension

Ong

Leung

Babińska

et al. 2009

American Journal of Hypertension

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“…126 Intriguingly, single-nucleotide polymorphisms in the junctional adhesion molecule-1 gene have recently been associated with blood pressure on a population-wide basis. 127 Experimental elevations in Ang II have been shown to concomitantly raise blood pressure and cause central inflammation and oxidative stress. 114 Specifically, Ang II-mediated hypertension is associated with increased brain levels of TNFa, nuclear factor kB and reactive oxygen species.…”

Section: Drug-resistant Hypertension-how To Treat?mentioning

confidence: 99%

The sympathetic nervous system and blood pressure in humans: implications for hypertension

2011

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A neurogenic component to primary hypertension (hypertension) is now well established. Along with raised vasomotor tone and increased cardiac output, the chronic activation of the sympathetic nervous system in hypertension has a diverse range of pathophysiological consequences independent of any increase in blood pressure. This review provides a perspective on the actions and interactions of angiotensin II, inflammation and vascular dysfunction/brain hypoperfusion in the pathogenesis and progression of neurogenic hypertension. The optimisation of current treatment strategies and the exciting recent developments in the therapeutic targeting of the sympathetic nervous system to control hypertension (for example, catheter-based renal denervation and carotid baroreceptor stimulation) will be outlined. Keywords: sympathetic nerve activity; neurogenic hypertension; immune-to-brain signalling The sympathetic renaissancePrimary (or essential) hypertension (termed hypertension from here on) accounts for the vast majority of hypertensive cases (B95%).1 Although the aetiology of this condition is incompletely understood, it appears that along with genetic factors, several environmental and behavioural 'hypertensiogenic' factors have been identified, such as obesity, insulin resistance, high-salt intake, low physical activity levels and stress.1 Given the elevated risk of stroke, renal failure, myocardial infarction and coronary heart disease in those afflicted with high blood pressure, the elucidation of the key pathogenic features and optimisation of effective therapeutic strategies are critical.The most common form of hypertension is neurogenic hypertension, defined as high blood pressure with sympathetic overdrive, loss of parasympathetically mediated cardiac variability and excessive angiotensin II (Ang II) activity.2 The importance of the sympathetic nervous system in the short-term regulation of blood pressure via the modulation of peripheral vascular tone and cardiac output is well established, while the role of the sympathetic nerve activity (SNA) in long-term blood pressure control is more controversial. [3][4][5] Although the concept of a potential neurogenic component to hypertension is not new, 4 it has perhaps received less attention than the renin-angiotensin system (RAS), which has been a prominent therapeutic and research target in hypertension over the past few decades. Nevertheless, the activation of the sympathetic nervous system and the RAS in hypertension appears inextricably, and reciprocally, linked. Evidence from studies in both patients and animal models of hypertension strongly implicate the chronic sympathetic neural activation in the aetiology and progression of hypertension (Figure 1). 2,[6][7][8][9] The use of regional surgical sympathectomy to treat hypertension over 50 years ago before the availability of antihypertensive medications that lower sympathetic activity provides an early indication of the clinical appreciation for a significant neurogenic component to hypertension.10 Recent clini...

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“…Local adenoviral overexpression of JAM-A in the NTS of normotensive rats resulted in a transient increase in blood pressure. 11 Since then, polymorphisms in JAM-A gene have been associated with human hypertension in a Hong Kong Chinese population, 12 suggesting that observations in SHRs are likely to be relevant to human hypertension. An elevated level of the soluble form of JAM-A was found in hypertensive patients.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension

Oliveira‐Sales

McBride

et al. 2012

Cardiovascular Research

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AimsEstablishing biochemical markers of pre-hypertension and early hypertension could help earlier diagnostics and therapeutic intervention. We assess dynamics of junctional adhesion molecule-A (JAM-A) expression in rat models of hypertension and test whether JAM-A expression could be driven by angiotensin (ANG) II and whether JAM-A contributes to the progression of hypertension. We also compare JAM-A expression in normo- and hypertensive humans.Methods and resultsIn pre-hypertensive and spontaneously hypertensive rats (SHRs), JAM-A protein was overexpressed in the brainstem microvasculature, lung, liver, kidney, spleen, and heart. JAM-A upregulation at early and late stages was even greater in the stroke-prone SHR. However, JAM-A was not upregulated in leucocytes and platelets of SHRs. In Goldblatt 2K-1C hypertensive rats, JAM-A expression was augmented before any increase in blood pressure, and similarly JAM-A upregulation preceded hypertension caused by peripheral and central ANG II infusions. In SHRs, ANG II type 1 (AT1) receptor antagonism reduced JAM-A expression, but the vasodilator hydralazine did not. Body-wide downregulation of JAM-A with Vivo-morpholinos in juvenile SHRs delayed the progression of hypertension. In the human saphenous vein, JAM-A mRNA was elevated in hypertensive patients with untreated hypertension compared with normotensive patients but reduced in patients treated with renin–angiotensin system antagonists.ConclusionBody-wide upregulation of JAM-A in genetic and induced models of hypertension in the rat precedes the stable elevation of arterial pressure. JAM-A upregulation may be triggered by AT1 receptor-mediated signalling. An association of JAM-A with hypertension and sensitivity to blockers of ANG II signalling were also evident in humans. We suggest a prognostic and possibly a pathogenic role of JAM-A in arterial hypertension.

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Association of F11 receptor gene polymorphisms with central obesity and blood pressure

Cited by 20 publications

References 41 publications

Elevated Plasma Level of Soluble F11 Receptor/Junctional Adhesion Molecule-A (F11R/JAM-A) in Hypertension

Elevated Plasma Level of Soluble F11 Receptor/Junctional Adhesion Molecule-A (F11R/JAM-A) in Hypertension

The sympathetic nervous system and blood pressure in humans: implications for hypertension

Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension

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