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352 results on '"Faraci, F M"'

7. Bioinformatic Analysis of Gene Sets Regulated by Ligand-Activated and Dominant-Negative Peroxisome Proliferator-Activated Receptor in Mouse Aorta

Author

Beyer, A. M., Maeda, N., Casavant, T. L., Liu, X., Sigmund, C. D., Faraci, F. M., de Lange, W. J., Keen, H. L., and Halabi, C. M.

Abstract

Drugs that activate PPARγ improve glucose sensitivity and lower blood pressure, whereas dominant negative mutations in PPARγ cause severe insulin resistance and hypertension. We hypothesize that these PPARγ mutants regulate target genes opposite to that of ligand-mediated activation and tested this hypothesis on a genome-wide scale.

Published
2010
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8. Interference With PPAR Signaling Causes Cerebral Vascular Dysfunction, Hypertrophy, and Remodeling

Author

Sigmund, C. D., Faraci, F. M., Gerhold, T. D., Ghoneim, S. M., Beyer, A. M., Lynch, C. M., Maeda, N., Keen, H. L., de Lange, W. J., Tsai, Y.-S., Modrick, M. L., Halabi, C. M., and Baumbach, G. L.

Abstract

The transcription factor PPARgamma is expressed in endothelium and vascular muscle where it may exert antiinflammatory and antioxidant effects. We tested the hypothesis that PPARgamma plays a protective role in the vasculature by examining vascular structure and function in heterozygous knockin mice expressing the P465L dominant negative mutation in PPARgamma (L/+). In L/+ aorta, responses to the endothelium-dependent agonist acetylcholine (ACh) were not affected, but there was an increase in contraction to serotonin, PGF(2alpha), and endothelin-1. In cerebral blood vessels both in vitro and in vivo, ACh produced dilation that was markedly impaired in L/+ mice. Superoxide levels were elevated in cerebral arterioles from L/+ mice and responses to ACh were restored to normal with a scavenger of superoxide. Diameter of maximally dilated cerebral arterioles was less, whereas wall thickness and cross-sectional area was greater in L/+ mice, indicating cerebral arterioles underwent hypertrophy and remodeling. Thus, interference with PPARgamma signaling produces endothelial dysfunction via a mechanism involving oxidative stress and causes vascular hypertrophy and inward remodeling. These findings indicate that PPARgamma has vascular effects which are particularly profound in the cerebral circulation and provide genetic evidence that PPARgamma plays a critical role in protecting blood vessels.

Published
2008
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9. Vascular dysfunction in monkeys with diet-induced hyperhomocyst(e)inemia

Author

Lentz, S R, Sobey, C G, Piegors, D J, Bhopatkar, M Y, Faraci, F M, Malinow, M R, and Heistad, D D

Subjects
Research Article
Abstract

Elevated plasma homocyst(e)ine may predispose to complications of vascular disease. Homocysteine alters vasomotor regulatory and anticoagulant properties of cultured vascular endothelial cells, but little is known about effects of hyperhomocyst(e)inemia on vascular function in vivo. We tested the hypothesis that diet-induced moderate hyperhomocyst(e)inemia is associated with vascular dysfunction in cynomolgus monkeys. Plasma homocyst(e)ine increased from 4.O +/- O.2 microM when monkeys were fed normal diet to 10.6 +/- 2.6 microM when they were fed modified diet (mean +/- SE; P = 0.02). Vasomotor responses were assessed in vivo by quantitative angiography and Doppler measurement of blood flow velocity. In response to activation of platelets by intraarterial infusion of collagen, blood flow to the leg decreased by 42 +/- 9% in monkeys fed modified diet, compared with 14 +/- 11% in monkeys fed normal diet (P = 0.008), Responses of resistance vessels to the endothelium-dependent vasodilators acetylcholine and ADP were markedly impaired in hyperhomocyst(e)inemic monkeys, which suggests that increased vasoconstriction in response to collagen may be caused by decreased vasodilator responsiveness to platelet-generated ADP. Relaxation to acetylcholine and, to a lesser extent, nitroprusside, was impaired ex vivo in carotid arteries from monkeys fed modified diet. Thrombomodulin anticoagulant activity in aorta decreased by 34 +/- 15% in hyperhomocyst(e)inemic monkeys (P = 0.03). We conclude that diet-induced moderate hyperhomocyst(e)inemia is associated with altered vascular function.

Published
1996

11. M 1 -M 5 Muscarinic Receptor Knockout Mice as Novel Tools to Study the Physiological Roles of the Muscarinic Cholinergic System

Author

Yamada, M., primary, Wess, J., additional, Duttaroy, A., additional, Zhang, W., additional, Gomeza, J., additional, Cui, Y., additional, Miyakawa, T., additional, Bymaster, F. P., additional, McKinzie, L., additional, Felder, C. C., additional, Lamping, K. G., additional, Faraci, F. M., additional, and Deng, C., additional

Published
2003
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13. M 1 -M 5 Muscarinic Receptor Knockout Mice as Novel Tools to Study the Physiological Roles of the Muscarinic Cholinergic System

Author

Wess, J., primary, Duttaroy, A., additional, Zhang, W., additional, Gomeza, J., additional, Cui, Y., additional, Miyakawa, T., additional, Bymaster, F. P., additional, Mckinzie, L., additional, Felder, C. C., additional, Lamping, K. G., additional, Faraci, F. M., additional, Deng, C., additional, and Yamada, M., additional

Published
2003
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