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1.
Lakartidningen ; 1132016 02 23.
Artículo en Sueco | MEDLINE | ID: mdl-26928685

RESUMEN

Cogans syndrome is a rare systemic inflammatory disease characterized by a combination of audiovestibular and ocular symptoms. In some cases, systemic complications occur with vascular inflammation. Aortitis and large vessel vasculitis are the most common forms, but medium-sized and small vessel involvement has also been described. The autoimmune reaction can lead to blindness, deafness and in worst case death, if these patients remain untreated or if treatment is delayed. There is no specific blood test or imaging method available and the diagnosis is clinical. It should be suspected in patients presenting with both inflammatory eye symptoms and audiovestibular dysfunction, when more common autoimmune and infectious diseases have been excluded. The treatment consists of high dose systemic steroids, topical steroids for the affected eye and in some cases addition of immunosuppressive drugs. Treatment is based on the severity of the symptoms and how well the patient responds to initial systemic corticosteroids. Here we present a case of suspected Cogan's syndrome where diagnosis was considered after exclusion of other possible autoimmune and infectious diseases.


Asunto(s)
Síndrome de Cogan/diagnóstico , Audiometría , Síndrome de Cogan/complicaciones , Síndrome de Cogan/tratamiento farmacológico , Síndrome de Cogan/fisiopatología , Cortisona/uso terapéutico , Femenino , Pérdida Auditiva Unilateral/etiología , Humanos , Inmunosupresores/uso terapéutico , Iritis/tratamiento farmacológico , Iritis/etiología , Imagen por Resonancia Magnética , Persona de Mediana Edad , Vértigo/etiología
2.
Arterioscler Thromb Vasc Biol ; 33(10): 2432-43, 2013 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-23908247

RESUMEN

OBJECTIVE: Carotid plaque instability is a major cause of ischemic stroke, but detailed knowledge about underlying molecular pathways is still lacking. Here, we evaluated large-scale transcriptomic and protein expression profiling in a biobank of carotid endarterectomies followed by characterization of identified candidates, as a platform for discovery of novel proteins differentially regulated in unstable carotid lesions. APPROACH AND RESULTS: Genes highly upregulated in symptomatic versus asymptomatic plaques were selected from Affymetrix microarray analyses (n=127 plaques), and tissue microarrays constructed from 34 lesions were assayed for 21 corresponding proteins by immunohistochemistry. Quantification of stainings demonstrated differential expression of CD36, CD137, and DOCK7 (P<0.05) in unstable versus stable lesions and the most significant upregulation of a proprotein convertase, PCSK6 (P<0.0001). Increased expression of PCSK6 in symptomatic lesions was verified by quantitative real-time polymerase chain reaction (n=233), and the protein was localized to smooth muscle α-actin positive cells and extracellular matrix of the fibrous cap by immunohistochemistry. PCSK6 expression positively correlated to genes associated with inflammation, matrix degradation, and mitogens in microarrays. Stimulation of human carotid smooth muscle cells in vitro with cytokines caused rapid induction of PCSK6 mRNA. CONCLUSIONS: Using a combination of transcriptomic and tissue microarray profiling, we demonstrate a novel approach to identify proteins differentially expressed in unstable carotid atherosclerosis. The proprotein convertase PCSK6 was detected at increased levels in the fibrous cap of symptomatic carotid plaques, possibly associated with key processes in plaque rupture such as inflammation and extracellular matrix remodeling. Further studies are needed to clarify the role of PCSK6 in atherosclerosis.


Asunto(s)
Estenosis Carotídea/enzimología , Estenosis Carotídea/genética , Perfilación de la Expresión Génica/métodos , Análisis de Secuencia por Matrices de Oligonucleótidos , Proproteína Convertasas/genética , Proproteína Convertasas/metabolismo , Serina Endopeptidasas/genética , Serina Endopeptidasas/metabolismo , Análisis de Matrices Tisulares , Enfermedades Asintomáticas , Estenosis Carotídea/inmunología , Estenosis Carotídea/patología , Células Cultivadas , Citocinas/metabolismo , Matriz Extracelular/metabolismo , Fibrosis , Humanos , Inmunohistoquímica , Mediadores de Inflamación/metabolismo , Músculo Liso Vascular/enzimología , Músculo Liso Vascular/inmunología , Miocitos del Músculo Liso/enzimología , Miocitos del Músculo Liso/inmunología , Placa Aterosclerótica , ARN Mensajero/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Rotura Espontánea , Regulación hacia Arriba
3.
Atherosclerosis ; 220(1): 102-9, 2012 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-22104117

RESUMEN

OBJECTIVE: Proliferation of smooth muscle cells (SMCs) in the fibrous cap of atherosclerotic lesions has been proposed to be important for plaque stability. Since the insulin-like growth factor (IGF) system has been implicated to play a role in atherosclerosis and plaque stability, we investigated the expression of members of the IGF system in carotid plaques, in particular IGFBP-1 and its role in the regulation of SMC proliferation. METHODS AND RESULTS: Gene expression profiles of the IGF system in 164 human carotid plaques obtained from our Biobank of Karolinska Endarterectomies (BiKE) were analyzed. Expression of IGFBP-1 mRNA was significantly increased in carotid plaques compared with normal iliac arteries in contrast to IGF-1, IGF-2, and IGFBP-3 to IGFBP-6. The expression of IGFBP-1 mRNA correlated positively to that of CD163, CD68, IL-1ß, IL-6, TNFα, IGFBP-4 and IGFBP-5. Immunohistochemistry demonstrated co-localization of IGFBP-1 with SMCs and macrophages. In vitro studies showed that IL-1ß, IL-6 and TNFα stimulated IGFBP-1 mRNA expression in SMCs. IGFBP-1 stimulated SMC proliferation through ERK1/2 activation but independently of the IGF-1 receptor. In addition, IGFBP-1 modulated the effect of IGF-1 on SMC proliferation and ERK1/2 activation. CONCLUSIONS: Our results demonstrate that IGFBP-1 mRNA and protein is detected at increased levels in human carotid plaques, possibly as a consequence of plaque inflammation. IGFBP-1 affects SMC proliferation and may be involved in the regulation of plaque stability.


Asunto(s)
Enfermedades de las Arterias Carótidas/metabolismo , Proliferación Celular , Proteína 1 de Unión a Factor de Crecimiento Similar a la Insulina/metabolismo , Músculo Liso Vascular/metabolismo , Miocitos del Músculo Liso/metabolismo , Somatomedinas/metabolismo , Adulto , Anciano , Anciano de 80 o más Años , Animales , Enfermedades de las Arterias Carótidas/genética , Enfermedades de las Arterias Carótidas/patología , Células Cultivadas , Femenino , Perfilación de la Expresión Génica/métodos , Humanos , Inmunohistoquímica , Proteína 1 de Unión a Factor de Crecimiento Similar a la Insulina/genética , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Macrófagos/metabolismo , Masculino , Persona de Mediana Edad , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Músculo Liso Vascular/patología , Miocitos del Músculo Liso/patología , Análisis de Secuencia por Matrices de Oligonucleótidos , ARN Mensajero/metabolismo , Ratas , Somatomedinas/genética , Factor de Necrosis Tumoral alfa/metabolismo , Regulación hacia Arriba
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