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Titolo:
Examination of the apoptotic pathway and proteolysis in the pathogenesis of popliteal artery aneurysms
Autore:
Jacob, T; Hingorani, A; Ascher, E;
Indirizzi:
Maimonides Med Ctr, Div Vasc Surg, Brooklyn, NY 11219 USA Maimonides Med Ctr Brooklyn NY USA 11219 asc Surg, Brooklyn, NY 11219 USA
Titolo Testata:
EUROPEAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY
fascicolo: 1, volume: 22, anno: 2001,
pagine: 77 - 85
SICI:
1078-5884(200107)22:1<77:EOTAPA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ABDOMINAL AORTIC-ANEURYSMS; ATHEROSCLEROTIC PLAQUES; DEATH; DNA; IDENTIFICATION; EXPRESSION; PROTEASES; PROTEINS; REPAIR; RAT;
Keywords:
popliteal artery aneurysms; apoptosis; proteolysis; molecular mechanisms;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Ascher, E Maimonides Med Ctr, Div Vasc Surg, 4802 10th Ave, Brooklyn, NY 11219 USA Maimonides Med Ctr 4802 10th Ave Brooklyn NY USA 11219 11219 USA
Citazione:
T. Jacob et al., "Examination of the apoptotic pathway and proteolysis in the pathogenesis of popliteal artery aneurysms", EUR J VAS E, 22(1), 2001, pp. 77-85

Abstract

Objectives: to investigate the role of apoptosis, expression of death-promoting molecules and mediators of apoptosis in the development of popliteal artery aneurysms. Methods: ten popliteal artery aneurysm (PAA) specimens were obtained from patients undergoing elective surgical repair. Normal controls were popliteal arteries obtained from patients without PAA undergoing infrainguinal bypass surgery (n = 8). Standard histochemistry techniques were used to assess elastic lamellae fragmentation and inflammatory infiltrate in PAA. Vascularsmooth muscle cells (VSMC), macrophages, T lymphocytes, death-promoting molecules, CPP-32, Fas, p53, perforin, apoptosis-mediating Bcl-2 family proteins and apoptotic death substrate, poly(ADP-ribose) polymerase (PARP) were detected immunohistochemically. Detection of apoptosis was by TUNEL assay. Proteolytic activity was determined by 10% gelatin gel zymography. Results: there is a conspicuous disruption and fragmentation of elastic lamellae in PAA as compared to normal arteries. Increased gelatinolytic activity was observed at 92, 84, 72 and 67 kDa in PAA tissues. There is a significant decrease of VSMCs in the PAA walls (p = 0.02). The control arteries had fewer CD68+ macrophages and CD3+ T cells in their media (p < 0.01). There was a significant increase in the number of cells undergoing apoptosis inaneurysmal tissue than in the normal vessels, (p < 0.02) as well as an increased expression of Bax, CPP- 32, Fas, p53 and perforin. Conclusions: the data confirm the architectural disruption of the PAA walland illustrate an apparent biological response involving inflammatory infiltrate, apoptosis and signalling molecules capable of initiating cell death. In addition to compromising the mechanical integrity of the vessel wall, VSMC loss may contribute to imbalance in the protein profile, accelerating extracellular matrix degradation that could favour PAA development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 09:04:41