Actin-Binding Rho Activating Protein (
            <i>Abra</i>
            ) Is Essential for Fluid Shear Stress-Induced Arteriogenesis

Troidl, Kerstin; Rüding, Inka; Cai, Wenju; Mücke, Yvonne; Großekettler, Leonie; Piotrowska, Izabela; Apfelbeck, H.; Schierling, Wilma; Volger, Oscar L.; Horrevoets, Anton J.G.; Grote, Karsten; Schmitz‐Rixen, Thomas; Schäper, Wolfgang; Troidl, Christian

doi:10.1161/atvbaha.109.195305

Cited by 65 publications

(69 citation statements)

References 42 publications

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“…Experiments using AV shunts such as performed with inhibitors of endothelial nitric oxide synthase efficiently showed mechanisms for modulating arteriogenesis. 28 Likewise, our results obtained from the angiographies showed that under high shear conditions, arteriogenesis is reduced with B1R antagonist treatment ( Figure 6I) and correlated with reduced leukocyte transmigration as presented in the histology. Immunostaining for CD11b (pan-leukocyte marker) showed a strong reduction in a number of positive cells in the collateral region of B1R antagonist-treated rats.…”

Section: Hillmeister Et Al Bradykinin Signaling Modulates Arteriogenesissupporting

confidence: 66%

Arteriogenesis Is Modulated By Bradykinin Receptor Signaling

Hillmeister

Gatzke

Dülsner

et al. 2011

Circulation Research

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Rationale: Positive outward remodeling of pre-existing collateral arteries into functional conductance arteries, arteriogenesis, is a major endogenous rescue mechanism to prevent cardiovascular ischemia. Collateral arterial growth is accompanied by expression of kinin precursor. However, the role of kinin signaling via the kinin receptors (B1R and B2R) in arteriogenesis is unclear.Objective: The purpose of this study was to elucidate the functional role and mechanism of bradykinin receptor signaling in arteriogenesis. Key Words: bone marrow transplantation Ⅲ bradykinin receptors Ⅲ collateral growth Ⅲ leukocytes A rteriogenesis is the process that involves the flow-induced outward remodeling of preexisting collateral arterial pathways into functional conductance arteries (biological bypass). As a result of the arteriogenesis process, blood perfusion to the compromised region is restored; 1 therefore, it is regarded as a clinically highly relevant target. It is established that arteriogenesis is triggered by changes in local hemodynamic conditions and subsequent activation of inflammatory pathways. We previously showed that expression of kininogen, a precursor of the vasoactive kinin peptides, was selectively expressed in growing collaterals of the rat brain. 2 Here we investigated the role of kinin signaling in bradykinin receptor-deficient mice for collateral growth and evaluated whether stimulation with bradykinin receptor antagonists/agonists may modulate arteriogenesis in mice and rats. Our data suggest that the kinin-receptor signaling pathway may act as a molecular link between changes in hemodynamic forces (artery occlusion) and the activation of inflammatory pathways, including attraction of bone marrow Original Methods and Results:

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Section: Hillmeister Et Al Bradykinin Signaling Modulates Arteriogenesissupporting

confidence: 66%

Arteriogenesis Is Modulated By Bradykinin Receptor Signaling

Hillmeister

Gatzke

Dülsner

et al. 2011

Circulation Research

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“…Clusters of variants in 7 loci were associated with childhood DBP (P≤5×10 −3 ; Table 3) and were investigated further using LocusZoom. 40 Regional associations for all of these associations are presented in Figure VI ) where all SNPs had an MAF>0.10 and all cohorts contributed to each SNP analyses (postpubertal) and at least 4 cohorts contributed to GWAS findings for the prepubertal and pubertal epochs. Beta values are in terms of Z-scores, the number of standard deviations away from the mean.…”

Section: Genome-wide Significancementioning

confidence: 99%

“…Repression of ABRA (STARS) within embryonic, neonatal, and adult hearts via gene GATA4 has shown major implications for MRTF-SRF signaling in the context of cardiac development and disease (mice studies) 39 . Fluid sheer stress-induced ABRA expression during arteriogenesis is triggered by NO and leads to stimulation of collateral growth by smooth muscle cell proliferation 40 . Has a vast range of effects in the cardiovascular, immune, and central and peripheral nervous systems 42 .…”

Section: Studymentioning

confidence: 99%

International Genome-Wide Association Study Consortium Identifies Novel Loci Associated With Blood Pressure in Children and Adolescents

Parmar¹,

Taal²,

Timpson³

et al. 2016

Circ Cardiovasc Genet

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266S ystolic and diastolic blood pressure (SBP and DBP) are complex phenotypes, with known environmental and genetic risk factors.1 Elevated SBP and DBP are associated with premature mortality 2,3 and cardiovascular diseases. 2,4-9 Clinical Perspective on p 278Recent genome-wide association studies (GWAS) have identified genetic variants associated with adult SBP and DBP and hypertension. [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] Several of these loci are in biologically plausible candidate genes, for example, those that influence the renin-angiotensin system. 25 There are established patterns of age-related changes in BP in industrialized populations, which support a potential interaction of genetic variants with age-related changes to environmental exposures in these populations. 26,27 For genetic variants that directly modulate childhood BP, effects might change with age, might differ between developmental periods (early life, childhood, and adolescence), and might also differ to those variants that act in adulthood.Children and adolescents are rarely treated with antihypertensives, whereas from middle age onwards, an increasing proportion of adults are using such medications. 26 Consequently, it is easier to examine genetic variants that are associated with untreated SBP and DBP in children. Variation in SBP, and to Background-Our aim was to identify genetic variants associated with blood pressure (BP) in childhood and adolescence. Methods and Results-Genome-wide association study data from participating European ancestry cohorts of the EarlyGenetics and Lifecourse Epidemiology (EAGLE) Consortium was meta-analyzed across 3 epochs; prepuberty (4-7 years), puberty (8-12 years), and postpuberty (13-20 years). Two novel loci were identified as having genome-wide associations with systolic BP across specific age epochs: rs1563894 (ITGA11, located in active H3K27Ac mark and transcription factor chromatin immunoprecipitation and 5′-C-phosphate-G-3′ methylation site) during prepuberty (P=2.86×10-8) and rs872256 during puberty (P=8.67×10 -9 ). Several single-nucleotide polymorphism clusters were also associated with childhood BP at P<5×10 -3. Using a P value threshold of <5×10 -3 , we found some overlap in variants across the different age epochs within our study and between several single-nucleotide polymorphisms in any of the 3 epochs and adult BPrelated single-nucleotide polymorphisms. Conclusions-Our results suggest that genetic determinants of BP act from childhood, develop over the lifecourse, and show some evidence of age-specific effects. Parmar et al Blood Pressure GWAS in Children 267a lesser extent DBP, in adolescence and early adulthood is associated with subsequent adult risk of coronary heart disease and stroke. 28,29 Understanding the risk factors, including genetic variation, that are associated with SBP and DBP through childhood and into adolescence may therefore inform an improved understanding of the life course pathogenesis of adult hypertension and cardiovascular disease...

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“…Genetik. Möglichkeiten des Gefäßwachs-tums auch im adulten Organismus [33,34], der dabei notwendigen Reprogrammierung von Zellen in pluripotente Vorläuferzellen und Mechanismen, diese reprogrammierten Zellen zielgerecht in den Regenerationsprozess eingreifen zu lassen ("foetal gene program") werden die Wissenschaftler für die nächsten 20 Jahre und darüber hinaus beschäftigen [35,36]. Translationale Forschungsansätze werden für die notwendige Dynamik sorgen und Irrwege vermeiden.…”

Section: Trend 5: Vaskuläre Biologieunclassified

Entwicklung der Gefäß- und Endovaskularchirurgie in den nächsten 20 Jahren

Schmitz‐Rixen

Lang

2009

Chirurg

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Vascular surgery is a young surgical discipline which has experienced a stormy development driven by internal motivation and external constraints. Changes in the field are primarily a result of diverse external influences which are expected to continue into the future. The most significant intrinsic change has been the development of stent graft technology. External influences include extensive demographic changes, rapid progress in endovascular techniques to treat obstructive vascular disease, improved advanced training, state and non-state controls, certification requests without considering the feasibility of professional and structural implementation and changing public expectations. Progress in vascular medicine is stimulated by advances in imaging techniques and subsequent improved endovascular procedures. Nevertheless, external influences have, at least within the 'surgical' sphere of influence, led to formidable innovative efforts on the part of associations representing vascular surgeons. These innovative efforts are concentrated in the Academy of the German Society of Vascular Surgery and Medicine and will determine trends in coming years. The future will reflect their quality.

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Actin-Binding Rho Activating Protein ( Abra ) Is Essential for Fluid Shear Stress-Induced Arteriogenesis

Cited by 65 publications

References 42 publications

Arteriogenesis Is Modulated By Bradykinin Receptor Signaling

Arteriogenesis Is Modulated By Bradykinin Receptor Signaling

International Genome-Wide Association Study Consortium Identifies Novel Loci Associated With Blood Pressure in Children and Adolescents

Entwicklung der Gefäß- und Endovaskularchirurgie in den nächsten 20 Jahren

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