Vascular Remodeling in the Internal Mammary Artery Graft and Association With In Situ Endothelin-1 and Receptor Expression

Sutherland, Allison J.; Nataatmadja, Maria; Walker, Philip J.; Cuttle, Leila; Garlick, Rhonda B.; West, Malcolm

doi:10.1161/circulationaha.105.582890

Cited by 35 publications

(25 citation statements)

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“…Although additional assessment of the association of their findings with endothelial function and neoangiogenesis would have strengthened this study by Sutherland et al, 9 their findings encourage further investigation on this unique and clinically important graft artery and the endogenous endothelin system as a mechanism for atherosclerosis. The choice of the most appropriate graft for coronary artery bypass surgery has been investigated by numerous clinical trials.…”

Section: Article P 1180mentioning

confidence: 56%

“…As shown by Sutherland et al, 9 there is increased and accentuated media necrosis, ET-1, and ET receptor expression in the media of the atherosclerotic IMA. It may be speculated that this may represent an imbalance between demand and perfusion and/or diffusion in this part of the vessel wall.…”

Section: Article P 1180mentioning

confidence: 62%

“…In summary, the report by Sutherland et al 9 elaborates nicely that atherosclerosis is a pathological process ubiquitously distributed throughout the vessel wall and that the endogenous endothelin system may play a significant role in its evolution, progression, and complications. Moreover, it underscores the fact that the outer vessel-wall layers (and with them, the vasa vasorum) appear to play an important role in atherosclerosis and may be suitable as a future therapeutic target.…”

Section: Article P 1180mentioning

confidence: 93%

“…6,7 Similar results have been reported with a nonselective ET A /ET B receptor blocker in rabbits. 8 In this issue of Circulation, Sutherland et al 9 extend the role of ET-1 in atherosclerosis and present their findings from a morphology-and immunohistochemistry-based study on internal mammary arteries (IMAs) collected from patients with coronary artery disease (CAD) undergoing coronary artery bypass graft surgery. They demonstrate that IMA specimens from CAD patients show increased medionecrosis, type-1 collagen, and ET-1, ET A , and ET B receptor expression.…”

Section: Article P 1180mentioning

confidence: 99%

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Endothelin

Gössl

Lerman

2006

Circulation

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A lmost 2 decades ago, endothelin-1 (ET-1) was identified as one of the most potent vasoconstrictors in the complex but well-balanced regulation of vascular tone. 1 Since then, through numerous clinical and experimental investigations, it has become evident that ET-1, beyond its function as a vasoactive peptide, also plays a seminal role in the atherogenic process by enhancing mitogenesis and inducing extracellular matrix formation. The role of ET-1 as an active participant in the atherogenic process is underscored by the observations that endothelin is highly and ubiquitously expressed in the extracellular space and the intracellular compartment (macrophages, myointimal cells, myofibroblasts, and endothelial cells) of human coronary atheromatous tissue. 2 Moreover, it has been demonstrated that circulating and tissue endothelin immunoreactivity correlates with the severity of human atherosclerotic disease. 3 Taken together, these findings strongly suggest a major role for ET-1 in the evolution and progression of coronary atherosclerosis in humans. At the molecular level, nuclear factor-B, a key transcription factor of the inflammation-cascade, is activated by ET-1 in human monocytes, 4 which further supports the role of ET-1 in the development of inflammation, a key feature of atherogenesis, within the vessel wall. Article p 1180Because of the development of endothelin antagonists suitable for experimental and human use, the functional role of ET-1 has been further elucidated. In experimental hypercholesterolemia, chronic endothelin receptor antagonism preserved coronary endothelial function and increased nitric oxide (NO) activity. 5 Moreover, in the rodent atherosclerosis model, chronic ET A receptor blockade not only normalized NO-mediated endothelial dysfunction but also significantly reduced atheroma formation. 6,7 Similar results have been reported with a nonselective ET A /ET B receptor blocker in rabbits. 8 In this issue of Circulation, Sutherland et al 9 extend the role of ET-1 in atherosclerosis and present their findings from a morphology-and immunohistochemistry-based study on internal mammary arteries (IMAs) collected from patients with coronary artery disease (CAD) undergoing coronary artery bypass graft surgery. They demonstrate that IMA specimens from CAD patients show increased medionecrosis, type-1 collagen, and ET-1, ET A , and ET B receptor expression. These findings underline the fact that the IMA is not simply a passive conduit vessel but is an autologous graft that responds to high levels of ET-1 in atherosclerosis with characteristic vessel-wall changes. In addition, they warrant further investigation regarding the potential use of ET-1 receptor antagonists in the medical regimen, which may further improve the already superior patency rate of the IMA in coronary artery bypass graft surgery. The concept that the IMA graft may profit from ET receptor blockade is supported by functional data showing that the IMA develops greater endothelium-dependent relaxation than vein grafts. 10 If the I...

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Section: Article P 1180mentioning

confidence: 56%

Section: Article P 1180mentioning

confidence: 62%

Section: Article P 1180mentioning

confidence: 93%

Section: Article P 1180mentioning

confidence: 99%

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Endothelin

Gössl

Lerman

2006

Circulation

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“…31,32 Si mi larly, ETA an ta gonism in hi bi ted ET-in du ced col la gen sti mu la ti on in por ci ne aor tic smo oth musc le cell cul tu re. 33 Ho wever, the pos sib le ef fects of ET an ta go nism on col lagen le vels and HSP47 ex pres si on in early at he rosc le ro sis mo del ha ve not be en stu di ed yet.…”

Section: Medical Pharmacologymentioning

confidence: 99%

Endothelin Receptor-Independent Correlation Between HSP47 and Collagen in Rabbit Model of Early Atherosclerosis

Reel¹,

Cavdar²,

Ergür³

et al. 2011

Turkiye Klinikleri J Med Sci

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A AB BS S T TR RA AC CT T O Ob b j je ec c t ti i v ve e: : Col la gen in the ex tra cel lu lar mat rix (ECM) plays an im por tant ro le in mo dula tion of res pon se to the vas cu lar in jury du ring the prog res si on of at he rosc le ro sis and res te no sis. Colla gen can re gu la te smo oth musc le cell (SMC) pro li fe ra ti on, mig ra ti on and mat rix me tal lop ro te i na se (MMP) pro duc ti on. The re fo re, col la gen tur no ver in the ar te ri es is an im por tant de ter mi nant of in timal thic ke ning. He at shock pro te in 47 (HSP47), a col la gen-spe ci fic mo le cu lar cha pe ro ne, is tho ught to be es sen ti al for the pro ces sing and sec re ti on of pro col la gen mo le cu les. En dot he lin (ET) is a strong che mo at rac tant and mi to gen pro mo ting SMC pro li fe ra ti on and mig ra ti on. The aim of this study was to in ves ti ga te the pos sib le ro le of HSP47 and its re la ti on to col la gen synthe sis, and the ef fects of a non se lec ti ve ETA/ETB re cep tor an ta go nist, TAK-044 in col lar-in du ced early at he rosc le ro sis mo del. M Ma a t te e r ri i a al l a an nd d M Me et t h ho od ds s: : New Ze a land whi te rab bits we re di vi ded in to two gro ups. Both gro ups re ce ived ve hic le (0.9% NaCl 0.8 ml/kg/day, s.c.) or TAK-044 (5 mg/kg/day, s.c.) for three we eks. On 8 th day, a non-occ lu si ve si li con col lar was pla ced aro und the left ca ro tid ar tery. The right ca ro tid ar tery was sham-ope ra ted. HSP47 ex pres si on in ca ro tid ar te ri es we re de ter mi ned im mu no his toc he mi cally. Furt her mo re, to tal col la gen le vels, col la gen ex pres si on and type I pro col la gen ex pres si on we re es tab lished. R Re e s su ul lt ts s: : HSP47 ex pres si on cor re la ted with col la gen ex pres si on did not chan ge in col la red ar te ri es. TAK-044 tre at ment did not af fect HSP47 and col la gen le vels. C Co on nc c l lu u s si i o on n: : The re was a cor re la ti on bet we en HSP47 ex pres si on and col la gen ex pres si on in ca ro tid ar te ri es. Ho we ver, in ti mal thic ke ning did not in du ce HSP47 ex pres si on and early col la gen de ve lop ment. The inef fec ti ve nes of TAK-044 sug gests that ET-1 sig na ling may not be imp li ca ted in HSP47 and col la gen in this mo del. K Ke ey y W Wo or rd ds s: : HSP47 he at-shock pro te ins; at he rosc le ro sis; col la gen; en dot he lin-1; rab bits Ö ÖZ ZE ET T A Am ma aç ç: : Eks tra sel lü ler mat riks te ki (ESM) ko la jen ate rosk le roz ve res te no zun ge li şi mi sı ra sın -da vas kü ler ha sa ra ya nı tın mo dü las yo nun da önem li bir rol oy nar. Ko la jen düz kas hüc re si pro li feras yo nu nu, mig ras yo nu nu ve mat riks me tal lop ro te i naz (MMP) üre ti mi ni dü zen le ye bi lir. Bu ne den le ar ter ler de ki ko la jen dön gü sü in ti mal ka lın laş ma nın önem li bir be lir te ci dir. Ko la je ne öz gü mo le kü -ler bir şape ron olan ısı şoku pro te i ni 47'nin (HSP47) pro ko la jen mo le kül le ri nin iş len me si ve sek resyo nu için te mel ol du ğu dü şü nül mek te dir. En do t...

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Endothelin receptors as drug targets in chronic cardiovascular diseases: the rationale for dual antagonism

Clozel¹,

Flores²

2006

Drug Development Research

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Endothelin has been described as the most potent vasoconstrictor known. Recent research shows that it is also a growth factor, a promoter of fibrosis and inflammation, and a key initiator of endothelial dysfunction. Endothelin becomes, therefore, a candidate in the pathogenesis of many chronic cardiovascular and fibrotic diseases, and inhibition of endothelin function is a potential therapeutic approach for those diseases. Endothelin receptor antagonists are now established therapy in the treatment of pulmonary arterial hypertension, and present promising perspectives in diabetic nephropathy, peripheral arterial disease, hypertension, heart failure, and pulmonary diseases. Endothelin binds to two endothelin receptors, ET A and ET B , and their respective roles are actively debated. A major challenge lies in the understanding of what is the preferred profile for new drugs: selective ET A antagonism or dual ET A and ET B receptor antagonism. A number of cardiovascular diseases are characterized by an up-regulation of smooth muscle cell ET B receptors mediating vasoconstriction and proliferation, and a down-regulation of endothelial ET B receptors, as compared to the physiological state, creating a situation where both ET A and ET B receptors contribute to vasoconstriction and remodeling. When these two receptor subtypes co-exist, a cross-talk between them, probably a result of receptor heterodimerization, suggests that dual ET A /ET B receptor antagonism may be necessary to obtain maximal efficacy. Drug Dev. Res. 67:825-834, 2006.

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Vascular Remodeling in the Internal Mammary Artery Graft and Association With In Situ Endothelin-1 and Receptor Expression

Cited by 35 publications

References 44 publications

Endothelin

Endothelin

Endothelin Receptor-Independent Correlation Between HSP47 and Collagen in Rabbit Model of Early Atherosclerosis

Endothelin receptors as drug targets in chronic cardiovascular diseases: the rationale for dual antagonism

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