scholarly journals Biomimetic Elastin Fiber Patch in Rat Aorta Angioplasty

ACS Omega ◽  
2021 ◽  
Author(s):  
Hualong Bai ◽  
Shunbo Wei ◽  
Peng Sun ◽  
Liwei Zhang ◽  
Yuanfeng Liu ◽  
...  
Keyword(s):  
1986 ◽  
Vol 103 (3) ◽  
pp. 1121-1128 ◽  
Author(s):  
H M Kagan ◽  
C A Vaccaro ◽  
R E Bronson ◽  
S S Tang ◽  
J S Brody

The localization of lysyl oxidase was examined in calf and rat aortic connective tissue at the ultrastructural level using polyclonal chicken anti-lysyl oxidase and gold conjugated rabbit anti-chicken immunoglobulin G to identify immunoreactive sites. Electron microscopy of calf aortic specimens revealed discrete gold deposits at the interface between extracellular bundles of amorphous elastin and the microfibrils circumferentially surrounding these bundles. The antibody did not react with microfibrils which were distant from the interface with elastin. There was negligible deposition of gold within the bundles of amorphous elastin and those few deposits seen at these sites appeared to be associated with strands of microfibrils. Lysyl oxidase was similarly localized in newborn rat aorta at the interface between microfibrils and nascent elastin fibers. Gold deposits were not seen in association with extracellular collagen fibers even after collagen-associated proteoglycans had been degraded by chondroitinase ABC. However, the antibody did recognize collagen-bound lysyl oxidase in collagen fibers prepared from purified collagen to which the enzyme had been added in vitro. No reaction product was seen if the anti-lysyl oxidase was preadsorbed with purified lysyl oxidase illustrating the specificity of the antibody probe. The present results are consistent with a model of elastogenesis predicting the radial growth of the elastin fiber by the deposition and crosslinking of tropoelastin units at the fiber-microfibril interface.


Author(s):  
E. N. Albert

Silver tetraphenylporphine sulfonate (Ag-TPPS) was synthesized in this laboratory and used as an electron dense stain for elastic tissue (Fig 1). The procedures for the synthesis of tetraphenylporphine sulfonate and the staining method for mature elastic tissue have been described previously.The fine structure of developing elastic tissue was observed in fetal and new born rat aorta using tetraphenylporphine sulfonate, phosphotungstic acid, uranyl acetate and lead citrate. The newly forming elastica consisted of two morphologically distinct components. These were a central amorphous and a peripheral fibrous. The ratio of the central amorphous and the peripheral fibrillar portion changed in favor of the former with increasing age.It was also observed that the staining properties of the two components were entirely different. The peripheral fibrous component stained with uranyl acetate and/or lead citrate while the central amorphous portion demonstrated no affinity for these stains. On the other hand, the central amorphous portion of developing elastic fibers stained vigorously with silver tetraphenylporphine sulfonate, while the fibrillar part did not (compare figs 2, 3, 4). Based upon the above observations it is proposed that developing elastica consists of two components that are morphologically and chemically different.


1995 ◽  
Vol 73 (03) ◽  
pp. 535-542 ◽  
Author(s):  
N Crawford ◽  
A Chajara ◽  
G Pfliegler ◽  
B EI Gamal ◽  
L Brewer ◽  
...  

SummaryDrugs can be electro-encapsulated within platelets and targeted to damaged blood vessels by exploiting the platelet’s natural haemostatic properties to adhere to collagen and other vessel wall constituents revealed by injury. A rat aorta balloon angioplasty model has been used to study the effect on platelet deposition of giving iloprost loaded platelets i.v. during the balloon injury. After labelling the circulating platelets with 111-Indium before balloon injury, time course studies showed maximum platelet deposition on the injured aorta occurred at about 1 h post-injury and the deposition remained stable over the next 2-3 h. When iloprost-loaded platelets were given i.v. during injury and the circulating platelet pool labelled with 111-Indium 30 min later, platelet deposition, measured at 2 h postinjury, was substantially and significantly reduced compared with control platelet treatment. Some antiproliferative effects of iloprost-loaded platelets given i.v. during injury have also been observed. Whereas the incorporation of [3H]-thymidine into aorta intima-media DNA at 3 days post injury was 62-fold higher in balloon injured rats than in control sham operated rats, thymidine incorporation into intima/media of rats which had received iloprost loaded platelets during injury was reduced as compared with rats subjected only to the injury procedure. The reduction was only of near significance, however, but at 14 days after injury the total DNA content of the aorta intima/media of rats given iloprost loaded platelets during injury was significantly reduced. Although iloprost loaded platelets can clearly inhibit excessive platelet deposition, other encapsulated agents may have greater anti-proliferative effects. These studies have shown that drug loaded platelets can be targeted to injured arteries, where they may be retained as depots for local release. We believe this novel drug delivery protocol may have therapeutic potential in reducing the incidence of occlusion and restenosis after angioplasty and thrombolysis treatment. Electro-encapsulation of drugs into platelets is a simple procedure and, using autologous and fully biocompatible and biodegradable platelets as delivery vehicles, might overcome some of the immunological and toxicological problems which have been encountered with other delivery vectors such as liposomes, microbeads, synthetic microcapsules and antibodies.


Diabetes ◽  
1986 ◽  
Vol 35 (9) ◽  
pp. 973-978 ◽  
Author(s):  
L. Capron ◽  
J. Jarnet ◽  
S. Kazandjian ◽  
E. Housset

Hypertension ◽  
1995 ◽  
Vol 26 (5) ◽  
pp. 738-743 ◽  
Author(s):  
Guy Berkenboom ◽  
Dmitri Brékine ◽  
Philippe Unger ◽  
Katrina Grosfils ◽  
Michel Staroukine ◽  
...  

Author(s):  
C Yang ◽  
L Zhang ◽  
R Dai ◽  
S Ji ◽  
F Li ◽  
...  
Keyword(s):  

2021 ◽  
Vol 22 (7) ◽  
pp. 3309
Author(s):  
Soo Hee Lee ◽  
Seong-Ho Ok ◽  
Seung Hyun Ahn ◽  
Hyun-Jin Kim ◽  
Sung Il Bae ◽  
...  

This study aimed to examine the effect of lipid emulsion (LE) on the vasoconstriction induced by dexmedetomidine (DMT) in the isolated rat aorta and elucidate the associated cellular mechanism. The effect of LE, NW-nitro-L-arginine methyl ester (L-NAME), and methyl-β-cyclodextrin (MβCD) on the DMT-induced contraction was examined. We investigated the effect of LE on the DMT-induced cyclic guanosine monophosphate (cGMP) formation and DMT concentration. The effect of DMT, LE, 4-Amino-3-(4-chlorophenyl)-1-(t-butyl)-1H-pyrazolo[3,4-d]pyrimidine,4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), and rauwolscine on the phosphorylation of endothelial nitric oxide synthase (eNOS), caveolin-1, and Src kinase was examined in the human umbilical vein endothelial cells. L-NAME, MβCD, and LE (1%, standardized mean difference (SMD): 2.517) increased the DMT-induced contraction in the endothelium-intact rat aorta. LE (1%) decreased the DMT (10−6 M) concentration (SMD: −6.795) and DMT-induced cGMP formation (SMD: −2.132). LE (1%) reversed the DMT-induced eNOS (Ser1177 and Thr496) phosphorylation. PP2 inhibited caveolin-1 and eNOS phosphorylation induced by DMT. DMT increased the Src kinase phosphorylation. Thus, LE (1%) enhanced the DMT-induced contraction by inhibition of NO synthesis, which may be caused by the decreased DMT concentration. DMT-induced NO synthesis may be caused by the increased eNOS (Ser1177) phosphorylation and decreased eNOS (Thr495) phosphorylation potentially mediated by Src kinase-induced caveolin-1 phosphorylation.


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