Cellular localization of matrix metalloproteinases in the abdominal aortic aneurysm wall

Newman, K M; Jean-Claude, Jessie; Li, Hong; Scholes, John V.; Osuga, Yutaka; Nagase, Hideaki; Tilson, M. David

doi:10.1016/s0741-5214(94)70169-5

Cited by 211 publications

(127 citation statements)

References 31 publications

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“…This occurs in the intima, and in atherosclerotic lesions, in the adventitia. In the latter area there is also perivascular cuffing (27,28) where the infiltrating leukocytes chronically secrete IL-1 and TNF, denoting an ongoing inflammatory process (28,29). We examined tissue sections from abdominal aortic aneurysms and found clusters of infiltrating mononuclear cells.…”

Section: Resultsmentioning

confidence: 99%

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Modur¹,

Feldhaus²,

Weyrich³

et al. 1997

J. Clin. Invest.

181

139

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Section: Resultsmentioning

confidence: 99%

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Modur¹,

Feldhaus²,

Weyrich³

et al. 1997

J. Clin. Invest.

181

139

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“…Phorbol esters have been reported to induce MMP-9 synthesis by human umbilical vein endothelial cells (42). Furthermore, rat carotid artery intimal smooth muscle cells have been found to produce 92-kd type IV collagenase after balloon catheter injury (29), and increased synthesis of MMP-9 by macrophages and smooth muscle cells has also been documented in atherosclerotic plaques (43) as well as abdominal aortic aneurysms (44). The circulating MMP-9 may thus originate from any of the above cells.…”

Section: Discussionmentioning

confidence: 99%

Elevated levels of 92‐kd type IV collagenase (matrix metalloproteinase 9) in giant cell arteritis

Sorbi

French

Nuovo

et al. 1996

Arthritis & Rheumatism

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Objective. To determine if circulating gelatinase activity and matrix metalloproteinase 9 (MMP-9) (gelatinase B, or 92-kd type IV collagenase) antigenic levels are elevated in sera of patients with giant cell arteritis (GCA), and to ascertain if MMP-9 messenger RNA (mRNA) is deposited in situ at sites of disease involvement.Methods. Serum samples were collected from 12 patients with GCA and 12 healthy volunteers. Vascular tissue was obtained a t the time of temporal artery biopsy. Type IV collagenase activity was determined by gelatin substrate zymography and the quantitative biotinylated gelatin substrate degradation assay. A doublesandwich immunoassay utilizing 2 different isotypes of monoclonal antibodies generated against MMP-9 was used for measuring serum MMP-9 antigenic levels. Finally, to localize sites of MMP-9 mRNA transcription in inflamed arteries, the method of reverse transcriptase in situ polymerase chain reaction (RTisPCR) was utilized.Results. Serum gelatinase activity and MMP-9 titers were significantly increased in patients with GCA (mean f SEM 198.9 f 36.9 p g gelatin/hour/ml serum, versus 21.2 f 4.0 in controls; P = 0.0006). The differences in antigenic MMP-9 levels were even more prominent (3005.4 & 900.6 ng/ml and 31.6 -C 9.8 ng/ml in GCA aIid control sera, respectively; P = 0.007). By

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“…Matrix metalloproteinases (MMPs) play important roles in such mechanisms of AAA, and pathological vascular remodeling is considered to be mediated by MMPs secreted by invasive macrophages, migrating vascular smooth muscle cells, and endothelial cells. [1][2][3] The expression of MMP-1, MMP-2, MMP-3, MMP-9, and MMP-12 are significantly increased in harvested human aneurysms. [1][2][3][4][5][6] These findings suggest that MMP are strongly associated with the activity of the disease.…”

mentioning

confidence: 99%

“…[1][2][3] The expression of MMP-1, MMP-2, MMP-3, MMP-9, and MMP-12 are significantly increased in harvested human aneurysms. [1][2][3][4][5][6] These findings suggest that MMP are strongly associated with the activity of the disease. From this viewpoint, pharmacological strategies to inhibit MMP might prevent the progression from asymptomatic to critical large AAA, resulting in a delay or avoidance of surgical repair.…”

mentioning

confidence: 99%

Inhibition of Experimental Abdominal Aortic Aneurysm in the Rat by Use of Decoy Oligodeoxynucleotides Suppressing Activity of Nuclear Factor κB and ets Transcription Factors

Nakashima

Aoki²,

Miyake³

et al. 2004

Circulation

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Background-Two phenomena, inflammation and matrix degradation, contribute to the progression of abdominal aortic aneurysm (AAA). Importantly, the inflammation is regulated by the transcription factor nuclear factor (NF)-B, whereas the destruction and degradation of elastin fibers by matrix metalloproteinases (MMP) are regulated by ets. Thus, we developed a novel strategy to treat AAA by simultaneous inhibition of both NF-B and ets by using chimeric decoy oligodeoxynucleotides (ODN). Methods and Results-AAA was induced in rats by transient aortic perfusion with elastase, whereas transfection of decoy ODN was performed by wrapping a delivery sheet containing decoy ODN around the aorta. Gel-mobility shift assay at 7 days after treatment demonstrated that both NF-B and ets binding activity were simultaneously inhibited by chimeric decoy ODN. Transfection of chimeric decoy ODN resulted in significant inhibition of the progression of AAA such as aneurysmal dilation at 4 weeks after treatment as compared with control, accompanied by a reduction of MMP expression. Moreover, the destruction of elastin fibers was inhibited in the aorta transfected with chimeric decoy ODN. Importantly, transfection of chimeric decoy ODN demonstrated potent inhibition of aneurysmal dilatation compared with NF-B decoy ODN alone, whereas scrambled decoy ODN had no effects. Interestingly, the migration of macrophages was significantly inhibited by chimeric decoy ODN. Conclusions-We

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Cellular localization of matrix metalloproteinases in the abdominal aortic aneurysm wall

Cited by 211 publications

References 31 publications

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Elevated levels of 92‐kd type IV collagenase (matrix metalloproteinase 9) in giant cell arteritis

Inhibition of Experimental Abdominal Aortic Aneurysm in the Rat by Use of Decoy Oligodeoxynucleotides Suppressing Activity of Nuclear Factor κB and ets Transcription Factors

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