Haematologica 2004;89: supplement no. 8 - Supplements ...

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XVIII Congress of the Italian Society for Hemostasis and Thrombosis Research, Rome, Sept. 30-Oct. 3, 200425tially expressed genes. MT confirms its pivotal role asscreening approach to identify novel genes.This work was supported by a grant from Ministerodella Salute.CO-012DIVERSITY AND SIMILARITY IN SIGNALING EVENTS LEADINGTO RAPID COX-2 SYNTHESIS BY PMA AND TNFα IN HUMANENDOTHELIAL CELLSEligini S,* Barbieri SS,* Cavalca V,° Camera M,°De Franceschi M,° Tremoli E,*° Colli S**E. Grossi Paoletti Center, Department ofPharmacological Sciences and °Department ofCardiac Surgery, Centro Cardiologico FondazioneMonzino I.R.C.C.S, University of Milan, ItalyCyclooxygenase 2 (Cox-2) is a key enzyme in vascularhomeostasis, inflammation, tumorigenesis, andangiogenesis. Specifically, endothelial Cox-2 activityis crucial for the availability of prostacyclin and,consequently, for the modulation of platelet-vascularinteractions. Aim. This study examines whetherCox-2 synthesis and activity in endothelial cellsinvolves distinct signaling pathways when inducedby the representative proinflammatory cytokinetumor necrosis factor α (TNFv) or by the tumor promoterphorbol ester (PMA). Moreover, the hypothesisthat reactive oxygen species (ROS) and alterationof cell redox status are fundamental steps in Cox-2synthesis is addressed. Methods. Human endothelialcells isolated from umbilical vein (HUVEC) wereexposed to TNFα or PMA. Cox-2 protein synthesiswas evaluated by Western blot analysis and its activityby measurement of prostaglandin E2 (PGE2) and6-keto prostaglandin F1α levels. Intracellular ROSgeneration was detected by flow cytometry in cellsloaded with the oxidant sensitive 2'7'-dichlorofluoresceindiacetate and by reduction of nitroblue tetrazolium.Reduced and oxidized glutathione (GSH andGSSG) levels were measured by HPLC. Distinct signalingpathways are involved in early Cox-2 inductionby TNFα and PMA. PMA signals through theinvolvement of a small GTPase, protein kinase C (PKC)and mitogen activated protein kinase (MAPK) ERK1/2activation whereas p38 MAPK is critical when Cox-2 is induced by TNFα. Conversely, intracellular ROSgeneration and consequent reduction of GSH/GSSGratio represent a common step for Cox-2 inductionby both stimuli. In addition, evidence that phosphatidylinositol3(PI3)-kinase activation plays a regulatoryrole for Cox-2 synthesis induced by PMA andTNFα is provided. Cox-2 represents a critical regulatorof vascular homeostasis, inflammatory response,angiogenesis and tumor growth. The finding that twoindependent pathways, together with overlappingupstream events signal for Cox-2 induction in HUVECmay be of relevance to develop strategies aimed atselectively interfering with regulating pathways.CO-013SYSTEMIC SCLEROSIS: GENE EXPRESSION PROFILING BYMICROARRAY TECHNOLOGY OF ENDOTHELIAL CELLSGiusti B, Del Rosso M,* Fibbi G,*Matucci-Cerinic M,^ Rossi L, Poggi F, Attanasio M,Lucarini L, Saracini C, Lapini I, Pepe G, Abbate RDipartimento Area Critica Medico-Chirugica,Università degli Studi di Firenze; *Dipartimento diPatologia e Oncologia Sperimentale, UNiversitàdegli Studi di Firenze; ^ Dipartimento di MedicinaInterna, Università degli Studi di Firenze, ItalySystemic sclerosis (SSc) is a clinically heterogeneous,systemic disorder which affects the connectivetissue of the skin, internal organs and the wallsof blood vessels. Defective angiogenesis, resulting intissue ischemia, is prominent in the diffuse form ofSSc, but its pathogenetic basis is unknown. We isolatedmicrovascular endothelial cells (MVEC) fromthe dermis of healthy individuals (N-MVEC) andpatients with diffuse SSc (SSc-MVEC) in order toidentify differences in the gene expression profiling.For this purpose we used a 14,000 gene oligonucleotidearray (70-mers oligonucleotide, Operontechnologies). Total RNA from cultured MVEC wasisolated by RNeasy Kit (QIAGEN). Pooling of MVECtotal RNA from patients and controls was performed.One hundred and ninety nine genes showed alteredexpression levels between SSc-MVEC and N-MVEC:153 were up-regulated and 46 were down-regulated.More than 25 of the genes (e.g. MIF, LAMR1, IL-8, CTGF, CFL1, PEA15, PGAR, KLKs, PLAT, PLAU, etc)which were differentially expressed in SSc-MVEC aredirectly or indirectly involved with angiogenesis.Interestingly, in contrast with the clinical data indicatinga vascular desert-like pattern, many proangiogeneticgenes were found to be over-expressed inSSc. These results suggest that an epigenetic eventwhich occurs in SSc may be able to vanish the angiogenicattitude of MVEC. Preliminary data indicatethat the truncation of the urokinase-plasminogenactivator receptor (uPAR) in SSc-MVEC may account,at least in part, for defective angiogenesis.haematologica vol. 89(suppl. n. 8):september 2004
26Oral CommunicationsCO-014ENOS GENE AFFECTS BLOOD VISCOSITY AND RED CELLDEFORMABILITY: ROLE OF ENOS T-786C, G894T AND 4A/4BPOLYMORPHISMSMannini L,* Fatini C,* Sticchi E,* Cecchi E,* Ilari I,*Bruschettini A,* Costanzo M,* Leprini E,° Pagnini P,°Gensini GF,* Prisco D,* Abbate R**Dipartimento Area Critica Medico-Chirurgica,Università degli Studi di Firenze; °Dipartimento diScienze Chirurgiche Oto-Neuro-Oftalmologiche,Università degli Studi di Firenze, ItalyPlasma viscosity and erythrocyte aggregation playa key role in maintaining and regulating microcirculation.In vitro and in vivo studies suggested a role fornitric oxide (NO) in modulating flow-mediated vasodilatationand red blood cell deformability. Impaired NOavailability due to mutations in eNOS gene might contributeto altered hemorheological state. Aim of thisstudy was to investigate the role of eNOS T-786C,G894T and 4a/4b polymorphisms in influencinghemorheological state. We studied 80 Idiopathic SuddenSensorineural Hearing Loss (ISSHL) patients and80 healthy subjects. From the multivariate analysis asignificant association between eNOS 894T rare variantand ISSHL (OR 894TT+GT=2.08, p=0.03) wasfound. A higher percentage of altered erythrocyte filtrationtest (EFT) both in patients and in controls carryingthe eNOS rare variants was found in comparisonto subjects carrying the wild-type. Apart from thedisease, eNOS T-786C and G894T polymorphismsindependently affected the EFT (OR -786CC+TC=2.81,p=0.01 and OR 894TT+GT=2.5, p=0.02, respectively),in particular in subjects in whom the contemporarypresence of the two rare alleles was observed (OR -786CC+TC and 894TT+GT combined genotype =6.9,p
Page 5 and 6: haematologicaThe origin and power o
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98PostersPO-008INTEGRIN α2β1 AND
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