0000000000373934

AUTHOR

Teresa Mateo

showing 6 related works from this author

A critical role for TNFα in the selective attachment of mononuclear leukocytes to angiotensin-II-stimulated arterioles

2007

Abstract Angiotensin II (Ang-II) exerts inflammatory activity and is involved in different cardiovascular disorders. This study has evaluated the involvement of tumor necrosis factor alpha (TNFα) in the leukocyte accumulation elicited by Ang-II. Ang-II (1 nM intraperitoneally in rats) induced TNFα release at 1 hour followed by neutrophil and mononuclear cell recruitment. The administration of an antirat TNFα antiserum had no effect on Ang-IIinduced neutrophil accumulation but inhibited the infiltration of mononuclear cells and reduced CC chemokine content in the peritoneal exudate. Pretreatment with either an anti-TNFα or an anti-IL-4 antiserum decreased Ang-II-induced arteriolar mononuclea…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliummedicine.medical_treatmentImmunologyBiologyBiochemistryPeripheral blood mononuclear cellMicrocirculationRats Sprague-DawleyInternal medicineCell AdhesionmedicineAnimalsHumansVasoconstrictor AgentsRNA MessengerVenuleReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAngiotensin IICell BiologyHematologyAngiotensin IIRatsArteriolesMononuclear cell infiltrationmedicine.anatomical_structureCytokineEndocrinologyLeukocytes MononuclearTumor necrosis factor alphaEndothelium VascularInterleukin-4ChemokinesInjections IntraperitonealBlood
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Angiotensin II Induces Neutrophil Accumulation In Vivo Through Generation and Release of CXC Chemokines

2004

Background—Angiotensin II (Ang II) is implicated in the development of cardiac ischemic disorders in which prominent neutrophil accumulation occurs. Ang II can be generated intravascularly by the renin-angiotensin system or extravascularly by mast cell chymase. In this study, we characterized the ability of Ang II to induce neutrophil accumulation.Methods and Results—Intraperitoneal administration of Ang II (1 nmol/L) induced significant neutrophil recruitment within 4 hours (13.3±2.3×106neutrophils per rat versus 0.7±0.5×106in control animals), which disappeared by 24 hours. Maximal levels of CXC chemokines were detected 1 hour after Ang II injection (577±224 pmol/L cytokine-inducible neut…

MaleChemokinemedicine.medical_specialtyEndotheliumCellsInflammationAngiotensin ; Interleukins ; Cells ; Endothelium ; InflammationPulmonary ArteryUmbilical CordRats Sprague-DawleyAngiotensin:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]Physiology (medical)Internal medicineRenin–angiotensin systemCell AdhesionLeukocytesAnimalsHumansMedicineMesenteryRNA MessengerEndotheliumPeritoneal CavityMacrophage inflammatory proteinCells CulturedUNESCO::CIENCIAS MÉDICAS ::Medicina internaInflammationbiologybusiness.industryAngiotensin IIMicrocirculationInterleukinsInterleukin-8Endothelial CellsChemotaxis:CIENCIAS MÉDICAS [UNESCO]Angiotensin IIRatsmedicine.anatomical_structureEndocrinologyNeutrophil InfiltrationUNESCO::CIENCIAS MÉDICASbiology.proteinmedicine.symptomCardiology and Cardiovascular MedicinebusinessChemokines CXCIntravital microscopy
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Angiotensin II-Induced Mononuclear Leukocyte Interactions with Arteriolar and Venular Endothelium Are Mediated by the Release of Different CC Chemoki…

2006

Abstract Angiotensin II (Ang-II) is associated with atherogenesis and arterial subendothelial mononuclear leukocyte infiltration. We have demonstrated that Ang-II causes the initial attachment of mononuclear cells to the arteriolar endothelium. We now report on the contribution of CC chemokines to this response. Intraperitoneal administration of 1 nM Ang-II induced MCP-1, RANTES, and MIP-1α generation, maximal at 4 h, followed by mononuclear leukocyte recruitment at 8 and 24 h. Using intravital microscopy within the rat mesenteric microcirculation 4 h after exposure to 1 nM Ang-II, arteriolar mononuclear cell adhesion was 80–90% inhibited by pretreatment with Met-RANTES, a CCR1 and CCR5 ant…

MaleCCR1EndotheliumImmunologyVascular Cell Adhesion Molecule-1Peripheral blood mononuclear cellUmbilical CordRats Sprague-DawleyLeukocyte CountCell MovementCell AdhesionLeukocytesmedicineAnimalsHumansImmunology and AllergyEndotheliumChemokine CCL5Cells CulturedChemokine CCL2Angiotensin II receptor type 1Chemokine CCL26business.industryAngiotensin IIMonocyteEpithelial Cellsmedicine.diseaseAngiotensin IIMolecular biologyRatsP-Selectinmedicine.anatomical_structureChemokines CCImmunologycardiovascular systembusinessInfiltration (medical)Intravital microscopyThe Journal of Immunology
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L-NAME induces direct arteriolar leukocyte adhesion, which is mainly mediated by angiotensin-II.

2005

Acute inhibition (1 h) of nitric oxide synthase (NOS) with L-NAME causes leukocyte recruitment in the rat mesenteric postcapillary venules that is angiotensin-II (Ang-II) dependent. Since 4-h exposure to Ang-II provokes arteriolar leukocyte adhesion, this study was designed to investigate whether subacute (4-h) NOS inhibition also causes this effect.Rats were intraperitoneally injected with saline, L-NAME, or 1H-[1,2,4]-oxidazolol-[4,3-a]-quinoxalin-1-one (ODQ). Leukocyte accumulation in the mesenteric microcirculation was examined 4 h later via intravital microscopy. Some groups were pretreated with losartan, an AT(1) Ang-II receptor antagonist.At 4-h, L-NAME caused a significant increase …

MaleEndotheliumPhysiologyPharmacologyLosartanNitric oxideRats Sprague-Dawleychemistry.chemical_compoundVenulesPhysiology (medical)medicineCell AdhesionLeukocytesAnimalsLeukocyte RollingSplanchnic CirculationReceptorMolecular BiologyAngiotensin II receptor type 1Microscopy VideobiologyAngiotensin IIAngiotensin IIRatsNitric oxide synthaseArteriolesmedicine.anatomical_structureLosartanNG-Nitroarginine Methyl EsterchemistryImmunologycardiovascular systembiology.proteinNitric Oxide SynthaseCardiology and Cardiovascular MedicineCell Adhesion MoleculesIntravital microscopymedicine.drugMicrocirculation (New York, N.Y. : 1994)
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Effect of boldine, secoboldine, and boldine methine on angiotensin II-induced neutrophil recruitment in vivo.

2005

AbstractAngiotensin-II (Ang-II) has inflammatory activity and is involved in different diseases associated with the cardiovascular system. This study has evaluated the effect of boldine (B), and two phenanthrene alkaloids semisynthesized by us, secoboldine (SB) and boldine methine (BM), on Ang-II-induced neutrophil recruitment. Intraperitoneal administration of 1 nM Ang-II induced significant neutrophil accumulation, which was maximal at 4–8 h. BM inhibited neutrophil infiltration into the peritoneal cavity at 4 h and 8 h by 73% and 77%, respectively, SB at 8 h by 55%, and B had no effect on this response. Although BM inhibited the release of cytokine-inducible neutrophil chemoattractant/ke…

KeratinocytesMaleChemokineAporphinesEndotheliumNeutrophilsImmunologyChemokine CXCL2InflammationPharmacologyRats Sprague-Dawleychemistry.chemical_compoundIn vivomedicineImmunology and AllergyBoldineAnimalsHumansInfusions ParenteralPlatelet Activating FactorReceptorchemistry.chemical_classificationReactive oxygen speciesbiologyMolecular StructureAngiotensin IIMonokinesInterleukin-8Endothelial CellsCell BiologyPhenanthrenesAngiotensin IIRatsP-Selectinmedicine.anatomical_structureBiochemistrychemistrybiology.proteinIntercellular Signaling Peptides and Proteinsmedicine.symptomChemokinesReactive Oxygen SpeciesChemokines CXCJournal of leukocyte biology
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