Glycated human serum albumin enhances macrophage inflammatory protein-1β mRNA expression through protein kinase C-δ and NADPH oxidase in macrophage-like differentiated U937 cells

Higai, Koji; Satake, Misaki; Nishioka, Haruka; Azuma, Yutaro; Matsumoto, Kojiro

doi:10.1016/j.bbagen.2007.11.010

Cited by 19 publications

(12 citation statements)

References 30 publications

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“…As shown in Figure 1B , PKC δ and p38 that involved in CCR5 signaling pathway in macrophages were predicted as targets of WTD. As reported in previous literature, PKC δ and p38 could promote the expression of cytokines and chemokines in macrophages (Higai et al, 2008; Tang et al, 2010; Si et al, 2012; Ren et al, 2014; Park et al, 2015). Then, in vitro and in vivo tests were designed to validate the effect of WTD on CCR5 signaling pathway in macrophages.…”

Section: Discussionsupporting

confidence: 78%

Wu-Tou Decoction in Rheumatoid Arthritis: Integrating Network Pharmacology and In Vivo Pharmacological Evaluation

et al. 2017

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Purpose: This study aimed to explore underlying action mechanism of Wu-Tou decoction (WTD) in rheumatoid arthritis (RA) through network pharmacology prediction and experimental verification.Methods: Chemical compounds and human target proteins of WTD as well as RA-related human genes were obtained from TCM Database @ Taiwan, PubChem and GenBank, respectively. Subsequently, molecular networks and canonical pathways presumably involved in the treatment of WTD on RA were generated by ingenuity pathway analysis (IPA) software. Furthermore, experimental validation was carried out with MIP-1β-induced U937 cell model and collagen induced arthritis (CIA) rat model.Results: CCR5 signaling pathway in macrophages was shown to be the top one shared signaling pathway associated with both cell immune response and cytokine signaling. In addition, protein kinase C (PKC) δ and p38 in this pathway were treated as target proteins of WTD in RA. In vitro experiments indicated that WTD inhibited MIP-1β-induced production of TNF-α, MIP-1α, and RANTES as well as phosphorylation of CCR5, PKC δ, and p38 in U937 cells. WTD treatment maintained the inhibitory effects on production of TNF-α and RANTES in MIP-1β-induced U937 cells after CCR5 knockdown. In vivo experiments demonstrated that WTD ameliorated symptoms in CIA rats, decreased the levels of IL-1β, IL-2, IL-6, TNF-α, MIP-1α, MIP-2, RANTES, and IP-10 in serum of CIA rats, as well as mRNA levels of MIP-1α, MIP-2, RANTES, and IP-10 in ankle joints of CIA rats. Furthermore, WTD also lowered the phosphorylation levels of CCR5, PKC δ and p38 in both ankle joints and macrophages in ankle joints from CIA rats.Conclusion: It was demonstrated in this research that WTD played a role in inhibiting inflammatory response in RA which was closely connected with the modulation effect of WTD on CCR5 signaling pathway in macrophages.

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Section: Discussionsupporting

confidence: 78%

Wu-Tou Decoction in Rheumatoid Arthritis: Integrating Network Pharmacology and In Vivo Pharmacological Evaluation

et al. 2017

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“…Signal pathways regulated by AGE-derived ROS are cell type specific and may be associated with an increase of proinflammatory or proapoptotic events, and/or with suppression of antioxidant systems (37,53,54,63). The significant increase in nuclear translocation of NF-B/p65 in aortic rings from LAGEϩMG-fed Fig.…”

Section: Discussionmentioning

confidence: 91%

“…The AGE-induced translocation of p47 phox to the membrane was blocked by a selective inhibitor of PKC-␦, a kinase sensitive to extrinsic oxidants (37,53), suggesting that induction of PKC-␦ kinase activity is required for NOX activation and superoxide anion generation by AGEs in ECs. Consistent with this view, AGEs induced marked phosphorylation of PKC-␦ at residues Tyr-311 and Tyr-332, as effectively as H 2 O 2 .…”

Section: Discussionmentioning

confidence: 98%

AGER1 regulates endothelial cell NADPH oxidase-dependent oxidant stress via PKC-δ: implications for vascular disease

Cai¹,

Torreggiani²,

Zhu³

et al. 2010

American Journal of Physiology-Cell Physiology

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Advanced glycated end-product receptor 1 (AGER1) protects against vascular disease promoted by oxidants, such as advanced glycated end products (AGEs), via inhibition of reactive oxygen species (ROS). However, the specific AGEs, sources, and pathways involved remain undefined. The mechanism of cellular NADPH oxidase (NOX)-dependent ROS generation by defined AGEs, N(epsilon)-carboxymethyl-lysine- and methylglyoxal (MG)-modified BSA, was assessed in AGER1 overexpressing (AGER1(+) EC) or knockdown (sh-mRNA-AGER1(+) EC) human aortic endothelial (EC) and ECV304 cells, and aortic segments from old (18 mo) C57BL6-F(2) mice, propagated on low-AGE diet (LAGE), or LAGE supplemented with MG (LAGE+MG). Wild-type EC and sh-mRNA-AGER1(+) EC, but not AGER1(+) EC, had high NOX p47(phox) and gp91(phox) activity, superoxide anions, and NF-kappaB p65 nuclear translocation in response to MG and N(epsilon)-carboxymethyl-lysine. These events involved epidermal growth factor receptor-dependent PKC-delta redox-sensitive Tyr-311 and Tyr-332 phosphorylation and were suppressed in AGER1(+) ECs and enhanced in sh-mRNA-AGER1(+) ECs. Aortic ROS, PKC-delta Tyr-311, and Tyr-332 phosphorylation, NOX expression, and nuclear p65 in older LAGE+MG mice were significantly increased above that in age-matched LAGE mice, which had higher levels of AGER1. In conclusion, circulating AGEs induce NADPH-dependent ROS generation in vascular aging in both in vitro and in vivo models. Furthermore, AGER1 provides protection against AGE-induced ROS generation via NADPH.

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“…Recently, the protein kinase C (PKC) family was shown to be involved in ROS induction by AGEs [22,23]. To test the possible participation of PKCs, we employed two PKC inhibitors: Rottlerin The result of cell fractioning as described in the Materials and methods.…”

Section: Rottlerin Inhibits Ros Production Induced By Agesmentioning

confidence: 99%

Advanced glycation end products induce production of reactive oxygen species via the activation of NADPH oxidase in murine hepatic stellate cells

Guimarães

Empsen

Geerts

et al. 2010

Journal of Hepatology

194

131

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Glycated human serum albumin enhances macrophage inflammatory protein-1β mRNA expression through protein kinase C-δ and NADPH oxidase in macrophage-like differentiated U937 cells

Cited by 19 publications

References 30 publications

Wu-Tou Decoction in Rheumatoid Arthritis: Integrating Network Pharmacology and In Vivo Pharmacological Evaluation

Wu-Tou Decoction in Rheumatoid Arthritis: Integrating Network Pharmacology and In Vivo Pharmacological Evaluation

AGER1 regulates endothelial cell NADPH oxidase-dependent oxidant stress via PKC-δ: implications for vascular disease

Advanced glycation end products induce production of reactive oxygen species via the activation of NADPH oxidase in murine hepatic stellate cells

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