Arterial Response to Gentle Injury is Modulated by Anti-Pdgf Immunoglobulin in the Nude Rat

Ferns, G.; Raines, EW; Reidy, M. A.; Ross, Russell

doi:10.1042/cs083013pa

Cited by 2 publications

(1 citation statement)

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“…In contrast to the extensive literature on the role of cellular and humoral immunity in progressive atherosclerosis, the effects of inflammatory cells in injury-induced neointimal hyperplasia have received considerably less attention. Studies in the rat model, both with athymic nude rats and T-lymphocytes-depleted rats yielded opposite results regarding the role of T lymphocytes in neointimal hyperplasia [48,49]. Additionally, although interferon-γ (IFNγ) secreted by activated T lymphocytes inhibits smooth muscle cell proliferation in vitro, and IFN-γ also limits arterial proliferative lesions in response to arterial injury in vivo [50], cyclosporine suppression of lymphocyte activation had no effect on injury-induced neointimal proliferation in cholesterol-clamped rabbits [51].…”

Section: Role Of T and B Lymphocytes In Vascular Response To Injurymentioning

confidence: 97%

Intimal Hyperplasia in Murine Models

Hui¹

2008

CDT

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The most commonly used procedures to induce arterial injury in mice are carotid artery ligation with cessation of blood flow and mechanically-induced denudation of endothelium in the carotid or the femoral arteries. Both procedures result in neointimal hyperplasia after two to three weeks. A survey of various inbred strains of mice shows that strain-specific differences in susceptibility to injury-induced neointimal hyperplasia are different than those for susceptibility to diet-induced atherosclerosis, with strains identified as susceptible to both neointimal hyperplasia and atherosclerosis, resistant to both, susceptible to atherosclerosis but resistant to neointimal hyperplasia, or resistant to atherosclerosis but susceptible to neointimal hyperplasia. Inflammatory cells such as T and B lymphocytes, which are contributory to atherosclerosis, are protective against injury-induced neointimal hyperplasia. In contrast, the infiltration of monocytes into the site of injury and their differentiation to macrophages favor neointimal hyperplasia similar to their pathogenic role in atherosclerosis. The regulatory role of lymphocytes and macrophages in neointimal hyperplasia is related to the production of cytokines such as interferon-gamma and tumor necrosis factor-alpha, respectively. Interestingly, inducible nitric oxide synthase (iNOS) activity appears to inhibit neointimal hyperplasia in the endothelial denudation model but contributes to neointimal hyperplasia when arterial injury is induced by periadventitial cuff placement. The difference appears to be due to the time required for endothelial recovery and the participation of inflammatory cells. Thus, although arterial injury-induced neointimal hyperplasia results in similar vascular occlusion as progressive atherosclerosis, the pathology and mechanism of the two disease processes are quite different.

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