Jo De Mey

Publications (131) View all

• Article: Prenatal stress changes rat arterial adrenergic reactivity in a regionally selective manner.

  Marijke Sanders, Gregorio Fazzi, Ger Janssen, Carlos Blanco, Jo De Mey
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  ABSTRACT: A suboptimal fetal environment has been linked to increased risk of cardiovascular disease in adulthood. We investigated whether intrauterine stress (IUS) alters the development of adrenergic reactivity in different types of rat arteries. Intrauterine stress was induced by ligation of the uterine arteries at day 13 of pregnancy in Wistar rats. First-order mesenteric, renal, femoral and saphenous arteries of the 21-day-old male offspring were studied in a myograph. IUS in the rat changes arterial adrenergic reactivity in a regionally selective manner. Adrenoceptor-mediated responses are altered in the renal artery. Maximal contractile responses to phenylephrine were increased, while sensitivity to the alpha(1)-adrenoceptor agonist was decreased. Intrauterine stress significantly reduced contractile responses to norepinephrine and enhanced relaxing responses to isoproterenol in the renal artery. Adrenergic responses were not modified in mesenteric, femoral and saphenous arteries. In the kidneys the densities of [(3)H]prazosin binding sites, periarterial adrenergic nerves and of the glomeruli were not altered after intrauterine stress at day 13 of gestation. The observed regionally selective alterations in arterial reactivity might link a suboptimal fetal environment to the development of cardiovascular disease in the adult.
  European Journal of Pharmacology 04/2004; 488(1-3):147-55. · 2.52 Impact Factor
• Article: The inhibitory effect of the flavonoid galangin on urinary bladder smooth muscle contractility is mediated in part by modulation of Ca2+ release from intracellular stores.

  Miriam Dambros, Marjanka van Deutekom, Rik de Jongh, Gommert A van Koeveringe, Jo G De Mey, Philip van Kerrebroeck
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  ABSTRACT: The present study was designed to examine the effect of the flavonoid galangin on the muscarinic receptor mediating a carbachol-induced contraction and to investigate the effect of the flavonoid on Ca (2+) release from intracellular stores in the urinary bladder of the pig. Galangin (10(-7) -10(-4)M) produced a concentration-dependent inhibition of the contractile responses to electrical field stimulation (EFS) and carbachol (10(-5)M). Galangin (3 x 10(-5)M) reduced muscle contractions evoked by carbachol (10(-5)M) in calcium-containing solution as well as contractions evoked by carbachol and caffeine (2 x 10(-2)M) in Ca(2+)-free solutions significantly. The flavonoid had a stronger effect on the maximal force of the contractions induced by caffeine, compared to contractions induced by carbachol. These results suggest that galangin has an important effect on the intracellular calcium mobilization, which might be attributed predominantly to its influence on ryanodine-receptors.
  Planta Medica 11/2005; 71(10):962-4. · 2.15 Impact Factor
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  Available from: Leon J Schurgers

  Article: Matrix Gla protein accumulates at the border of regions of calcification and normal tissue in the media of the arterial vessel wall.

  H M Spronk, B A Soute, L J Schurgers, J P Cleutjens, H H Thijssen, J G De Mey, C Vermeer
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  ABSTRACT: Vitamin K-dependent matrix Gla protein (MGP) has been suggested to play a role in the inhibition of soft-tissue calcification. Here we report the expression of recombinant prokaryotic MGP as part of a fusion protein and the preparation of two antibodies that specifically recognize MGP. Monoclonal antibodies were raised against synthetic peptides homologous to the sequences 3-15 and 63-75 of human MGP. Both antibodies recognize recombinant and synthetic human MGP. Immunohistochemical analysis showed that MGP was associated with the extracellular matrix of noncalcified bone and with chondrocytes in cartilage. In the healthy human arterial vessel wall, MGP antigen was demonstrated in association with smooth muscle cells and elastic laminae of the tunica media and with the extracellular matrix of the adventitia. Colocalization with the elastic laminae was lost at sites of medial calcification; in both human and rat arteries, high amounts of MGP were found in the extracellular matrix at borders of intimal and medial calcification. Our data demonstrate the close association between MGP and calcification. It is suggested that undercarboxylated MGP is biologically inactive and that poor vascular vitamin K status may form a risk factor for vascular calcification.
  Biochemical and Biophysical Research Communications 12/2001; 289(2):485-90. · 2.48 Impact Factor
• Article: Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries.

  C L Buus, F Pourageaud, G E Fazzi, G Janssen, M J Mulvany, J G De Mey
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  ABSTRACT: To obtain information on the molecular and cellular mechanisms of flow-induced arterial remodeling, we analyzed the morphology and smooth muscle cell (SMC) characteristics in rat mesenteric resistance arteries after interventions that decreased and increased flow. Juvenile male Wistar Kyoto rats were subjected to surgery that, compared with control arteries, provided arteries with chronic low flow and chronic high flow. Low flow resulted in a decreased passive lumen diameter, hypotrophy of the artery wall, and both loss and decreased size of SMCs. Time course studies, with intervention length ranging from 2 to 32 days of altered blood flow, showed that the narrowing of the lumen diameter in low-flow arteries appeared within 2 days and that an early dedifferentiation of SMC phenotype was indicated by markedly reduced levels of desmin mRNA. High flow resulted in an increased passive lumen diameter and in hypertrophy of the artery wall. The hypertrophy resulted from SMC proliferation because SMC number, measured by the 3D-dissector technique, was increased and immunohistochemical assessment of proliferating cell nuclear antigen also showed an increase. The widening of high-flow arteries required 16 days to become established, at which time desmin mRNA was reduced. This time was also required to establish changed wall mass in both low-flow and high-flow arteries. Apoptotic cells detected by TdT-mediated dUTP-biotin nick end labeling staining were mainly located in the medial layer, and evaluation of DNA fragmentation indicated that increased apoptosis occurred in both low flow and high flow. This study shows for the first time direct evidence that reduced and elevated blood flow in resistance arteries produce, respectively, decrease and increase in SMC number, with dedifferentiation of the SMCs in both cases.
  Circulation Research 08/2001; 89(2):180-6. · 9.49 Impact Factor
• Article: Diadenosine polyphosphates cause contraction and relaxation in isolated rat resistance arteries.

  M Steinmetz, E Schlatter, H A Boudier, K H Rahn, J G De Mey
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  ABSTRACT: The effects of diadenosine polyphosphates (APnA; n = 3-6) and adenine nucleotides on contractile reactivity of isolated rat mesenteric resistance arteries (MrA) and superior epigastric arteries (SEA), which display a dense and sparse autonomic innervation, respectively, were evaluated. All agonists examined, except adenosine and AMP, induced contractions. The rank order of potency was similar in both arteries: alpha,beta-methylene ATP (alpha,beta-meATP) > AP5A > AP6A > AP4A > ATP > ADP > AP3A. Contractions were stable during several minutes in SEA but highly transient in MrA. They were reduced after exposure to 10 microM alpha,beta-meATP and by 10 microM of the P2X antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid. During phenylephrine (10 microM)-induced contractions, the agonists induced a further contraction in SEA. In MrA, however, further contraction was followed by marked relaxation. The rank order of relaxing potency was comparable to that of the contractile potency of agonists. Also, the relaxing effects of APnA were blunted by 10 microM pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and after exposure to alpha,beta-meATP. In vitro and in vivo sympathectomy with 6-hydroxydopamine and removal of the endothelium did not modify the effects of APnA in MrA. Thus, the contractile effects of APnA in resistance arteries 1) are due to a P2X purinoceptor-mediated stimulation of the smooth muscle; 2) depend on the length of the phosphate chain; and 3) are followed by endothelium-independent relaxing effects in MrA but not SEA, which may involve receptors that are similar to those mediating contraction. The regional heterogeneity of APnA effects cannot be attributed to a direct neurogenic influence.
  Journal of Pharmacology and Experimental Therapeutics 09/2000; 294(3):1175-81. · 3.83 Impact Factor