Use este identificador para citar ou linkar para este item: https://observatorio.fm.usp.br/handle/OPI/2815
Título: Expression of SMAD proteins, intracellular effectors of TGF-beta signalling, in non-Marfan patients with thoracic aortic aneurysms and dissections
Autor(es): GUTIERREZ, P. S.APARECIDA-SILVA, R.BORGES, L. F.MOREIRA, L. F. P.DIAS, R. R.KALIL, J.STOLF, N. A. G.
Parte de: CARDIOVASCULAR RESEARCH, v.93, suppl.1, p.S82-S83, 2012
Resumo: Introduction a role for TGF-beta (TGFb) in thoracic aortic aneurysms and dissections (TAAD) has been evidenced by many studies. For example, around 5% of TAAD patients present Marfan's syndrome (MFS), in which there is a defect in fibrillin, that regulates TGFb signalling. Nevertheless, most TAAD patients have no known syndrome, but rather systemic arterial hypertension (SAH); other alterations in TGFb pathway might be involved in those cases. In this study, we analysed the expression of SMAD proteins, a family of intracellular effectors of TGFb signalling, in TAAD patients without MFS. Since aortic dissections occur always at the external half of the medial layer, we compared both halves. Patients and methods Five micrometre-thick sections of ascending aorta samples obtained at surgery were submitted to immunoperoxidase reactions to detect SMAD-2, -3, -4, and -7. The positive and total cells were counted in each half of the medial layer in the aortas from 10 patients with ascending aorta aneurysms, 10 with aortic dissections (all without MFS, most with SAH), 8 control cases (patients submitted to coronary artery bypass surgery) with SAH, and 9 control cases without SAH. The positive/ total cell ratios in each half of the media were compared by two-way repeated measure ANOVA after ranking transformation (since the distribution was not normal), and Bonferroni t-test as post-hoc test both in all these 4 groups and considering the cases as only two groups (patients with TAAD versus controls). Significance was established in p < or = 0.05. Results No significant difference was detected between halves for any SMAD. No difference was also found considering separately the 4 groups; however, when analyzing TAAD as a whole (table), the expression of SMAD 4 was significantly increased in comparison with controls (p=0.02). Conclusion an increase in SMAD 4 protein, one of the intracellular effectors of TGFb, may be related to TAAD. TAAD Controls p SMAD 2 0.84 0.86 0.61 SMAD 3 0.62 0.63 0.72 SMAD 4 0.95 0.87 0.02 SMAD 7 0.95 0.95 0.61 Abstract P410 figure Medians for SMAD proteins positive cell/total cell ratio at the medial layer of thoracic aortas with aneurysms or dissections (TAAD) and controls
Aparece nas coleções:

Comunicações em Eventos - FM/MCM
Departamento de Clínica Médica - FM/MCM

Comunicações em Eventos - FM/MCP
Departamento de Cardio-Pneumologia - FM/MCP

Comunicações em Eventos - HC/ICHC
Instituto Central - HC/ICHC

Comunicações em Eventos - HC/InCor
Instituto do Coração - HC/InCor

Comunicações em Eventos - LIM/11
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação

Comunicações em Eventos - LIM/19
LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular


Arquivos associados a este item:
Não existem arquivos associados a este item.

Os itens no repositório estão protegidos por copyright, com todos os direitos reservados, salvo quando é indicado o contrário.