MIGRATION RESPONSES OF HUMAN MONOCYTIC CELL LINES TO Α- AND Β-Chemokines

Cross, Alison K.; Richardson, V. J.; Ali, Selman A.; Palmer, Ian R.; Taub, Dennis D.; Rees, RC

doi:10.1006/cyto.1996.0196

Cited by 56 publications

(40 citation statements)

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“…This is consistent with our data, where all the chemokines induced (MIP-1␣, MIP-1␤, MCP-1, IP-10, and RANTES) have been implicated in the chemotaxis of macrophages (56,57) and microglia (50,51,53), the predominant cell types recruited into the demyelinating lesion during cuprizone treatment (23). MIP-2, lymphotactin, eotaxin, and TCA-3 were not observed (Fig.…”

Section: Discussionsupporting

confidence: 93%

Absence of Macrophage-Inflammatory Protein-1α Delays Central Nervous System Demyelination in the Presence of an Intact Blood-Brain Barrier

McMahon

Cook

Suzuki

et al. 2001

The Journal of Immunology

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Chemokines are small chemotactic cytokines that modulate leukocyte recruitment and activation during inflammation. Here, we describe the role of macrophage inflammatory protein-1α (MIP-1α) during cuprizone intoxication, a model where demyelination of the CNS features a large accumulation of microglia/macrophage without T cell involvement or blood-brain barrier disruption. RNase protection assays showed that mRNA for numerous chemokines were up-regulated during cuprizone treatment in wild-type, C57BL/6 mice. RANTES, inflammatory protein-10, and monocyte chemoattractant protein-1 showed greatest expression with initiation of insult at 1–2 wk of treatment, whereas MIP-1α and β increased later at 4–5 wk, coincident with peak demyelination and cellular accumulation. The function of MIP-1α during demyelination was tested in vivo by exposing MIP-1α knockout mice (MIP-1α−/−) to cuprizone and comparing pathology to wild-type mice. Demyelination at 3.5 wk of treatment was significantly decreased in MIP-1α−/− mice (∼36% reduction), a result confirmed by morphology at the electron microscopic level. The delay in demyelination was correlated to apparent decreases in microglia/macrophage and astrocyte accumulation and in TNF-α protein levels. It was possible that larger effects of the MIP-1α deficiency were being masked by other redundant chemokines. Indeed, RNase protection assays revealed increased expression of several chemokine transcripts in both untreated and cuprizone-treated MIP-1α−/− mice. Nonetheless, despite this possible compensation, our studies show the importance of MIP-1α in demyelination in the CNS and highlight its effect, particularly on cellular recruitment and cytokine regulation.

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Section: Discussionsupporting

confidence: 93%

Absence of Macrophage-Inflammatory Protein-1α Delays Central Nervous System Demyelination in the Presence of an Intact Blood-Brain Barrier

McMahon

Cook

Suzuki

et al. 2001

The Journal of Immunology

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“…32,58 The above data prompted us to investigate the relationships that might exist between the different MAPK pathways and the migration of MonoMac6 cells in response to MCP-1. To address this question, 2 types of migratory conditions were tested corresponding to a transendothelial migration or a simple chemotaxis through an acellular filter.…”

Section: Discussionmentioning

confidence: 99%

Signal transduction involved in MCP-1–mediated monocytic transendothelial migration

Cambien

Pomeranz

Millet

et al. 2001

Blood

121

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“…For these experiments we adopted as a model the MonoMac-6 cell line [45,46] . At a concentration of AVE8134 specifically activating PPARα but not the other subtypes (1 µmol/L), we observed increases in the expression of the scavenger receptor genes CD36 and MSR1.…”

Section: Comparison Of Ave8134 To Other Pparα Agonistsmentioning

confidence: 99%

The peroxisome proliferator-activated receptor-α (PPAR-α) agonist, AVE8134, attenuates the progression of heart failure and increases survival in rats

Linz

Wohlfart

Baader³

et al. 2009

Acta Pharmacol Sin

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Aim: To investigate the efficacy of the peroxisome proliferator-activated receptor-α (PPARα) agonist, AVE8134, in cellular and experimental models of cardiac dysfunction and heart failure. Methods: In Sprague Dawley rats with permanent ligation of the left coronary artery (post-MI), AVE8134 was compared to the PPARγ agonist rosiglitazone and in a second study to the ACE inhibitor ramipril. In DOCA-salt sensitive rats, efficacy of AVE8134 on cardiac hypertrophy and fibrosis was investigated. Finally, AVE8134 was administered to old spontaneously hypertensive rats (SHR) at a nonblood pressure lowering dose with survival as endpoint. In cellular models, we studied AVE8134 on hypertrophy in rat cardiomyocytes, nitric oxide signaling in human endothelial cells (HUVEC) and LDL-uptake in human MonoMac-6 cells. Results: In post-MI rats, AVE8134 dose-dependently improved cardiac output, myocardial contractility and relaxation and reduced lung and left ventricular weight and fibrosis. In contrast, rosiglitazone exacerbated cardiac dysfunction. Treatment at AVE8134 decreased plasma proBNP and arginine and increased plasma citrulline and urinary NOx/creatinine ratio. In DOCA rats, AVE8134 prevented development of high blood pressure, myocardial hypertrophy and cardiac fibrosis, and ameliorated endothelial dysfunction. Compound treatment increased cardiac protein expression and phosphorylation of eNOS. In old SHR, treatment with a low dose of AVE8134 improved cardiac and vascular function and increased life expectancy without lowering blood pressure. AVE8134 reduced phenylephrine-induced hypertrophy in adult rat cardiomyocytes. In HUVEC, Ser-1177-eNOS phosphorylation but not eNOS expression was increased. In monocytes, AVE8134 increased the expression of CD36 and the macrophage scavenger receptor 1, resulting in enhanced uptake of oxidized LDL. Conclusion: The PPARα agonist AVE8134 prevents post-MI myocardial hypertrophy, fibrosis and cardiac dysfunction. AVE8134 has beneficial effects against hypertension-induced organ damages, resulting in decreased mortality. The compound exerts its protective properties by a direct effect on cardiomyocyte hypertrophy, but also indirectly via monocyte signaling and increased endothelial NO production.

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MIGRATION RESPONSES OF HUMAN MONOCYTIC CELL LINES TO Α- AND Β-Chemokines

Cited by 56 publications

References 0 publications

Absence of Macrophage-Inflammatory Protein-1α Delays Central Nervous System Demyelination in the Presence of an Intact Blood-Brain Barrier

Absence of Macrophage-Inflammatory Protein-1α Delays Central Nervous System Demyelination in the Presence of an Intact Blood-Brain Barrier

Signal transduction involved in MCP-1–mediated monocytic transendothelial migration

The peroxisome proliferator-activated receptor-α (PPAR-α) agonist, AVE8134, attenuates the progression of heart failure and increases survival in rats

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