.ALPHA.1-Acid Glycoprotein Suppresses Rat Acute Inflammatory Paw Edema through the Inhibition of Neutrophils Activation and Prostaglandin E2 Generation

Matsumoto, Kazuaki; Nishi, Koji; Kikuchi, Mari; Kadowaki, Daisuke; Tokutomi, Yoshiko; Tokutomi, Naofumi; Nishi, Katsuhide; Suenaga, Atsushi; Otagiri, Masaki

doi:10.1248/bpb.30.1226

Cited by 23 publications

(13 citation statements)

References 38 publications

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“…29,35 Orosomucoid is also bound to the surface of cultured bovine pulmonary microvascular endothelial cells. 36 It has been found that orosomucoid modulates the transport of charged solutes across the wall of peripheral and cerebral microvessels in vivo by decreasing the transport of negatively charged molecules but increasing that of positively charged ones, 13,23,46 suggesting that orosomucoid plays an essential role in maintaining the permeability property of endothelium by adding negative charge to the SGL.…”

Section: Introductionmentioning

confidence: 99%

Effect of Surface Charge of Immortalized Mouse Cerebral Endothelial Cell Monolayer on Transport of Charged Solutes

Yuan

2010

Ann Biomed Eng

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Abstract-Charge carried by the surface glycocalyx layer (SGL) of the cerebral endothelium has been shown to significantly modulate the permeability of the blood-brain barrier (BBB) to charged solutes in vivo. The cultured monolayer of bEnd3, an immortalized mouse cerebral endothelial cell line, is becoming a popular in vitro BBB model due to its easy growth and maintenance of many BBB characteristics over repeated passages. To test whether the SGL of bEnd3 monolayer carries similar charge as that in the intact BBB and quantify this charge, which can be characterized by the SGL thickness (L f ) and charge density (C mf ), we measured the solute permeability of bEnd3 monolayer to neutral solutes and to solutes with similar size but opposite charges: negatively charged a-lactalbumin (À11) and positively charged ribonuclease (+3). Combining the measured permeability data with a transport model across the cell monolayer, we predicted the L f and the C mf of bEnd3 monolayer, which is~160 nm and~25 mEq/L, respectively. We also investigated whether orosomucoid, a plasma glycoprotein modulating the charge of the intact BBB, alters the charge of bEnd3 monolayer. We found that 1 mg/mL orosomucoid would increase SGL charge density of bEnd3 monolayer to~2-fold of its control value.

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Section: Introductionmentioning

confidence: 99%

Effect of Surface Charge of Immortalized Mouse Cerebral Endothelial Cell Monolayer on Transport of Charged Solutes

Yuan

2010

Ann Biomed Eng

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“…3) We have seen that thalidomide acts at different levels of regulation and there are reports of this molecule acting at the very fundamental level of DNA. A very recent in situ electrochemical and atomic force microscopy (AFM) study of thalidomide-DNA interaction has been reported by Oliveira et al (2009) [145]. The main findings of the study convey that, thalidomide interacts specifically with the dsDNA by intercalating between the bases and inducing structural changes in B-DNA, in a time-dependent manner.…”

Section: Other Mechanisms Involved In the Inhibition Of Tnf-by Thalidmentioning

confidence: 96%

“…Interestingly, thalidomide is seen to have specific interaction with GC-rich promoter sequences [96]. Reports convey that, thalidomide can regulate the GC-rich promoter of vascular endothelial growth factor (VEGF) and also down regulate the basic fibroblast growth factor (bFGF) expression in glioma cells [145]. Drucker et al(2003) and group showed that thalidomide down regulates transcription levels of GC-rich promoter genes in multiple myeloma (MM) [146].…”

Section: Other Mechanisms Involved In the Inhibition Of Tnf-by Thalidmentioning

confidence: 99%

TNF α Signaling Beholds Thalidomide Saga: A Review of Mechanistic Role of TNF-α Signaling Under Thalidomide

Majumder¹,

Sreedhara²,

Banerjee³

et al. 2012

CTMC

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Tumor necrosis factor alpha (TNF-α) is a pleiotropic inflammatory cytokine. The cytokine possesses both growth stimulating properties and growth inhibitory processes, and it appears to have self regulatory properties as well. Agents like etanercept and infliximab showed beneficial effects against rheumatoid arthritis by modulationg TNF-α proteins, however, these agents are largely unable to penetrate the blood-brain barrier, which severely limits their use in different conditions. Thalidomide, an inhibitor of TNF-α protein synthesis is readily capable of crossing the blood-brain barrier and thus thalidomide and its analogs are excellent candidates for use in determining the potential value of anti-TNF-α therapies in a variety of diseases. Thalidomide blocks TNF-α expression by different possible mechanisms. Down regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), an essential transcription factor for TNF and other cytokines under thalidomide treatment leads to reduction in the TNF-α expression. Additionally, myeloid differentiation factor 88 (MyD88), an adapter protein regulates the expression of TNF under thalidomide treatment. Thalidomide treatment also leads to destruction of TNF-α mRNA thus, reducing the total expression of TNF-α protein. Thalidomide also targets reactive oxygen species (ROS) and α(1)-acid glycoprotein (AGP) to regulate TNF-α. In the present review, we discuss different possible mechanism that regulates TNF-α under thalidomide treatment. Additionally, we suggest novel strategies for the future targeting combination therapies of thalidomide and its analogs with different other anti-inflammatory drug to curb TNF-α associated diseases.

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“…Alpha-(1)-acid glycoprotein (AGP) (normal range=0-130 ng/ml), an acute-phase protein, was measured on days 0 (preoperative), 7 and 14 (19).…”

Section: S Aureus Strains and Infection Processmentioning

confidence: 99%

Active and Passive Immunization Against Staphylococcus aureus Periprosthetic Osteomyelitis in Rats

Søe

Jensen

et al. 2017

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.ALPHA.1-Acid Glycoprotein Suppresses Rat Acute Inflammatory Paw Edema through the Inhibition of Neutrophils Activation and Prostaglandin E2 Generation

Abstract: a 1 -Acid glycoprotein (AGP), a member of the lipocalin family, is a polypeptide containing 2 disulfide bonds and 5 carbohydrate chains, the latter of which account for about 40% of its total mass of 40 kDa.1-4) The half-life of 125

Cited by 23 publications

References 38 publications

Effect of Surface Charge of Immortalized Mouse Cerebral Endothelial Cell Monolayer on Transport of Charged Solutes

Effect of Surface Charge of Immortalized Mouse Cerebral Endothelial Cell Monolayer on Transport of Charged Solutes

TNF α Signaling Beholds Thalidomide Saga: A Review of Mechanistic Role of TNF-α Signaling Under Thalidomide

Active and Passive Immunization Against Staphylococcus aureus Periprosthetic Osteomyelitis in Rats

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.ALPHA.1-Acid Glycoprotein Suppresses Rat Acute Inflammatory Paw Edema through the Inhibition of Neutrophils Activation and Prostaglandin E2 Generation

Abstract: a 1 -Acid glycoprotein (AGP), a member of the lipocalin family, is a polypeptide containing 2 disulfide bonds and 5 carbohydrate chains, the latter of which account for about 40% of its total mass of 40 kDa.1-4) The half-life of 125

Cited by 23 publications

References 38 publications

Effect of Surface Charge of Immortalized Mouse Cerebral Endothelial Cell Monolayer on Transport of Charged Solutes

Effect of Surface Charge of Immortalized Mouse Cerebral Endothelial Cell Monolayer on Transport of Charged Solutes

TNF &alpha; Signaling Beholds Thalidomide Saga: A Review of Mechanistic Role of TNF-&alpha; Signaling Under Thalidomide

Active and Passive Immunization Against Staphylococcus aureus Periprosthetic Osteomyelitis in Rats

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TNF α Signaling Beholds Thalidomide Saga: A Review of Mechanistic Role of TNF-α Signaling Under Thalidomide