Hakusana:
ELASTASE and Aortic Aneyrysm- association
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- (1) Hyperglykemian merkitys aortan aneurysmassa.
Miyama N, Dua MM et al. Hyperglycemia limits experimental aortic aneurysm progression.
J Vasc Surg. 2010 Jul 31.PMID: 20678880
CONCLUSIONS: Hyperglycemia reduces progression of experimental AAA disease; lowering of serum glucose levels with insulin treatment diminishes this protective effect. Identifying mechanisms of hyperglycemic aneurysm inhibition may accelerate development of novel clinical therapies for AAA disease
- (2) Ateroskleroosin ja vatsa-aortan aneurysmataudin riskiin assosioituu kohonnut MMP-8 ja alentunut myeloperoksidaasi.
Pradhan-Palikhe P, Vikatmaa P et al. Elevated MMP-8 and decreased myeloperoxidase concentrations associate significantly with the risk for peripheral atherosclerosis disease and abdominal aortic aneurysm. Scand J Immunol. 2010 Aug;72(2):150-7.PMID: 20618774
. Combination of high MMP-8 and low MPO level in serum eventually reflecting selectively modified neutrophil degranulation may indicate increased risk for arterial disease.
- (3) Transglutaminaasi 2 aktivoitumisen protektiivinen vaikutus vatsa-aortan kehittymisen suhteen koe-eläimessä. TG2 mahdollisesti on extrasellulaarimatriksia suojaava.
Munezane T, Hasegawa T et al. A
ctivation of transglutaminase type 2 for aortic wall protection in a rat abdominal aortic aneurysm formation. J Vasc Surg. 2010 Jul 6 ]PMID: 20615646
---Similar mRNA upregulation of TNF-alpha, interleukin-1beta, matrix metalloproteinases (MMP)-2, MMP-9, and tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2 was observed in the AAAs, and TG2 and TNF-alpha were colocalized in the aortic walls at 1 week.---
Ex vivo experiments showed that mRNA expressions of TNF-alpha, MMP-2, and MMP-9 in the cultured AAA tissue were decreased by exogenous TG2, whereas were increased by cystamine (TG2 inhibitor) . TNF-alpha exposure to the AAA tissues was significantly upregulated TG2 mRNA expression (P = .0333).
CONCLUSION: TG2 expression and activity in AAA formation were enhanced, possibly due to compensatory reaction. TG2 has a potential role of ECM protector in aortic walls during remodeling of the AAAs.
- (4) Vatsa-aortan aneurysman nopeaa kasvua heijastava seikka. Hp 2-1 fenotyyppi. Elastaasi ja CRP koholla.
Wiernicki I, Safranow K et al. Haptoglobin 2-1 phenotype predicts rapid growth of abdominal aortic aneurysms. J Vasc Surg. 2010 Jun 4.
Elastase and
C-reactive protein (CRP) levels are elevated in patients with AAAs.
Haptoglobin (Hp) polymorphism is associated with the prevalence and clinical evolution of many inflammatory diseases and atherosclerosis. Circulating neutrophils and neutrophil-associated proteases are an important initial component of experimental abdominal aortic aneurysm (AAA) formation.
CONCLUSIONS: The
Hp 2-1 phenotype showed a strong association with increased rates of the expansion of AAAs and may be a useful independent predictor of growth rate. Further large follow-up studies will be needed to investigate the pathomechanisms of association and the role of elastase and inflammation in the progression of AAA
- (5) Hyperglysemia moduloi PAI-1 ilmenemää ja aortan diametria kokeellisessa aneurysmassa koe-eläimellä. Fibrinolyyttisellä tiellä on osuutta vatsa-aortan aneurysman patofysiologiassa
Dua MM, Miyama N et al. Hyperglycemia modulates plasminogen activator inhibitor-1 expression and aortic diameter in experimental aortic aneurysm disease. Surgery. 2010 Aug;148(2):429-35. Epub 2010 Jun 19.PMID: 20561659
CONCLUSION: Hyperglycemia increases PAI-1 expression and attenuates AAA diameter in experimental AAA disease. These results emphasize
the role of the fibrinolytic pathway in AAA pathophysiology, and suggest a candidate mechanism for hyperglycemic inhibition of AAA disease. Copyright 2010 Mosby, Inc. All rights reserved.
- (6.) Vatsa-aortan aneurysman ohuen trombin kattamassa pinnassa on matrixia hajoittava proteolyyttinen aktiivisuus suurempaa kuin paksussa trombissa. Aortan elastiinin säilyminen on tärkeää , jotta aneurysman muodostus estyisi. Jos trombi vaikuttaa ohuelta, elastaasiaktiivisuus voi olla kiihtyneempää.
Wiernicki I, Stachowska E et al. .Enhanced matrix-degrading proteolytic activity within the thin thrombus-covered wall of human abdominal aortic aneurysms.
Atherosclerosis. 2010 May 6.PMID: 20537648
OBJECTIVE: The maintenance of an arterial elastin's integrity is essential in the prevention of abdominal aortic aneurysm (AAA) development. So far, the effect of intraluminal thrombus (ILT) thickness on the elastolytic activity within the AAA wall has not been studied. In the present study the hypothesis that thin thrombus is associated with enhanced proteolytic activity within human AAA wall was investigated
Schultz G, Tedesco MM et al. Enhanced abdominal aortic aneurysm formation in thrombin-activatable procarboxypeptidase B-deficient mice. Arterioscler Thromb Vasc Biol. 2010 Jul;30(7):1363-70. Epub 2010 Apr 29.PMID: 20431069 [PubMed - indexed for MEDLINE]Related citations
OBJECTIVE: To determine whether procarboxypeptidase B (pCPB)(-/-) mice are susceptible to accelerated abdominal aortic aneurysm (AAA) development secondary to unregulated OPN-mediated mural inflammation in the absence of
CPB inhibition. METHODS AND RESULTS:
Thrombin/thrombomodulin cleaves thrombin-activatable pCPB or thrombin-activatable fibrinolysis inhibitor, activating CPB, which inhibits the generation of plasmin and inactivates proinflammatory mediators (complement C5a and thrombin-cleaved osteopontin [OPN]). Apolipoprotein E(-/-)OPN(-/-) mice are protected from experimental AAA formation. Murine AAAs were created via intra-aortic porcine pancreatic elastase (PPE) infusion. Increased mortality secondary to AAA rupture was observed in pCPB(-/-) mice at the standard PPE dose. At reduced doses of PPE, pCPB(-/-) mice developed larger AAAs than wild-type controls (1.01+/-0.27 versus 0.68+/-0.05 mm; P=0.02 [mean+/-SD]). C5(-/-) and OPN(-/-) mice were not protected against AAA development. Treatment with tranexamic acid inhibited plasmin generation and abrogated enhanced AAA progression in pCPB(-/-) mice. CONCLUSIONS:
This study establishes the role of CPB in experimental AAA disease, indicating that
CPB has a broad anti-inflammatory role in vivo. Enhanced AAA formation in the PPE model is the result of increased plasmin generation, not unregulated C5a- or OPN-mediated mural inflammation.
TÄTÄ ASIAA TÄYTYY KATSOA TARKEMMIN. Muistiin 16.4. 2014. Päivitys jatkuu.
8.
Acoustic radiation force impulse imaging on ex vivo abdominal aortic aneurysm model.
Tierney AP, Dumont DM, Callanan A, Trahey GE, McGloughlin TM.
Ultrasound Med Biol. 2010 May;36(5):821-32. Epub 2010 Apr 9.PMID: 20381946 [PubMed - indexed for MEDLINE]Related citations
9.
Efficacy of
neutrophil elastase inhibitor on type A acute aortic dissection.
Niino T, Hata M, Sezai A, Yoshitake I, Unosawa S, Fujita K, Shimura K, Osaka S, Minami K.
Thorac Cardiovasc Surg. 2010 Apr;58(3):164-8. Epub 2010 Apr 7.PMID: 20376727 [PubMed - indexed for MEDLINE]Related citations
BACKGROUND: Surgery for type A acute aortic dissection (AAD) is associated with a high mortality and incidence of postoperative complications, including acute respiratory failure and coagulopathy. Aim of the study was to investigate the effects of sivelestat on pulmonary function and coagulopathy in patients undergoing surgery for AAD.
METHODS: The platelet count, antithrombin III (AT III) level, leukocyte count, C-reactive protein (CRP) level, prothrombin time (PT), activated partial thrombin time (APTT), and prothrombin time-international normalized ratio (PT-INR) were measured.
RESULTS: The postoperative decrease of AT III and the platelet count on admission to the intensive care unit (ICU) and 3 hours later were significantly less in group I. The leukocyte count and the values of CRP, PT, APTT, and PT-INR did not differ significantly between the groups. The duration of mechanical ventilation after surgery tended to be shorter in group I.
CONCLUSIONS:
Sivelestat significantly reduced the postoperative decreases in AT III and platelet count in patients undergoing emergency surgery for AAD. Georg Thieme Verlag KG Stuttgart New York
10.
Thrombus versus wall biological activities in experimental aortic aneurysms.
Coutard M, Touat Z, Houard X, Leclercq A, Michel JB.
J Vasc Res. 2010;47(4):355-66. Epub 2009 Dec 16.PMID: 20016209 [PubMed - indexed for MEDLINE]Free ArticleRelated citations
11.
A novel rat model of abdominal aortic aneurysm using a combination of intraluminal elastase infusion and extraluminal calcium chloride exposure.
Tanaka A, Hasegawa T, Chen Z, Okita Y, Okada K.
J Vasc Surg. 2009 Dec;50(6):1423-32.PMID: 19958989 [PubMed - indexed for MEDLINE]Related citations
CONCLUSION: The rat AAA model using a combination of intraluminal elastase infusion and extraluminal calcium chloride exposure is simple and easy to perform and is highly reliable and reproducible to create a saccular aneurysm similar to human AAAs. This model could be more useful to clarify AAA pathogenesis, mechanisms, and treatment interventions in experimental researches.
12.
Smooth muscle phenotypic modulation is an early event in aortic aneurysms.
Ailawadi G, Moehle CW, Pei H, Walton SP, Yang Z, Kron IL, Lau CL, Owens GK.
J Thorac Cardiovasc Surg. 2009 Dec;138(6):1392-9.PMID: 19931668 [PubMed - indexed for MEDLINE]Related citations
13.
Nitric oxide induces the progression of abdominal aortic aneurysms through the matrix metalloproteinase inducer EMMPRIN.
Lizarbe TR, Tarín C, Gómez M, Lavin B, Aracil E, Orte LM, Zaragoza C.
Am J Pathol. 2009 Oct;175(4):1421-30. Epub 2009 Sep 24.PMID: 19779140 [PubMed - indexed for MEDLINE]Related citations
14.
Decreased collagen and increased matrix metalloproteinase-13 in experimental abdominal aortic aneurysms in males compared with females.
Cho BS, Roelofs KJ, Ford JW, Henke PK, Upchurch GR Jr.
Surgery. 2010 Feb;147(2):258-67. Epub 2009 Sep 20.PMID: 19767051 [PubMed - indexed for MEDLINE]Related citations
15.
Expression of annexin II in experimental abdominal aortic aneurysms.
Hayashi T, Morishita E, Ohtake H, Oda Y, Asakura H, Nakao S.
Int J Hematol. 2009 Oct;90(3):336-42. Epub 2009 Sep 16.PMID: 19756921 [PubMed - indexed for MEDLINE]Related citations
Annexin II is a receptor of tissue-type plasminogen activator (t-PA). We have previously identified annexin II by immunolocalization in human atherosclerotic abdominal aortic aneurysms (AAAs). To investigate possible interactions between annexin II and AAA development, we examined annexin II mRNA and protein expression in a rat model of experimental AAA. AAAs were induced in rats by transient aortic infusion of elastase.
16.
Critical role of
mast cell chymase in mouse abdominal aortic aneurysm formation.
Sun J, Zhang J, Lindholt JS, Sukhova GK, Liu J, He A, Abrink M, Pejler G, Stevens RL, Thompson RW, Ennis TL, Gurish MF, Libby P, Shi GP.
Circulation. 2009 Sep 15;120(11):973-82. Epub 2009 Aug 31.PMID: 19720934 [PubMed - indexed for MEDLINE]Free PMC ArticleFree textRelated citations
CONCLUSIONS: High chymase-positive mast cell content in human AAA lesions,
greatly reduced AAA formation in Mcpt4(-/-) mice, and significant correlation of serum chymase levels with human AAA expansion rate suggests participation of mast cell chymase in the progression of human and mouse AAA.
17.
Immune cells and molecular mediators in the pathogenesis of the abdominal aortic aneurysm.
Rizas KD, Ippagunta N, Tilson MD 3rd.
Cardiol Rev. 2009 Sep-Oct;17(5):201-10. Review.PMID: 19690470 [PubMed - indexed for MEDLINE]Related citations
Abdominal aortic aneurysm is a multifactorial disease with genetic risk factors and an immunologic component. Immune cells, including macrophages, neutrophils, mast cells, B- and T- lymphocytes, along with vascular smooth muscle cells and adventitial fibroblasts, produce cytokines and enzymes, promoting an inflammatory reaction, extracellular matrix (ECM) degradation, and neovascularization. Among the different enzymes secreted by immune and stromal cells, matrix metalloproteinase (MMP)-2, MMP-9, MMP-12, cathepsins, and neutrophil elastase (NE) cause medial degeneration. Chymase causes smooth muscle cell apoptosis, and MMP-3, MMP-8, and MMP-13 cause adventitial collagen degradation, promoting abdominal aortic aneurysm rupture. At the same time chemokines (interleukin 8, macrophage inflammatory protein 1 alpha, monocyte chemotactic protein-1) cause recruitment and proliferation of inflammatory cells, whereas cytokines (vascular endothelial growth factor and transforming growth factor-beta) promote neoangiogenesis.
18.
Fusiform aneurysm model in rabbit carotid artery.
Reinald N, Fournier B, Naveau A, Couty L, Lemitre M, Seguier S, Coulomb B, Gogly B, Lafont A, Durand E.
J Vasc Res. 2010;47(1):61-8. Epub 2009 Aug 7.PMID: 19672109 [PubMed - indexed for MEDLINE]Related citations
19.
Creation of murine experimental abdominal aortic aneurysms with elastase.
Azuma J, Asagami T, Dalman R, Tsao PS.
J Vis Exp. 2009 Jul 23;(29). pii: 1280. doi: 10.3791/1280.PMID: 19629030 [PubMed - indexed for MEDLINE]Related citations
20.
Gender-dependent differential phosphorylation in the ERK signaling pathway is associated with increased MMP2 activity in rat aortic smooth muscle cells.
Ehrlichman LK, Ford JW, Roelofs KJ, Tedeschi-Filho W, Futchko JS, Ramacciotti E, Eliason JL, Henke PK, Upchurch GR Jr.
J Surg Res. 2010 May 1;160(1):18-24. Epub 2009 May 8.PMID: 19592018 [PubMed - indexed for MEDLINE]Related citations
These data provide evidence implicating alterations in p-ERK signaling via the up-regulation of MMPs as a potential explanation for gender-related discrepancies in AAA formation
