2017
A p190BRhoGAP mutation and prolonged RhoB activation in fatal systemic capillary leak syndrome
Pierce RW, Merola J, Lavik JP, Kluger MS, Huttner A, Khokha MK, Pober JS. A p190BRhoGAP mutation and prolonged RhoB activation in fatal systemic capillary leak syndrome. Journal Of Experimental Medicine 2017, 214: 3497-3505. PMID: 29097442, PMCID: PMC5716031, DOI: 10.1084/jem.20162143.Peer-Reviewed Original ResearchConceptsTumor necrosis factorSystemic capillary leakDermal microvascular endothelial cellsMicrovascular endothelial cellsPatient-derived endothelial cellsEndothelial cellsCapillary leakNormal human dermal microvascular endothelial cellsSystemic capillary leak syndromeBarrier functionCapillary leak syndromeHuman dermal microvascular endothelial cellsTransendothelial electrical resistanceEC barrier functionNormal endothelial cellsLeak syndromeCritical illnessFatal casesNecrosis factorBarrier recoverySiRNA knockdownEC culturesRhoB activationGreater increaseJunctional proteinsCo-expression of tissue factor and IL-6 in immature endothelial cells of cerebral cavernous malformations
Noshiro S, Mikami T, Kataoka-Sasaki Y, Sasaki M, Ohnishi H, Ohtaki S, Wanibuchi M, Mikuni N, Kocsis JD, Honmou O. Co-expression of tissue factor and IL-6 in immature endothelial cells of cerebral cavernous malformations. Journal Of Clinical Neuroscience 2017, 37: 83-90. PMID: 28087183, DOI: 10.1016/j.jocn.2016.12.023.Peer-Reviewed Original ResearchConceptsCerebral cavernous malformationsInterleukin-6Immature endothelial cellsTissue factorMRNA expression levelsEndothelial cellsCavernous malformationsSporadic cerebral cavernous malformationDistribution of TFExpression levelsNormal endothelial cellsClinical factorsPrognostic rolePathological findingsUnderlying pathologyOperative specimensMRNA expressionAssociation of TFAbnormal clustersMalformationsProgressive eventsMessenger RNACellsExpressionAssociation
2016
Biological relevance of tissue factor and IL-6 in arteriovenous malformations
Noshiro S, Mikami T, Kataoka-Sasaki Y, Sasaki M, Hashi K, Ohtaki S, Wanibuchi M, Mikuni N, Kocsis JD, Honmou O. Biological relevance of tissue factor and IL-6 in arteriovenous malformations. Neurosurgical Review 2016, 40: 359-367. PMID: 27542852, DOI: 10.1007/s10143-016-0780-1.Peer-Reviewed Original ResearchConceptsInterleukin-6Vascular endothelial growth factor receptor 2Arteriovenous malformationsTissue factorControl tissuesMRNA expressionEndothelial cellsAbnormal endothelial cellsPlatelet-derived growth factor receptor betaGrowth factor receptor 2Growth factor receptor betaEndothelial growth factor receptor 2Factor receptor 2Distribution of TFSporadic arteriovenous malformationsNormal endothelial cellsMessenger RNAAsymptomatic groupSymptomatic groupClinical factorsPrognostic rolePathological findingsShunt bloodUnderlying pathologyOperative specimens
2010
Induction of Podocyte VEGF164 Overexpression at Different Stages of Development Causes Congenital Nephrosis or Steroid-Resistant Nephrotic Syndrome
Veron D, Reidy K, Marlier A, Bertuccio C, Villegas G, Jimenez J, Kashgarian M, Tufro A. Induction of Podocyte VEGF164 Overexpression at Different Stages of Development Causes Congenital Nephrosis or Steroid-Resistant Nephrotic Syndrome. American Journal Of Pathology 2010, 177: 2225-2233. PMID: 20829436, PMCID: PMC2966782, DOI: 10.2353/ajpath.2010.091146.Peer-Reviewed Original ResearchConceptsNephrotic syndromePodocyte effacementTransgenic miceSteroid-resistant nephrotic syndromeEndothelial cellsSingle transgenic miceMultiple renal diseasesSwollen endothelial cellsCongenital nephrotic syndromeVascular endothelial growthInducible transgenic miceNormal endothelial cellsGlomerular filtration barrierRenal diseasePathogenic rolePodocyte lossMice expressMassive albuminuriaEndothelial growthCongenital nephrosisMinimal changesFoot processesMiceGlomerulomegalyAlbuminuria
2006
Granzyme B‐dependent Matrix Degradation Generates Anti‐Angiostatic Activity in Scleroderma Patients
Mulligan‐Kehoe M, Drinane M, Hummers L, Hall A, Rosen A, Wigley F, Simons M. Granzyme B‐dependent Matrix Degradation Generates Anti‐Angiostatic Activity in Scleroderma Patients. The FASEB Journal 2006, 20: a1099-a1099. DOI: 10.1096/fasebj.20.5.a1099-a.Peer-Reviewed Original ResearchSSc patientsRA patientsScleroderma patientsGranzyme BSystemic connective tissue diseasesExtensive vascular componentConnective tissue diseasePAI-1 levelsNormal control patientsAngiostatin K1-3Impaired wound healingAnti-angiogenic factorsAnti-angiogenic activityNormal endothelial cellsAberrant microvasculatureControl patientsRheumatoid arthritisTissue diseaseVascular abnormalitiesUncertain etiologyVascular componentPatientsEndothelial cellsEndothelial cell migrationWound healing
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