The role of endothelin receptor antagonism in collar-induced intimal thickening and vascular reactivity changes in rabbits

Reel, Buket; Sozer, Gonen Ozsarlak; Türkseven, Saadet; Kerry, Zeliha; Özkal, Şermin; Özer, Erdener; İşlekel, Hüray; Oktay, Gülgün; Tanriverdi, Serpil

doi:10.1211/jpp.57.12.0010

Cited by 11 publications

(15 citation statements)

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“…[19][20][21] In our previous study, we demonstrated that endothelin contributes to the development of intimal thickening in the collar model and also that endothelin receptor antagonism had an inhibitory effect on thickening of intima. 22 In this study, using the same model, we aimed to investigate (1) the role of gelatinases (MMP-2 and MMP-9) in the development of collar-induced intimal thickening and (2) the effects of TAK-044 {cyclo [D-a-aspartyl-3-[(4-phenylpiperazin-1-yl) carbonyl]-L-alanyl-L-a-aspartyl-D-2-(2-thienyl) glycyl-L-leucyl-D-tryptophyl] disodium}, a nonselective ETA/ETB receptor antagonist, on the expression and activities of these enzymes.…”

Section: Introductionmentioning

confidence: 99%

MMP-2 and MMP-9 Alteration in Response to Collaring in Rabbits: The Effects of Endothelin Receptor Antagonism

Reel

Oktay

Özkal

et al. 2009

J Cardiovasc Pharmacol Ther

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Matrix metalloproteinases (MMPs), and, in particular, gelatinases (MMP-2 and MMP-9), have been implicated in vascular cell proliferation and/or migration, contributing to intimal thickening, an essential stage in the development of atherosclerosis and restenosis following balloon angioplasty. Endothelin, a strong chemoatractant and mitogen, has been shown to promote smooth muscle cell proliferation and migration by activating MMPs via endothelin-A (ETA) receptors. The positioning of a soft silicon collar around the left carotid artery in rabbits results in intimal thickening. In this study, we investigate the possible role of gelatinases and the effect of a nonselective ETA/ETB receptor antagonist, TAK-044 (5 mg/kg body weight/day, subcutaneously [sc]), on these enzymes. Our results demonstrated that both MMP-2 and MMP-9 activities increased in response to collaring in placebo group, while treatment with TAK-044 significantly suppressed both gelatinase activities and proMMP-2 levels, and inhibited intimal thickening in collared arteries. These results suggest that either enhanced MMP expression or endothelin receptor antagonism may be involved in the formation of intimal thickening in this model.

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Section: Introductionmentioning

confidence: 99%

MMP-2 and MMP-9 Alteration in Response to Collaring in Rabbits: The Effects of Endothelin Receptor Antagonism

Reel

Oktay

Özkal

et al. 2009

J Cardiovasc Pharmacol Ther

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“…We ha ve al so shown that ET has an im por tant ro le in the prog res si on of in ti mal thic ke ning in this mo del and the non se lec ti ve en dot helin re cep tor an ta go nist TAK-044 in hi bi ted in ti mal thic ke ning, ge la ti na se up re gu la ti on and ac ti va ti on in col la red ar te ri es. 15,16 It is known that ge la ti na se up re gu la ti on in du ces deg ra da ti on of col la gen. Howe ver, in this study, col la gen con tent was not af- fec ted by TAK-044 tre at ment. The re fo re, this eviden ce sug gests that HSP47 and col la gen are expres sed in de pen dently from ET re cep tor-me di a ted cell sig na ling path ways in the col lar in du ced early at he rosc le ro sis mo del.…”

Section: Medical Pharmacologymentioning

confidence: 99%

“…We al so sho wed that a non se lec ti ve en dot he lin recep tor an ta go nist, TAK-044, in hi bi ted in ti mal thicke ning, MMP up re gu la ti on and ac ti va ti on in this mo del. 15,16 Thus, in this study, we ai med to in ves tiga te the pos sib le ro le of HSP47, the re la ti on betwe en HSP47 and col la gen sythe sis, and al so the ef fects of a non se lec ti ve ETA/ETB re cep tor an tago nist, TAK-044 in col lar-in du ced early at he roscle ro sis mo del.…”

mentioning

confidence: 97%

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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“…32 In this res pect, the inef fec ti ve ness of ni fe di pi ne may be cau sed by the inef fi ci ency of ni fe di pi ne on cyto ki nes, en dot he lin and/or ad he si on mo le cu les. 33,34 On the ot her hand, this study de mons tra ted that the re si du al lu men ra ti o and lu men pe ri me ter sig ni fi cantly dec re a sed and the lu men are a ten ded to be re du ced du e to col lar-in du ced in ti mal thic ke ning.…”

Section: Fi Gu Rementioning

confidence: 99%

Nifedipine Induces Expansive Vascular Remodeling of Carotid Arteries in Rabbit Collar Model

Reel¹,

Ergür²

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: : In ti mal thic ke ning is an adap ti ve res pon se to in jury and to sti mu li ac ting on the ves sel wall. Vas cu lar re mo de ling (VR) is de fi ned as the chan ges in the si ze and/or com po si ti on of the vessels in res pon se to dyna mic and trop hic sti mu li. Inap prop ri a te VR plays a cru ci al ro le in lu men loss and pat ho ge ne sis of car di o vas cu lar di se a ses. Cal ci um chan nel bloc kers (CCBs) ha ve be en known to ha ve vascu lar pro tec ti ve ef fects. Ho we ver, the pre ci se mo le cu lar mec ha nisms of the se ef fects ha ve not be en fully elu ci da ted. The aim of this study was to in ves ti ga te the ef fects of ni fe di pi ne on in ti mal thic ke ning and patho lo gi cal VR, and to exa mi ne the ro le of the dis co i din do ma in re cep tors (DDRs), which are col la gen recep tors, in the VR pro cess in the col lar 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: : Whi te rab bits we re ran do mi zed in to two gro ups. The gro ups re ce i ved ve hic le or ni fe di pi ne (40 mg/kg/day, p.o.) for three we eks. Af ter seven days, a non-occ lu si ve si li co ne col lar was pla ced aro und the left ca ro tid ar tery. To eva lu a te in ti mal thic ke ning and VR, the in ti mal are a, me di al and lu mi nal pe ri me ters we re me a su red. Furt her mo re, DDR ex pressi ons we re as ses sed im mu no his toc he mi cally. R Re e s su ul lt ts s: : Ni fe di pi ne did not in hi bit in ti mal thic ke ning. The col lar pro vo ked in ward VR. Ne it her col la gen con tent nor DDR ex pres si ons we re af fec ted by the col lar. Ni fe di pi ne cons ti tu ted hyper trop hic out ward ex pan si ve VR by in vol ving lu mi nal and ar te ri al en lar gement. Ho we ver ni fe di pi ne did not chan ge eit her col la gen in gre di ent or DDR ex pres si ons. C Co on nc c l lu u s si i o on n: : Nife di pi ne did not in hi bit in ti mal thic ke ning. Ho we ver, it re sul ted in fa vo rab le ex pan si ve VR wit ho ut chan ging col la gen con tents and DDR ex pres si ons. Thus, ni fe di pi ne may help to ma in ta in lu mi nal pa tency and to pre vent res te no sis af ter bal lo on an gi op lasty.K Ke ey y W Wo or rd ds s: : Cal ci um chan nel bloc kers; dis co i din re cep tor; rab bits; at he rosc le ro sis; vas cu lar pa tency Ö ÖZ ZE ET T A Am ma aç ç: : İnti mal ka lın laş ma ha sa ra ve da mar du va rı nı et ki le yen uya rı la ra kar şı ve ri len adap tif bir cevap tır.Vas kü ler ye ni den mo del len me (VYM) di na mik ve tro fik uya rı lar dan do la yı da mar la rın bü yük lük ve/ve ya bi le şi min de olu şan de ği şik lik ler ola rak ta nım lan mak ta dır. Uy gun suz VYM lü men kay bın da ve kar di yo vas kü ler has ta lık la rın pa to je ne zin de kri tik rol oy nar. Kal si yum ka nal blo kör le ri nin vas kü ler koru yu cu et ki le ri ol du ğu bi lin mek te dir. Bu nun la bir lik te bu et ki le rin ke sin mo le kü ler me ka niz ma la rı tam ola rak ay dın la tıl ma mış tır. Bu ça lış ma nın ama cı ni fe di pi nin in ti mal...

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The role of endothelin receptor antagonism in collar-induced intimal thickening and vascular reactivity changes in rabbits

Cited by 11 publications

References 50 publications

MMP-2 and MMP-9 Alteration in Response to Collaring in Rabbits: The Effects of Endothelin Receptor Antagonism

MMP-2 and MMP-9 Alteration in Response to Collaring in Rabbits: The Effects of Endothelin Receptor Antagonism

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

Nifedipine Induces Expansive Vascular Remodeling of Carotid Arteries in Rabbit Collar Model

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