MCP-1-induced enhancement of THP-1 adhesion to vascular endothelium was modulated by HMG-CoA reductase inhibitor through RhoA GTPase-, but not ERK1/2-dependent pathway

Hiraoka, M; Nitta, Noriko; Nagai, Megumi; Shimokado, Kentaro; Yoshida, Masayuki

doi:10.1016/j.lfs.2004.02.028

Cited by 40 publications

(34 citation statements)

References 9 publications

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“…This apparent discord may relate to the different cell types used. In support of our data, a study by Hiraoka et al on monocyte motility found that pitavastatin treatment of THP-1 cells reduced RhoA activity (24), corroborating our finding of reduced RhoA activity in THP-1 cells.…”

Section: Prenylation-deficient Rhoa Has Reduced Gtp Binding Activity supporting

confidence: 93%

“…Patients suffering from MKD have severely reduced protein prenylation, but it is not fully understood how decreased prenylation is related to function of proteins that would normally be prenylated. As we and others have shown, lack of prenylation can affect activity of small GTPases (16,24). However these effects can differ between cell types and tissues.…”

Section: Discussionmentioning

confidence: 80%

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Unprenylated RhoA Contributes to IL-1β Hypersecretion in Mevalonate Kinase Deficiency Model through Stimulation of Rac1 Activity

Burgh

Pervolaraki

Turkenburg

et al. 2014

Journal of Biological Chemistry

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Background: Shortage of isoprenoids causes aberrant activity of prenylated small GTPases. Results: Inactivation of RhoA due to lack of prenylation leads to Rac1 activation and subsequent priming for IL-1␤ secretion. Conclusion: RhoA inactivation contributes to the pathology of isoprenoid deficiency. Significance: Insight into the multiple networks involving RhoA will benefit new intervention strategies in prenylation-related pathologies.

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Section: Prenylation-deficient Rhoa Has Reduced Gtp Binding Activity supporting

confidence: 93%

Section: Discussionmentioning

confidence: 80%

Unprenylated RhoA Contributes to IL-1β Hypersecretion in Mevalonate Kinase Deficiency Model through Stimulation of Rac1 Activity

Burgh

Pervolaraki

Turkenburg

et al. 2014

Journal of Biological Chemistry

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“…Recent studies have shown that pitavastatin has multiple effects, such as reducing inflammation 11) and the generation of reactive oxygen species 12) , improving endothelial function 13) , increasing nitric oxide production 14) , inhibiting cell adhesion 15) , inhibiting the contraction of smooth muscle cells 16) , and promoting apolipoprotein (apo) A-production 17) . Pitavastatin has a potent lipid-lowering effect, and the reduction of LDL-C is comparable to that achieved with atorvastatin 10) .…”

Section: Discussionmentioning

confidence: 99%

Influence of Pitavastatin on Glucose Tolerance in Patients with Type 2 Diabetes Mellitus

Yamakawa

Tajiri

Tanaka

et al. 2008

JAT

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Aim:We previously reported that glycemic control deteriorated in patients receiving atorvastatin, which is useful for the treatment of hypercholesterolemia in patients with type 2 diabetes. Pitavastatin has a strong lipid-lowering effect, comparable to that of atorvastatin, but it is unknown whether pitavastatin has an adverse influence on glycemic control. The aim of this study was to examine. The effects of three different statins (pravastatin, atorvastatin, and pitavastatin) on blood glucose and HbA1c levels in diabetic patients. Methods: We retrospectively compared glycemic control between groups receiving atorvastatin (10 mg/day, group A, n 99), pravastatin (10 mg/day, group Pr, n 85), and pitavastatin (2 mg/day, group Pi, n 95) from the start of treatment until 3 months later. Patients were excluded if the dosage of their antidiabetic drugs was changed, if their drug therapy was altered within 3 months before starting statin therapy, or if events occurred that could affect glycemic control such as hospitalization. Results: The subjects available for analysis were 74 patients from group A, 71 patients from group Pr, and 74 patients from group Pi. Arbitrary blood glucose levels increased from 147 51 mg/dL (mean SD) to 176 69 mg/dL in group A, but only changed minimally from 136 31 to 134 32 mg/dL in group Pr and from 155 53 to 154 51 mg/dL in group Pi. HbA1c increased from 7.0 1.1% to 7.4 1.2% in group A, while it was 6.9 0.9% versus 6.9 1.0% in group Pr, and 7.3 1.0% versus 7.2 1.0% in group Pi. There was no correlation between LDL-C and HbA1c (the change from baseline to 3 months) in any of the groups. Conclusion: The glycemic parameters only increased significantly in group A, suggesting that pitavastatin and pravastatin did not have an adverse influence on glycemic control in type 2 diabetic patients. J Atheroscler

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“…24) Pitavastatin (10 mM) was suggested to play an anti-inflammatory role through the RhoA-dependent pathway in monocytic THP-1 cells. 38) Other studies have demonstrated that statins may regulate cytokine-induced IL-6 level through different signal pathways that involve both Y27632-sensitive and -insensitive molecular signaling, in particular the NF-kB pathway. 25) Our results demonstrate that the effect of pitavastatin at a low dose appears to be specific to the inhibition of HMG-CoA reductase, as the addition of MEV abolishes the inhibitory effect of pitavastatin.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory Effect of Pitavastatin on NF-.KAPPA.B Activated by TNF-.ALPHA. in Hepatocellular Carcinoma Cells

Wang

Tokoro

Higa

et al. 2006

Biological & Pharmaceutical Bulletin

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MCP-1-induced enhancement of THP-1 adhesion to vascular endothelium was modulated by HMG-CoA reductase inhibitor through RhoA GTPase-, but not ERK1/2-dependent pathway

Cited by 40 publications

References 9 publications

Unprenylated RhoA Contributes to IL-1β Hypersecretion in Mevalonate Kinase Deficiency Model through Stimulation of Rac1 Activity

Unprenylated RhoA Contributes to IL-1β Hypersecretion in Mevalonate Kinase Deficiency Model through Stimulation of Rac1 Activity

Influence of Pitavastatin on Glucose Tolerance in Patients with Type 2 Diabetes Mellitus

Anti-inflammatory Effect of Pitavastatin on NF-.KAPPA.B Activated by TNF-.ALPHA. in Hepatocellular Carcinoma Cells

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