The effect of tumor necrosis factor binding protein and interleukin-1 receptor antagonist on the development of abdominal aortic aneurysms in a rat model

Hingorani, Anil; Ascher, Enrico; Scheinman, Marcel; Yorkovich, William; DePippo, Patrick; Ladoulis, Charles T.; Salles-Cunha, Sérgio X.

doi:10.1016/s0741-5214(98)70139-9

Cited by 34 publications

(42 citation statements)

References 10 publications

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“…Since this model exhibits several similarities with hu- man abdominal aortic aneurysms [5], various laboratories have used it to investigate the pathogenesis and prevention of aneurysm growth. Unfortunately, the mortality rate in this model has not been mentioned in previous reports [1][2][3][4][5][6][7][8][9][10][11]. Although 2 h of elastase infusion time and a 1-cm segment of aorta have been used in all studies since Anidjar et al first described this model in 1990 [1], we noted a high mortality rate in the experimental animals.…”

Section: Discussionmentioning

confidence: 65%

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Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

Yamaguchi¹,

Yokokawa

Suzuki

et al. 1999

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 65%

“…The elastase-induced rat aneurysm model is one of a few established in vivo aneurysm models and is used in many laboratories [1][2][3][4][5][6][7][8][9][10][11]. Commonly the rats are given drugs containing anti-inflammatory agents before or after elastase infusion to investigate the pathogenesis and prevention of aneurysm formation.…”

Section: Introductionmentioning

confidence: 99%

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

Yamaguchi¹,

Yokokawa

Suzuki

et al. 1999

Journal of Surgical Research

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“…Since this experimental model exhibits several similarities to human abdominal aortic aneurysms, 14 a variety of laboratories have used it to investigate the pathogenesis and prevention of aneurysm growth. 10,12,13,[15][16][17][18][19][21][22][23][24] In this study, we used a modification of the model that we recently described. 25 An inflammatory response is a critical step in this model.…”

Section: Discussionmentioning

confidence: 99%

“…8 An elastase-induced rat aneurysm model is commonly used to investigate the pathogenesis and prevention of abdominal aortic aneurysms. [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] In this model, inflammatory cell infiltration of the aortic wall occurs in temporal relation to an increase in the aortic diameter. 9,11,13,14 Inflammatory cell infiltration is considered to be a critical step in the development of aortic aneurysms in these rats.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Immunosuppression on Aortic Dilatation in a Rat Aneurysm Model

et al. 2000

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This study was conducted to investigate whether systemic immunosuppression attenuated aortic dilatation in a rat aneurysm model. Sprague-Dawley rats were subjected to elastase infusion of the infrarenal aorta and divided into two groups of 12 rats each. The immunosuppression group (group 1) was given subcutaneous injections of cyclosporine A (5 mg/kg per day), azathioprine (2 mg/kg per day), and methylprednisolone (2 mg/kg per day) from the operative day until postoperative day (POD) 6. An additional subcutaneus injection of cyclophosphamide 30 mg/kg was also given on the operative day. The control group (group 2) was given subcutaneous injections of saline. Relaparotomy was performed on POD 7. After measurement of the aortic diameter, aortography and ultrasonography were performed in three rats from each group, following which the aortas were excised for histologic examination. The aortic diameter was significantly smaller in group 1 (2.58 +/- 0.37 mm) than in group 2 (6.21 +/- 1.74 mm) (P < 0.01) and the aortic lumen was slightly dilated in group 1, whereas it was spherically dilated in group 2. Total loss of elastic tissue was seen in both groups. Inflammatory cell infiltration and collagen fiber fragmentation were noted in group 2, whereas very little inflammatory cell infiltration and well-preserved collagen fibers were seen in group 1. These findings showed that immunosuppression attenuates aortic dilatation, partly by preserving the collagen fibers, in this rat aneurysm model.

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“…Previous studies have demonstrated the critical role of inflammatory cytokines in the pathogenesis of AAA through animal models. For example, it was demonstrated thataneurysm formation was attenuated in an elastase-induced rat AAA model by blocking the action of tumor necrosis factor-α (TNF-α) [13]. Furthermore, inflammatory cells such as monocytes have an important role in AAA pathogenesis through the secretion and activation of MMPs [14].…”

Section: Introductionmentioning

confidence: 99%

MCP-1 Stimulates MMP-9 Expression via ERK 1/2 and p38 MAPK Signaling Pathways in Human Aortic Smooth Muscle Cells

Yang¹,

Wen

Li³

et al. 2014

Cell Physiol Biochem

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Objective: We investigated the molecular mechanism underlying the role of monocyte chemoattractant protein-1 (MCP-1) in the formation and development of human abdominal aortic aneurysm (AAA). Methods: We examined protein expression profiles using a protein array and found that MCP-1 was the most highly expressed protein in AAA tissues compared with normal aortas. To investigate the potential mechanism of MCP-1 involvement in the pathogenesis of AAA, we treated human aortic smooth muscle cells (HASMCs) with human recombinant MCP-1. Results: MCP-1 was the most highly expressed protein in AAA tissues compared with normal aorta; matrix metalloproteinase-9 (MMP-9) expression was also significantly increased. Treatment with MCP-1 significantly increased the expression and activation of MMP-9 and activated the three major mitogen activated protein kinases (MAPKs) extracellular signal regulated kinase (ERK), c-Jun amino terminal kinase (JNK1/2) and p38 MAPK. Furthermore, MCP-1-induced secretion of MMP-9 was inhibited by U0126 (inhibitor of the ERK 1/2 pathway) and SB203580 (inhibitor of the p38 MAPK pathway), but not SP600125 (inhibitor of the JNK1/2 pathway). Conclusion: These data demonstrate that MCP-1 stimulates secretion of MMP-9 directly through the ERK1/2 and p38 MAPK mediated pathways in HASMCs. Thus, inhibition of this molecular mechanism might be a potential therapeutic target in the non-surgical treatment of AAA.

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The effect of tumor necrosis factor binding protein and interleukin-1 receptor antagonist on the development of abdominal aortic aneurysms in a rat model

Abstract: TNF-BP, but not IL-1RA, may inhibit the development of AAAs in this model.

Cited by 34 publications

References 10 publications

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

Shortened Elastase Infusion Time in the Elastase-Induced Rat Aneurysm Model

The Effect of Immunosuppression on Aortic Dilatation in a Rat Aneurysm Model

MCP-1 Stimulates MMP-9 Expression via ERK 1/2 and p38 MAPK Signaling Pathways in Human Aortic Smooth Muscle Cells

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