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Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury

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Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury. / Cole, Marsha P; Rudolph, Tanja K; Khoo, Nicholas K H; Motanya, Uche N; Golin-Bisello, Franca; Wertz, Jeffrey W; Schopfer, Francisco J; Rudolph, Volker; Woodcock, Steven R; Bolisetty, Subhashini; Ali, Muhammad S; Zhang, Jifeng; Chen, Y Eugene; Agarwal, Anupam; Freeman, Bruce A; Bauer, Philip M.

In: CIRC RES, Vol. 105, No. 10, 06.11.2009, p. 965-972.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Cole, MP, Rudolph, TK, Khoo, NKH, Motanya, UN, Golin-Bisello, F, Wertz, JW, Schopfer, FJ, Rudolph, V, Woodcock, SR, Bolisetty, S, Ali, MS, Zhang, J, Chen, YE, Agarwal, A, Freeman, BA & Bauer, PM 2009, 'Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury', CIRC RES, vol. 105, no. 10, pp. 965-972. https://doi.org/10.1161/CIRCRESAHA.109.199075

APA

Cole, M. P., Rudolph, T. K., Khoo, N. K. H., Motanya, U. N., Golin-Bisello, F., Wertz, J. W., Schopfer, F. J., Rudolph, V., Woodcock, S. R., Bolisetty, S., Ali, M. S., Zhang, J., Chen, Y. E., Agarwal, A., Freeman, B. A., & Bauer, P. M. (2009). Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury. CIRC RES, 105(10), 965-972. https://doi.org/10.1161/CIRCRESAHA.109.199075

Vancouver

Cole MP, Rudolph TK, Khoo NKH, Motanya UN, Golin-Bisello F, Wertz JW et al. Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury. CIRC RES. 2009 Nov 6;105(10):965-972. https://doi.org/10.1161/CIRCRESAHA.109.199075

Bibtex

@article{4fc3e0f76fec42b486afa91ae347a601,
title = "Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury",
abstract = "RATIONALE: Fatty acid nitroalkenes are endogenously generated electrophilic byproducts of nitric oxide and nitrite-dependent oxidative inflammatory reactions. Existing evidence indicates nitroalkenes support posttranslational protein modifications and transcriptional activation that promote the resolution of inflammation.OBJECTIVE: The aim of this study was to assess whether in vivo administration of a synthetic nitroalkene could elicit antiinflammatory actions in vivo using a murine model of vascular injury.METHODS AND RESULTS: The in vivo administration (21 days) of nitro-oleic acid (OA-NO(2)) inhibited neointimal hyperplasia after wire injury of the femoral artery in a murine model (OA-NO(2) treatment resulted in reduced intimal area and intima to media ratio versus vehicle- or oleic acid (OA)-treated animals,P<0.0001). Increased heme oxygenase (HO)-1 expression accounted for much of the vascular protection induced by OA-NO(2) in both cultured aortic smooth muscle cells and in vivo. Inhibition of HO by Sn(IV)-protoporphyrin or HO-1 small interfering RNA reversed OA-NO(2)-induced inhibition of platelet-derived growth factor-stimulated rat aortic smooth muscle cell migration. The upregulation of HO-1 expression also accounted for the antistenotic actions of OA-NO(2) in vivo, because inhibition of neointimal hyperplasia following femoral artery injury was abolished in HO-1(-/-) mice (OA-NO(2)-treated wild-type versus HO-1(-/-) mice, P=0.016).CONCLUSIONS: In summary, electrophilic nitro-fatty acids induce salutary gene expression and cell functional responses that are manifested by a clinically significant outcome, inhibition of neointimal hyperplasia induced by arterial injury.",
keywords = "Animals, Cell Movement/drug effects, Femoral Artery/enzymology, Gene Expression Regulation, Enzymologic/drug effects, Heme Oxygenase (Decyclizing)/biosynthesis, Inflammation/metabolism, Mice, Mice, Knockout, Nitric Oxide/metabolism, Nitro Compounds/metabolism, Oleic Acids/metabolism, Oxidation-Reduction/drug effects, Platelet-Derived Growth Factor/pharmacology, Rats, Tunica Intima/enzymology, Up-Regulation/drug effects",
author = "Cole, {Marsha P} and Rudolph, {Tanja K} and Khoo, {Nicholas K H} and Motanya, {Uche N} and Franca Golin-Bisello and Wertz, {Jeffrey W} and Schopfer, {Francisco J} and Volker Rudolph and Woodcock, {Steven R} and Subhashini Bolisetty and Ali, {Muhammad S} and Jifeng Zhang and Chen, {Y Eugene} and Anupam Agarwal and Freeman, {Bruce A} and Bauer, {Philip M}",
year = "2009",
month = nov,
day = "6",
doi = "10.1161/CIRCRESAHA.109.199075",
language = "English",
volume = "105",
pages = "965--972",
journal = "CIRC RES",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "10",

}

RIS

TY - JOUR

T1 - Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury

AU - Cole, Marsha P

AU - Rudolph, Tanja K

AU - Khoo, Nicholas K H

AU - Motanya, Uche N

AU - Golin-Bisello, Franca

AU - Wertz, Jeffrey W

AU - Schopfer, Francisco J

AU - Rudolph, Volker

AU - Woodcock, Steven R

AU - Bolisetty, Subhashini

AU - Ali, Muhammad S

AU - Zhang, Jifeng

AU - Chen, Y Eugene

AU - Agarwal, Anupam

AU - Freeman, Bruce A

AU - Bauer, Philip M

PY - 2009/11/6

Y1 - 2009/11/6

N2 - RATIONALE: Fatty acid nitroalkenes are endogenously generated electrophilic byproducts of nitric oxide and nitrite-dependent oxidative inflammatory reactions. Existing evidence indicates nitroalkenes support posttranslational protein modifications and transcriptional activation that promote the resolution of inflammation.OBJECTIVE: The aim of this study was to assess whether in vivo administration of a synthetic nitroalkene could elicit antiinflammatory actions in vivo using a murine model of vascular injury.METHODS AND RESULTS: The in vivo administration (21 days) of nitro-oleic acid (OA-NO(2)) inhibited neointimal hyperplasia after wire injury of the femoral artery in a murine model (OA-NO(2) treatment resulted in reduced intimal area and intima to media ratio versus vehicle- or oleic acid (OA)-treated animals,P<0.0001). Increased heme oxygenase (HO)-1 expression accounted for much of the vascular protection induced by OA-NO(2) in both cultured aortic smooth muscle cells and in vivo. Inhibition of HO by Sn(IV)-protoporphyrin or HO-1 small interfering RNA reversed OA-NO(2)-induced inhibition of platelet-derived growth factor-stimulated rat aortic smooth muscle cell migration. The upregulation of HO-1 expression also accounted for the antistenotic actions of OA-NO(2) in vivo, because inhibition of neointimal hyperplasia following femoral artery injury was abolished in HO-1(-/-) mice (OA-NO(2)-treated wild-type versus HO-1(-/-) mice, P=0.016).CONCLUSIONS: In summary, electrophilic nitro-fatty acids induce salutary gene expression and cell functional responses that are manifested by a clinically significant outcome, inhibition of neointimal hyperplasia induced by arterial injury.

AB - RATIONALE: Fatty acid nitroalkenes are endogenously generated electrophilic byproducts of nitric oxide and nitrite-dependent oxidative inflammatory reactions. Existing evidence indicates nitroalkenes support posttranslational protein modifications and transcriptional activation that promote the resolution of inflammation.OBJECTIVE: The aim of this study was to assess whether in vivo administration of a synthetic nitroalkene could elicit antiinflammatory actions in vivo using a murine model of vascular injury.METHODS AND RESULTS: The in vivo administration (21 days) of nitro-oleic acid (OA-NO(2)) inhibited neointimal hyperplasia after wire injury of the femoral artery in a murine model (OA-NO(2) treatment resulted in reduced intimal area and intima to media ratio versus vehicle- or oleic acid (OA)-treated animals,P<0.0001). Increased heme oxygenase (HO)-1 expression accounted for much of the vascular protection induced by OA-NO(2) in both cultured aortic smooth muscle cells and in vivo. Inhibition of HO by Sn(IV)-protoporphyrin or HO-1 small interfering RNA reversed OA-NO(2)-induced inhibition of platelet-derived growth factor-stimulated rat aortic smooth muscle cell migration. The upregulation of HO-1 expression also accounted for the antistenotic actions of OA-NO(2) in vivo, because inhibition of neointimal hyperplasia following femoral artery injury was abolished in HO-1(-/-) mice (OA-NO(2)-treated wild-type versus HO-1(-/-) mice, P=0.016).CONCLUSIONS: In summary, electrophilic nitro-fatty acids induce salutary gene expression and cell functional responses that are manifested by a clinically significant outcome, inhibition of neointimal hyperplasia induced by arterial injury.

KW - Animals

KW - Cell Movement/drug effects

KW - Femoral Artery/enzymology

KW - Gene Expression Regulation, Enzymologic/drug effects

KW - Heme Oxygenase (Decyclizing)/biosynthesis

KW - Inflammation/metabolism

KW - Mice

KW - Mice, Knockout

KW - Nitric Oxide/metabolism

KW - Nitro Compounds/metabolism

KW - Oleic Acids/metabolism

KW - Oxidation-Reduction/drug effects

KW - Platelet-Derived Growth Factor/pharmacology

KW - Rats

KW - Tunica Intima/enzymology

KW - Up-Regulation/drug effects

U2 - 10.1161/CIRCRESAHA.109.199075

DO - 10.1161/CIRCRESAHA.109.199075

M3 - SCORING: Journal article

C2 - 19797175

VL - 105

SP - 965

EP - 972

JO - CIRC RES

JF - CIRC RES

SN - 0009-7330

IS - 10

ER -