Monocyte activation by smooth muscle cell-derived matrices

Kaufmann, J; Jorgensen, Robin W.; Martin, Bernice M.; Franzblau, Carl

doi:10.1016/0021-9150(90)90103-p

Cited by 8 publications

(2 citation statements)

References 41 publications

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“…Kauffman et al (65) demonstrated that monocytes adhering to smooth muscle cell-derived matrix develop a functional phenotype change leading to an activated state. Furthermore, Pacifi et al (66) showed that bone matrix constituents including collagen fragments stimulate IL-1 release from human blood monocytes in a dose-dependent manner requiring physical contact.…”

Section: Discussionmentioning

confidence: 99%

Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.

Bernard

Szekély²,

Philip³

et al. 1992

J. Clin. Invest.

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Inflammatory mediators released by macrophages (M+) are believed to be involved in septic vasoplegia. To investigate the effect of My on vascular reactivity, excised rabbit carotids were exposed intraluminally either to peritoneal rabbit ME, activated by 18 h of incubation with 1 gg/ml lipopolysaccharide, or to the supernatants (SPN) derived from them. The contractile responses to phenylephrine (PE, 10-6 M) were determined by measuring changes in diameter using an ultrasonic microdimensiometer 1, 2, and 3 h after the first control contraction. In control arteries (n = 12), PE-induced contractions were, respectively, 102.9±3.3%, 95.2±4.1%, and 89.7±3.8% of the first contraction, after 1, 2, and 3 h. Activated M4 significantly reduced PE-stimulated contractions after as little as 1 h of carotid exposure (percentage of controls at 1, 2, or 3 h: 74.1±5.6, 57.2±5.2, and 34.2±5.6, n = 10, P < 0.001). The activated macrophage-derived SPN took longer to diminish carotid contractility than the Mt themselves, and became significant only after 2 h. The greater effect of Mt might be due to cooperation between Mt and vascular cells, as suggested by the amplified interleukin-1 release observed after Mt infusion. The presence of the endothelium partially protected carotid contractility from depression by activated Mt. Extraluminal addition of NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis prevented this depression in arteries with or without endothelium. No products of the oxidative pathway of L-arginine were detected in rabbit activated Mt. These results suggest that activation of this pathway in smooth muscle cells seems to be involved in vascular hypocontractility. (J. Clin.

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Section: Discussionmentioning

confidence: 99%

Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.

Bernard

Szekély²,

Philip³

et al. 1992

J. Clin. Invest.

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“…58,59 In some cases, the exposed ECMs were treated for 18 hours with chondroitinase ABC (2.0 U/mL) or heparitinase I (4.0 U/mL) in a buffer containing 10 mmol/L HEPES, pH 7.4, 140 mmol/L NaCl, 10 mol/L CaCl 2 , and 0.4% BSA (binding buffer). After the 18-hour incubation the enzymes were removed, and the wells were washed 3 times with binding buffer before proceeding with the binding studies.…”

Section: Preparation Of Plates With Whole Ecm and Individual Ecm Compmentioning

confidence: 99%

Sphingomyelinase, an Enzyme Implicated in Atherogenesis, Is Present in Atherosclerotic Lesions and Binds to Specific Components of the Subendothelial Extracellular Matrix

Marathe¹,

Kuriakose²,

Williams³

et al. 1999

ATVB

113

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Abstract-Atherosclerotic lesions contain an extracellular sphingomyelinase (SMase) activity that hydrolyzes the sphingomyelin of subendothelial low density lipoprotein (LDL). This SMase activity may promote atherosclerosis by enhancing subendothelial LDL retention and aggregation, foam cell formation, and possibly other atherogenic processes.The results of recent cell-culture studies have led to the hypothesis that a specific molecule called secretory SMase (S-SMase) is responsible for the SMase activity known to be in lesions, although its presence in atheromata had not been examined directly. Herein we provide immunohistochemical and biochemical support for this hypothesis. First, 2 different antibodies against S-SMase detected extracellular immunoreactive protein in the intima of mouse, rabbit, and human atherosclerotic lesions. Much of this material in lesions appeared in association with the subendothelial matrix. Second, binding studies in vitro demonstrated that 125 I-S-SMase adheres to the extracellular matrix of cultured aortic smooth muscle and endothelial cells, specifically to the laminin and collagen components. Third, in its bound state, S-SMase retains substantial enzymatic activity against lipoprotein substrates. Overall, these data support the hypothesis that S-SMase is an extracellular arterial wall SMase that contributes to the hydrolysis of the sphingomyelin of subendothelial LDL. S-SMase may therefore be an important participant in atherogenesis through local enzymatic effects that stimulate subendothelial retention and aggregation of atherogenic lipoproteins. (Arterioscler Thromb Vasc

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Routine Cell Culture

Martin

1994

Tissue Culture Techniques

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Monocyte activation by smooth muscle cell-derived matrices

Cited by 8 publications

References 41 publications

Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.

Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.

Sphingomyelinase, an Enzyme Implicated in Atherogenesis, Is Present in Atherosclerotic Lesions and Binds to Specific Components of the Subendothelial Extracellular Matrix

Routine Cell Culture

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