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MeSH Review

Tunica Intima

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Disease relevance of Tunica Intima


High impact information on Tunica Intima


Chemical compound and disease context of Tunica Intima


Biological context of Tunica Intima


Anatomical context of Tunica Intima


Associations of Tunica Intima with chemical compounds

  • Heparin treatment inhibited intimal thickening and decreased the elastin content in the ECM domain in the upper and lower arterial intima [20].
  • Two other acid cysteine proteases, cathepsins S and K, which have been shown to be present in the arterial intima, were also capable of degrading apoB-100, albeit less efficiently [21].
  • These results suggest that the chemotactic gradient by IL-8 is established between arterial intima and media in response to high glucose levels in diabetic patients, and that it may be one of the key factors for SMC migration to the intima leading to diabetic macroangiopathy [22].
  • The tunica intima of l-NAME + captopril-treated rats was moderately thickened (60% increase in comparison with that of controls and 65% thinner as compared with L-NAME-treated rats) [23].
  • In the scoparone treated rabbits, the proportion of the aortic surface area covered with macroscopic plaques was 30%, and the thickness of the tunica intima 17%, of that of the non-scoparone treated hyperlipidaemic diabetic rabbits [24].

Gene context of Tunica Intima

  • CONCLUSIONS: Our study does not support the view that MCP-1 plasma levels and CCR-2 gene expression in circulating monocytes are directly responsible for the monocyte recruitment into the arterial intima in patients with severe asymptomatic hypercholesterolaemia [25].
  • These qualitative and quantitative features were the consequence of TIMP-1 infiltration from plasma to arterial intima, as immunohistochemical analyses revealed an abundance of TIMP-1 specifically in lesions of rAd.RSV [26].
  • HIF-1alpha protein in control was poorly positive (0.05 +/- 0.01), but was up-regulated in pulmonary arterial tunica intima of all hypoxic rats [27].
  • Thus, enhanced expression of TGF-beta, MMP-2, and ICAM-1 in the thickened vascular intima of aged rats may in part be produced by exaggerated SMC responses to cytokines and may have potential roles in intimal remodeling with aging [28].
  • The normal antithrombotic condition of the vascular intima probably results from lack of tissue factor activity and the presence of significant antithrombotic components comprising, among others, antithrombin III and the protein C-protein S system [29].

Analytical, diagnostic and therapeutic context of Tunica Intima

  • Analysis of EC-SOD by immunohistochemistry indicates an even distribution in the vessel wall, including large amounts of the arterial intima [30].
  • Following injection of 125I-labelled autologous P-LDL prior to reconstructive arterial surgery, polyacrylamide and agarose gel electrophoresis of A-LDL extracted from arterial intima showed that the A-LDL and its apolipoprotein B moiety were derived from P-LDL; the electrophoretic mobility of the product A-LDL was greater than that of native P-LDL [31].
  • The viability of an epigastric flap transferred to a recipient site with thickened arterial intima was significantly improved in a rabbit model by a seven-day continuous local intraarterial infusion of heparin at 10 U/kg/hr and urokinase at 100 IU/kg/hr, compared with control or intravenous infusion [32].
  • Epidemiological studies indicate that increased levels of fibrinogen and clotting activity are associated with accelerated atherosclerosis, and although blood fibrinolytic activity has given inconsistent results, in arterial intima both fibrinolytic activity and plasminogen concentration are decreased in cardiovascular disease [33].


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  17. Recognition of oxidized low density lipoprotein by the scavenger receptor of macrophages results from derivatization of apolipoprotein B by products of fatty acid peroxidation. Steinbrecher, U.P., Lougheed, M., Kwan, W.C., Dirks, M. J. Biol. Chem. (1989) [Pubmed]
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  21. Cysteine protease cathepsin F is expressed in human atherosclerotic lesions, is secreted by cultured macrophages, and modifies low density lipoprotein particles in vitro. Oörni, K., Sneck, M., Brömme, D., Pentikäinen, M.O., Lindstedt, K.A., Mäyränpää, M., Aitio, H., Kovanen, P.T. J. Biol. Chem. (2004) [Pubmed]
  22. High glucose enhances the gene expression of interleukin-8 in human endothelial cells, but not in smooth muscle cells: possible role of interleukin-8 in diabetic macroangiopathy. Temaru, R., Urakaze, M., Satou, A., Yamazaki, K., Nakamura, N., Kobayashi, M. Diabetologia (1997) [Pubmed]
  23. Chronic inhibition of NO synthesis per se promotes structural intimal remodeling of the rat aorta. Rossi, M.A., Colombini-Netto, M. J. Hypertens. (2001) [Pubmed]
  24. Morphological evidence for the antiatherogenic effect of scoparone in hyperlipidaemic diabetic rabbits. Chen, Y.L., Huang, H.C., Weng, Y.I., Yu, Y.J., Lee, Y.T. Cardiovasc. Res. (1994) [Pubmed]
  25. Monocyte chemoattractant protein-1 and CC-chemokine receptor-2 in severe hypercholesterolaemia. Blomqvist, H.M., Olsson, A.G. Scand. J. Clin. Lab. Invest. (2003) [Pubmed]
  26. Adenovirus-mediated overexpression of tissue inhibitor of metalloproteinase-1 reduces atherosclerotic lesions in apolipoprotein E-deficient mice. Rouis, M., Adamy, C., Duverger, N., Lesnik, P., Horellou, P., Moreau, M., Emmanuel, F., Caillaud, J.M., Laplaud, P.M., Dachet, C., Chapman, M.J. Circulation (1999) [Pubmed]
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  28. Increased expression of matrix metalloproteinase-2 in the thickened intima of aged rats. Li, Z., Froehlich, J., Galis, Z.S., Lakatta, E.G. Hypertension (1999) [Pubmed]
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  30. The interstitium of the human arterial wall contains very large amounts of extracellular superoxide dismutase. Strålin, P., Karlsson, K., Johansson, B.O., Marklund, S.L. Arterioscler. Thromb. Vasc. Biol. (1995) [Pubmed]
  31. Modified plasma-derived lipoproteins in human atherosclerotic plaques. Shaikh, M., Martini, S., Quiney, J.R., Baskerville, P., La Ville, A.E., Browse, N.L., Duffield, R., Turner, P.R., Lewis, B. Atherosclerosis (1988) [Pubmed]
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  33. Fibrinogen, fibrin and fibrin degradation products in relation to atherosclerosis. Smith, E.B. Clinics in haematology. (1986) [Pubmed]
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