Genetic Regulation of Endothelial Vasomotor Function

Kim, Seung Kyum; Massett, Michael P.

doi:10.3389/fphys.2016.00571

Cited by 10 publications

(10 citation statements)

References 87 publications

(105 reference statements)

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“…A portion of data presented here is reproduced from our previous publish (Kim et al . Front Physiol 2016;7:571 [16]).…”

Section: Figmentioning

confidence: 99%

“…We and others showed that EDR is determined by genetic background in mice [101112]. In humans, the estimated heritability of FMD ranges from 0.14 to 0.44 [13141516], suggesting that up to 45% of the variation in FMD is due to genetic factors. Others also reported that changes in FMD in response to training are more correlated in monozygotic than dizygotic twins [1718], implying that endothelial responses to exercise training are also partially affected by genetic factors.…”

Section: Introductionmentioning

confidence: 99%

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Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

Kim

Avila

Massett

2020

Korean J Physiol Pharmacol

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The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed across SED groups. For responses to exercise training, there was a significant interaction between mouse strain and training intensity on EDR. Exercise training had no effect on EDR in aortas from 129S1 and B6 mice. In NON, EDR was improved in aortas from MOD and HIT compared with respective SED, accompanied by diminished responses to PE in those groups. Interestingly, EDR was impaired in aorta from SJL HIT compared with SED. The transcriptional activation of endothelial genes was also influenced by the interaction between mouse strain and training intensity. The number of genes altered by HIT was greater than MOD, and there was little overlap between genes altered by HIT and MOD. HIT was associated with gene pathways for inflammatory responses. NON MOD genes showed enrichment for vessel growth pathways. These findings indicate that exercise training has non-uniform effects on endothelial function and transcriptional activation of endothelial genes depending on the interaction between genetic background and training intensity.

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“…A portion of data presented here is reproduced from our previous publish (Kim et al . Front Physiol 2016;7:571 [16]).…”

Section: Figmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

Kim

Avila

Massett

2020

Korean J Physiol Pharmacol

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“…In conclusion, this was the first study to report that the atherosclerotic process previously observed in coronary arteries also involves the peripheral vessels in HAE patients. Nitric oxide production impairment, through the still poorly-understood bradykinin receptor-ADMA pathway activation, was hypothesized to be involved (Rastaldo et al, 2007 ; Kim and Massett, 2016 ; Wang et al, 2016 ). This may indicate a much more extensive hardening of the arteries, involving the entire arterial tree.…”

Section: Discussionmentioning

confidence: 99%

Impaired Endothelial Function in Hereditary Angioedema During the Symptom-Free Period

et al. 2018

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Introduction: The presence of coronary endothelial dysfunction was previously shown in Hereditary Angioedema (HAE) patients. The aim of our study was to evaluate the effect of HAE on systemic endothelial function and whether there was a relationship among endothelial function, asymmetric dimethylarginine (ADMA) -which is a strong inhibitor of nitric oxide synthesis-, and disease severity scores.Methods: Twenty-four HAE patients (18 females, aged 47.9 ± 2 years) without factors known to interfere with endothelial function were studied and compared with 24 healthy peers age- and gender-matched. Endothelial function was assessed by means of non-invasive finger plethysmography (reactive hyperaemia index: RHI) and ADMA levels by high-performance liquid chromatography. HAE severity scores have been calculated according to published literature.Results: In HAE patients RHI was lower (2.03 ± 0.46 vs. 2.82 ± 0.34, p < 0.0001) and ADMA higher (0.636 ± 7 vs. 585 ± 5 micromol/L, p < 0.01) than in controls. A statistically significant inverse correlation was revealed between RHI and patients' ADMA levels (r = −0.516, p = 0.009) as well as between RHI and patients' chronological age (r = −0.49, p = 0.015). A statistically significant correlation between RHI and ADMA was confirmed even when excluding the possible influence of cholesterol (r = −0.408, p = 0.048). No other significant correlations were found with the examined laboratory and clinical parameters (chronological age, age at disease onset, disease duration, severity scores, and gender).Conclusion: The dysfunction previously shown in HAE patients at the coronary arteries seems to involve the peripheral vessels as well, without a correlation with disease severity.

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“…So far, the pathophysiology of CSFP is not exact; it is thought to be caused by various causes in blood vessels, in the form of coronary microvascular disease, inflammation and endothelial dysfunction [9], [10], [11]. The pathogenesis of CSFP also involves a vital role of the renin-angiotensin-aldosterone system (RAAS).…”

Section: Introductionmentioning

confidence: 99%

“…This system consists of hormones and enzymes, which include angiotensinogen, angiotensin-converting enzyme (ACE), angiotensin I (AT1), angiotensin II (AT2), and aldosterone. AT2 has two receptor subtypes, namely, type 1 receptor (AT1R) and type 2 receptors (AT2R) [10]. The function of AT2 not only to stimulating aldosterone secretion but also to constrict blood vessel, stimulates various growth factors, initiates hypertrophy and smooth muscle hyperplasia of blood vessels, making the condition of arterial stiffness.…”

Section: Introductionmentioning

confidence: 99%

The Role of AT1R A1166C Gene Polymorphism in Coronary Slow Flow Phenomenon of Undergoing Coronary Angiography Patients

Indrajaya

Saleh

Alpian

2020

Open Access Maced J Med Sci

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BACKGROUND: The presence of gene polymorphisms in the renin-angiotensin-aldosterone system associated with an impaired endothelial function that causes atherosclerosis and also myocardial fibrosis such as the polymorphism of the angiotensin-converting enzyme gene and the angiotensin I receptor (AT1R) gene. AIM: This research was aimed to explore the role of AT1R A1166C gene polymorphism in the incidence of coronary slow flow phenomenon (CSFP) in the Malay population, South Sumatra, Indonesia. METHODS: This study is a comparative analysis using a case-control study design to analyze the effect of the AT1R A1166C gene polymorphism on the incidence of slow flow phenomenon in patients undergoing elective coronary angiography at Mohammad Hoesin Hospital Palembang, Indonesia. Examination of AT1R gene polymorphism was carried out with several steps starting from deoxyribonucleic acid extraction, polymerase chain reaction process, followed by restriction fragment length polymorphism stages with Ddel restriction enzymes and visualization. RESULTS: Thirty-two patients participated in these study-baseline characteristics between homogeneous coronary regular flow groups and homogeneous coronary slow flow groups. There is no difference between genotype distribution, allele frequency, and genotype between the CSFP and the coronary standard flow group. CONCLUSION: There is no influence of AT1R A1166C gene polymorphism on the CSFP in patients undergoing coronary angiography.

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Genetic Regulation of Endothelial Vasomotor Function

Cited by 10 publications

References 87 publications

Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

Impaired Endothelial Function in Hereditary Angioedema During the Symptom-Free Period

The Role of AT1R A1166C Gene Polymorphism in Coronary Slow Flow Phenomenon of Undergoing Coronary Angiography Patients

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