on October 6, 2005
Published online before print October 6, 2005, doi: 10.1161/01.ATV.0000189298.62240.5d
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Submitted on April 7, 2005
Accepted on September 13, 2005
Upregulation of Proinflammatory Proteins Through NF-
B Pathway by Shed Membrane Microparticles Results in Vascular Hyporeactivity
Angela Tesse ;
From Pharmacologie et Physico-Chimie des Interactions Cellulaires et Moléculaires (A.T., K.C., C.M., F.M., R.A.), UMR CNRS 7034, Illkirch, France; Dipartimento di Farmacologia e Fisiologia Umana (A.T., D.M.-C.), Università di Bari, Italia; Institut d’Hématologie et d’Immunologie (M.C.M., B.H., J.-M.F.), Université Louis Pasteur, Strasbourg, France & Unité 143 INSERM, Le Kremlin-Bicêtre, France
* To whom correspondence should be addressed. E-mail: ramaroson.andriantsitohaina{at}pharma.u-strasbg.fr.
Objective--Microparticles are membrane vesicles with procoagulant and proinflammatory properties released during cell activation, including apoptosis. The present study was designed in dissecting the effects evoked by microparticles on vascular reactivity.
Methods and Results--Microparticles from either apoptotic T lymphocytic cells or from plasma of diabetic patients with vascular complications induced vascular hyporeactivity in response to vasoconstrictor agents in mouse aorta. Hyporeactivity was reversed by nitric oxide (NO) synthase plus cyclooxygenase-2 inhibitors, and associated with an increased production of vasodilatory products such as NO and prostacyclin. Microparticles induced an upregulation of proinflammatory protein expressions, inducible NO-synthase and cyclooxygenase-2, mainly in the medial layer of the vessels as evidenced by immunochemical staining. In addition, microparticles evoke NF-
B activation probably through the interaction with the Fas/Fas Ligand pathway. Finally, in vivo treatment of mice with lymphocyte-derived MPs induces vascular hyporeactivity, which was reversed by the combination of NO and COX-2 inhibitors.
Conclusion--These data provide a rationale to explain the paracrine role of microparticles as vectors of transcellular exchange of message in promoting vascular dysfunction during inflammatory diseases.
Key words: Fas/Fas Ligand • microvesicles • proinflammatory proteins • vascular dysfunction • vasoactivity
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