Model of Arterial Injury by Balloon De-Endothelialization: Reappraisal, Improvement, and Application to Measurement of Endothelial Growth

Insull, William; Chidi, Christopher C.

doi:10.1007/978-3-642-95308-8_54

Cited by 1 publication

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“…Incubations were carried out in 2 ml of Krebs-Ringer bicarbonate buffer at 37° for specified times under a 95% air-5% CO 2 atmosphere. The tracers, added in the buffer, were [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C] acetate (57 mCi/mmole), [2][3][4][5][6][7][8][9][10][11][12][13][14] C] mevalonate (22 mCi/ mmole), [4, H(N)] L-leucine (5 Ci/mmole), and methyl[ 3 H] thymidine (2 Ci/mmole). Incubations were carried out with two labeled substrates simultaneously, paired as: acetate + leucine, 14 X 10 6 and 12 X 10 6 cpm, respectively, and mevalonate + thymidine, 7 X 10" and 16 X 10 8 cpm, respectively.…”

Section: Incubationsmentioning

confidence: 99%

In vitro synthesis of DNA, protein, and lipids by the de-endothelialized rabbit aorta.

Rosenfeld¹,

Drouet²,

Cintron³

et al. 1981

Arteriosclerosis

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The uptake of [3H] leucine, [3H] thymidine, [14C] acetate, and [14C] mevalonic acid by aortic intima media from normal rabbits and from rabbits subjected to a single balloon de-endothelialization as measured 6 days, 2 months, and 4 months after treatment to determine how long the injury-induced stimulation of incorporation of these precursors into tissue components persisted beyond 6 days, the time of maximum proliferative response of the smooth muscle cells. We found that [3H] thymidine incorporation (indicative of DNA synthesis and the potential for cell proliferation) was about three times greater in the de-endothelialized tissue than in the control tissue 6 days after vessel injury, but that by 2 months it was normal. Labeled leucine incorporation into the de-endothelialized tissue (a measure of protein synthesis) was eight times higher than normal at the time of maximum proliferative response to injury (6 days), and showed no decrease under identical incubation conditions in ballooned tissue obtained 2 months after de-endothelialization; it continued high at 4 months. Both [14C] acetate and [14C] mevalonate uptake into lipids by the aortic tissue were enhanced by the injury; this increased incorporation was still evident at 4 months. Thus, de-endothelialization of the aorta triggers a vessel wall response characterized by augmented protein synthesis and lipogenesis, which persists at least 4 months after injury and at least 2 months after DNA synthesis has normalized.

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