Time course of increased collateral arterial and venous endothelial cell turnover after renal artery stenosis in the rat.

Ilich, Nenad; Hollenberg, Norman K.; Williams, Deborah H.; Abrams, Herbert L.

doi:10.1161/01.res.45.5.579

Cited by 30 publications

(16 citation statements)

References 8 publications

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“…92 Even a relatively low percentage of endothelial cell proliferation observed in response to arterial occlusion or exogenous growth factors may therefore represent considerable enhancement of endothelial cell proliferative activity and, when considered in relation to a denominator of thousands of endothelial cells, is clearly sufficient to provide the basis for new blood vessel formation. Second, endothelial cell proliferation that contributes to naturally occurring collateral development in the setting of vascular occlusion varies from 2.6% to 3.5% in the canine coronary 90,93 and from 5% to 6% in the rodent renal vasculature 94 and is Ͻ1% in swine coronary arteries. 95 The contrasting rates of endothelial cell proliferation between the canine and swine coronary circulations are in parallel with the relative propensity for natural collateral artery development in these 2 species.…”

Section: Mechanisms Of Angiogenesismentioning

confidence: 99%

Estrogen and Angiogenesis

Losordo

Isner

2001

ATVB

304

194

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Abstract-Multiple lines of evidence suggest that estrogen directly modulates angiogenesis via effects on endothelial cells.Under physiological conditions, angiogenesis is routinely observed in the uterus in association with fluctuations in the levels of circulating estradiol and other sex steroids. In pathological circumstances, such as breast cancer, a clear association between estrogen, estrogen receptor expression by endothelial cells, angiogenic activity, and/or tumor invasiveness has been made. Studies performed in our laboratory have revealed that estradiol accelerates functional endothelial recovery after arterial injury. Despite these consistent observations, the mechanisms by which estrogen regulates angiogenesis under physiological and pathological circumstances have not been defined. Key Words: estrogen Ⅲ angiogenesis Ⅲ vasculogenesis Ⅲ endothelium Ⅲ endothelial progenitor cells I n adult organisms, angiogenesis is virtually absent under normal conditions, except in the female reproductive tract. This observation suggests the potential for sex steroids to influence neovascularization. Several other associations, including the predilection of certain diseases (such as Takayasu's arteritis and lupus, both of which involve endothelial cell proliferation) for premenopausal females, also imply the potential role of estrogen in angiogenesis. 1,2 The role of estradiol in uterine angiogenesis, mediated by at least 1 of the estrogen receptors, has been further suggested by findings in the estrogen receptor-␣ knockout mouse, in which angiogenesis is impaired, 3 and by the demonstration that estrogen receptor antagonists can inhibit angiogenesis. 4 The positive correlation between estrogen receptor expression, angiogenic activity, and breast tumor invasiveness also supports the angiogenic effect of estrogen mediated by the estrogen receptor(s). [5][6][7][8] Finally, some reports suggest that the antitumor effect of tamoxifen may in fact relate to an antiangiogenic action of this estrogen receptor agonist/antagonist. 9 Several additional lines of experimental evidence suggest that estrogen and other sex steroids play important roles in physiological and pathological angiogenesis. One of the first observations suggesting a hormonal influence on angiogenesis was an inhibitory effect on tumor vascularization by medroxyprogesterone. 10 Subsequent studies have indicated that the mechanism of this inhibition may relate to the regulation of thrombospondin-1, an angiogenesis inhibitor, by this hormone. 11 Angiogenesis has been noted to be a prognostic marker in breast cancer, 12 and inhibition of angiogenesis in these tumors has been effected by antiestrogens. 4 In addition, the estrogen metabolite 2-methoxyestradiol has been shown to be a potent antiangiogenic agent 13 mediated by actions on cytoskeletal structure 14 and by increasing endothelial cell apoptosis. 15,16 Vascular Endothelial Cell Proliferation and Migration Are Enhanced by EstradiolEstradiol induces endothelial proliferation and migration 17 mediated by t...

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Section: Mechanisms Of Angiogenesismentioning

confidence: 99%

Estrogen and Angiogenesis

Losordo

Isner

2001

ATVB

304

194

View full text Add to dashboard Cite

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“…As previously, the nucleus was considered to be endothelial when it was unequivocally at the surface of the lumen, with no evidence of cytoplasm medially. Because of the large number of rats and sections examined, and the convenience of the method, 1 we employed an ordinal assessment system, which ranged from 0 to 3 + . Zero (0) indicated no positive endothelial cells and 1 + indicated an occasional tritiated thymidine-labelled endothelial cell, 2 + an unequivocal increase over the low, spontaneous normal turnover rate, and 3 + an unequivocal, striking increase in endothelial cell turnover.…”

Section: Methodsmentioning

confidence: 99%

“…Indeed, as pointed out in our earlier studies, 1 ' " the quantitative assessment of total collateral vascular mass is difficult. It was evident in the histologic sections and on gross examination, however, that there was both an increase in the number and size of arterial vessels supplying the kidney through various arteries following renal artery stenosis.…”

mentioning

confidence: 86%

“…W E have documented a hyperplastic response of the endothelium and smooth muscle elements of growing arterial collateral vessels in the rat 1 and dog 2 following renal artery stenosis. Because biophysical factors are thought to influence vascular proliferative responses, 3 and hypertension (a common feature in the models in our earlier studies) is known to promote an increase in arterial cell turnover, 4 we initiated a systematic assessment of the role of hypertension in the hyperplastic response.…”

mentioning

confidence: 99%

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Increase in collateral arterial endothelial cell proliferation induced by captopril after renal artery stenosis in the rat.

Odori¹,

Paskins-Hurlburt²,

Hollenberg³

1983

Hypertension

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SUMMARY Studies to assess the role of blood pressure rise in the growth of the collateral arterial supply following renal artery stenosis were performed in 70 rats. Assessment of the proliferative response was made by coded reading of endothelial cell turnover following tritiated thymidine administration, 5 days after renal artery stenosis. Stenosis induced the anticipated brisk increase in endothelial cell turnover in arterial collaterals and in the ipsilateral renal vein, and ureteric epithelium. Blood pressure elevation did not appear to play the dominant role, as the proliferative response did not parallel blood pressure changes; moreover, neither bilateral renal artery stenosis, designed to enhance the hypertension, nor hydralazine administration, to reduce the blood pressure, influenced endothelial cell turnover. A contribution of elevated blood pressure to the vasoproliferative response, however, was not ruled out definitively in this study. Captopril, also administered to assess the same question, resulted in an enhanced endothelial cell proliferative response, both in frequency and in degree, an observation that became the central thrust of our study. The mechanism by which converting enzyme inhibitor modified endothelial cell turnover is not clear, but may well provide insight into the responsible factors. (Hypertension 5: 307-311, 1983) KEY WORDS • tritiated thymidine • hypertension • anglotensin converting enzyme inhibition W E have documented a hyperplastic response of the endothelium and smooth muscle elements of growing arterial collateral vessels in the rat 1 and dog 2 following renal artery stenosis. Because biophysical factors are thought to influence vascular proliferative responses, 3 and hypertension (a common feature in the models in our earlier studies) is known to promote an increase in arterial cell turnover, 4 we initiated a systematic assessment of the role of hypertension in the hyperplastic response. Maneuvers were designed either to promote increased hypertension, or to prevent the hypertension with antihypertensive drugs. A surprising finding that the converting enzyme inhibitor, captopril, increased the vascular proliferative response rather than reduced it represents the primary thrust of this report.

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“…[1][2][3] Turnover of the endothelium in adults is relatively low, but proliferation can be triggered by inflammation, matrix disruption, or ischemia. 4 Our appreciation of this cell lining is acutely apparent following percutaneous coronary intervention, where delayed reendothelialization can cause thrombosis and exacerbate restenosis. 5 An even greater challenge is the aging patient with eroding endothelial function.…”

mentioning

confidence: 99%