Correlation of inflammatory infiltrate with the enlargement of experimental aortic aneurysms

Anidjar, Samy; Dobrin, Philip B.; Eichorst, Mariann; Graham, Galen P.; Chejfec, Gregorio

doi:10.1016/0741-5214(92)90101-d

Cited by 200 publications

(140 citation statements)

References 14 publications

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“…For example, type IV collagenase mRNA was detected in cells surrounding vasa vasorum within the plaque (8), and macrophage elastase may induce aortic aneurysm in rats (9). Furthermore, enlargement of elastase-induced aortic aneurysm was shown to correlate with the presence of inflammatory infiltrates within the aortic wall (10). These observations suggest that the enzymes required for ECM degradation are synthesized and subsequently activated in situ within the aneurysm wall.…”

Section: Introductionmentioning

confidence: 71%

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

Schneiderman¹,

Bordin²,

Engelberg³

et al. 1995

J. Clin. Invest.

131

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Expansion of atherosclerotic abdominal aortic aneurysm (AAA) has been attributed to remodeling of the extracellular matrix by active proteolysis. We used in situ hybridization to analyze the expression of fibrinolytic genes in aneurysm wall from eight AAA patients. All specimens exhibited specific areas of inflammatory infiltrates with macrophagelike cells expressing urokinase-type plasminogen activator (u-PA) and tissue-type PA (t-PA) mRNA. Type 1 PA inhibitor (PAM-) mRNA was expressed at the base of the necrotic atheroma of all specimens and also within some of the inflammatory infiltrates where it frequently colocalized in regions contining u-PA and t-PA mRNA expressing cells.However, in these areas, the cellular distribution of the transcripts for t-PA and u-PA extended far beyond the areas of PAT-i expression. These observations suggest a local ongoing proteolytic process, one which is only partially counteracted by the more restricted expression of PAT-i mRNA. An abundance of capillaries was also obvious in all inflammatory infiltrates and may reflect local angiogenesis in response to active pericellular fibrinolysis. The increased fibrinolytic capacity in AAA wall may promote angiogenesis and contribute to local proteolytic degradation of the aortic wall leading to physical weakening and active expansion of the aneurysm. (J. Clin. Invest. 1995. 96:639-645.)

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Section: Introductionmentioning

confidence: 71%

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

Schneiderman¹,

Bordin²,

Engelberg³

et al. 1995

J. Clin. Invest.

131

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“…1,3,14,15 The association of some aneurysms with connective tissue disorders led to genetic evaluations of families with multiple members affected and to the search for culprit genes. 1,2,16,17 Experiments have sought to identify enzymes in the aorta that might break down collagen and elastin, which compose major structural elements of the vessel wall. Recently, Knox et al 4 compared MMP expression in aneurysmal and occlusive aortic diseases with normal controls and found no difference in MMP or TIMP expression that would explain aneurysm formation versus occlusive disease.…”

Section: Discussionmentioning

confidence: 99%

Death of Smooth Muscle Cells and Expression of Mediators of Apoptosis by T Lymphocytes in Human Abdominal Aortic Aneurysms

et al. 1999

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Background-Thinning of the tunica media and rarefaction of smooth muscle cells (SMCs) characterize aneurysmal aortas. Apoptosis determines the cellularity and morphogenesis of tissue. Macrophages and T lymphocytes infiltrate the wall of abdominal aortic aneurysms (AAAs) and produce death-promoting proteins (perforin, Fas, and FasL). This study investigated whether apoptosis occurs in association with the expression of these proteins. Methods and Results-We examined signs of apoptosis and expression of death-promoting mediators in segments of AAAs from patients undergoing elective repair (nϭ20). Anti-␣-actin immunostaining showed a reduced number of SMCs in AAAs. In situ terminal transferase-mediated dUTP nick end-labeling (TUNEL) showed higher levels of DNA fragmentation in AAAs than in controls (nϭ5). The AAA walls contained more cells bearing markers of apoptosis than normal aorta (PϽ0.05, Student's t test). Double immunostaining identified SMCs and macrophages as the principal cell types displaying fragmented DNA. Immunohistochemistry revealed that AAAs but not normal aorta contained CD4

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“…Collagen is produced by fibre-producing cells such as fibroblasts and smooth muscle cells, and collagen degradation is accomplished by collagenases (Dobrin and Canfield, 1984;Murphy and Reynolds, 1985). Increased levels of collagenases have also been observed in aneurysmal tissue (AAssar et al, 2003;Anidjar et al, 1992;McMillan et al, 1995;Sluijter et al, 2004;Webster et al, 1991). The production of collagen (Type I) in cerebral aneurysms is mainly accomplished by fibroblasts (Eastwood et al, 1998;Espinosa et al, 1984;Kamphorst et al, 1991;Sluijter et al, 2004;Tóth et al, 1998), and these cells therefore play a key role in aneurysmal growth.…”

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confidence: 99%

A theoretical model for fibroblast-controlled growth of saccular cerebral aneurysms

Kroon

Holzapfel

2009

Journal of Theoretical Biology

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A new theoretical model for the growth of saccular cerebral aneurysms is proposed by extending the recent constitutive framework of Kroon and Holzapfel (J. Theor. Biol., 247:775-787, 2007). The continuous turnover of collagen is taken to be the driving mechanism in aneurysmal growth. The collagen production rate depends on the magnitude of the cyclic deformation of fibroblasts, caused by the pulsating blood pressure during the cardiac cycle. The volume density of fibroblasts in the aneurysmal tissue is taken to be constant throughout the growth process. The growth model is assessed by considering the inflation of an axisymmetric membranous piece of aneurysmal tissue, with material characteristics representative of a cerebral aneurysm. The diastolic and systolic states of the aneurysm are computed, together with its load-free state. It turns out that the value of collagen pre-stretch, that determines growth speed and stability of the aneurysm, is of pivotal importance. The model is able to predict aneurysms with typical berry-like shapes observed clinically, and the predicted wall stresses correlate well with the experimentally obtained ultimate stresses of this type of tissue. The model predicts that aneurysms should fail when reaching a size of about 1.2-3.6 mm, which is smaller than what has been clinically observed. With some refinements, the model may, however, be used to predict future growth of diagnosed aneurysms.

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Correlation of inflammatory infiltrate with the enlargement of experimental aortic aneurysms

Cited by 200 publications

References 14 publications

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

Death of Smooth Muscle Cells and Expression of Mediators of Apoptosis by T Lymphocytes in Human Abdominal Aortic Aneurysms

A theoretical model for fibroblast-controlled growth of saccular cerebral aneurysms

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