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Wnt1 Participates in Inflammation Induced by Lipopolysaccharide Through Upregulating Scavenger Receptor A and NF-kB.

Zhao W, Sun Z, Wang S, Li Z, Zheng L - Inflammation (2015)

Bottom Line: THP-1 cells were activated with phorbol-12-myristate-13-acetate (PMA) and treated with LPS to induce inflammation.Inhibitor of β-catenin and siRNA of FZD1were used to investigate the signaling events involved in SRA activation induced by wnt1.Wnt1 promoted SRA expression through activation of canonical wnt pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, 79Qingchun Road, Hangzhou, 310003, China.

ABSTRACT
The study investigated the role of wnt1 in the inflammatory response initiated by lipolysaccharide (LPS), and analyzed the association between wnt1, NF-KB, and inflammatory factors. THP-1 cells were activated with phorbol-12-myristate-13-acetate (PMA) and treated with LPS to induce inflammation. THP-1 cells were transfected with wnt1siRNA and overexpression plasmid to explore the relationship among wnt1, SRA, and NF-KB. Inhibitor of β-catenin and siRNA of FZD1were used to investigate the signaling events involved in SRA activation induced by wnt1. Levels of NF-kB protein and inflammatory cytokines were assessed followingwnt1 siRNA and LPS treatment. PMA activation and LPS treatment of THP-1 cells increased wnt1 protein levels. Wnt1 promoted SRA expression through activation of canonical wnt pathway. Wnt1 increased NF-kB protein levels and enhanced the secretion of IL-6, TNF-α, and iNOS through binding to SRA. These findings suggest that wnt1 increased SRA and NF-kB protein levels and participated in the inflammatory response.

No MeSH data available.


Related in: MedlinePlus

NF-kB was activated by wnt1 through increasing SRA expression. a SRA protein level was decreased in THP-1 cells transfected with wnt1 siRNA while ectopic expression of wnt1 increased it (p < 0.05), and TLR4 protein level was unchanged with either siRNA-wnt1 transfection or ectopic expression of wnt1. bwnt1 siRNA transfection decreased SRA expression induced by LPS (p < 0.05). c SRA protein level was increased following concentration gradient of human wnt1 recombination protein (p < 0.05). d p65 protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with SRA siRNA (p < 0.05). e p65 protein level was increased following concentration gradient of human wnt1 recombination protein (from 0 to 15 ug/ml) (p < 0.05). Results were normalized against levels of GAPDH protein.
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Fig3: NF-kB was activated by wnt1 through increasing SRA expression. a SRA protein level was decreased in THP-1 cells transfected with wnt1 siRNA while ectopic expression of wnt1 increased it (p < 0.05), and TLR4 protein level was unchanged with either siRNA-wnt1 transfection or ectopic expression of wnt1. bwnt1 siRNA transfection decreased SRA expression induced by LPS (p < 0.05). c SRA protein level was increased following concentration gradient of human wnt1 recombination protein (p < 0.05). d p65 protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with SRA siRNA (p < 0.05). e p65 protein level was increased following concentration gradient of human wnt1 recombination protein (from 0 to 15 ug/ml) (p < 0.05). Results were normalized against levels of GAPDH protein.

Mentions: To explore the detail mechanism involved in NF-kB activation induced by wnt1, the expression of SRA andTLR4 was detected through transfection of wnt1 siRNA or overexpression plasmid. As shown in Fig. 3a, wnt1 increased SRA expression but had no effect on levels of TLR4. Transfection with wnt1 siRNA also decreased levels of SRA protein by LPS-stimulated THP-1 cells (Fig. 3b). Moreover, levels of SRA protein were also increased in a dose-dependent manner of wnt1 recombination protein (Fig. 3c). Transfection with SRA siRNA decreased levels of NF-kB protein induced by wnt1 overexpression (Fig. 3d), predicting that SRA was involved in wnt1-mediated NF-KB activation. More importantly, protein levels of p65 were also increased following concentration gradient of human wnt1 recombination protein (Fig. 3e).Fig. 3


Wnt1 Participates in Inflammation Induced by Lipopolysaccharide Through Upregulating Scavenger Receptor A and NF-kB.

Zhao W, Sun Z, Wang S, Li Z, Zheng L - Inflammation (2015)

NF-kB was activated by wnt1 through increasing SRA expression. a SRA protein level was decreased in THP-1 cells transfected with wnt1 siRNA while ectopic expression of wnt1 increased it (p < 0.05), and TLR4 protein level was unchanged with either siRNA-wnt1 transfection or ectopic expression of wnt1. bwnt1 siRNA transfection decreased SRA expression induced by LPS (p < 0.05). c SRA protein level was increased following concentration gradient of human wnt1 recombination protein (p < 0.05). d p65 protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with SRA siRNA (p < 0.05). e p65 protein level was increased following concentration gradient of human wnt1 recombination protein (from 0 to 15 ug/ml) (p < 0.05). Results were normalized against levels of GAPDH protein.
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Related In: Results  -  Collection

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Fig3: NF-kB was activated by wnt1 through increasing SRA expression. a SRA protein level was decreased in THP-1 cells transfected with wnt1 siRNA while ectopic expression of wnt1 increased it (p < 0.05), and TLR4 protein level was unchanged with either siRNA-wnt1 transfection or ectopic expression of wnt1. bwnt1 siRNA transfection decreased SRA expression induced by LPS (p < 0.05). c SRA protein level was increased following concentration gradient of human wnt1 recombination protein (p < 0.05). d p65 protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with SRA siRNA (p < 0.05). e p65 protein level was increased following concentration gradient of human wnt1 recombination protein (from 0 to 15 ug/ml) (p < 0.05). Results were normalized against levels of GAPDH protein.
Mentions: To explore the detail mechanism involved in NF-kB activation induced by wnt1, the expression of SRA andTLR4 was detected through transfection of wnt1 siRNA or overexpression plasmid. As shown in Fig. 3a, wnt1 increased SRA expression but had no effect on levels of TLR4. Transfection with wnt1 siRNA also decreased levels of SRA protein by LPS-stimulated THP-1 cells (Fig. 3b). Moreover, levels of SRA protein were also increased in a dose-dependent manner of wnt1 recombination protein (Fig. 3c). Transfection with SRA siRNA decreased levels of NF-kB protein induced by wnt1 overexpression (Fig. 3d), predicting that SRA was involved in wnt1-mediated NF-KB activation. More importantly, protein levels of p65 were also increased following concentration gradient of human wnt1 recombination protein (Fig. 3e).Fig. 3

Bottom Line: THP-1 cells were activated with phorbol-12-myristate-13-acetate (PMA) and treated with LPS to induce inflammation.Inhibitor of β-catenin and siRNA of FZD1were used to investigate the signaling events involved in SRA activation induced by wnt1.Wnt1 promoted SRA expression through activation of canonical wnt pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, First Affiliated Hospital, College of Medicine, Zhejiang University, 79Qingchun Road, Hangzhou, 310003, China.

ABSTRACT
The study investigated the role of wnt1 in the inflammatory response initiated by lipolysaccharide (LPS), and analyzed the association between wnt1, NF-KB, and inflammatory factors. THP-1 cells were activated with phorbol-12-myristate-13-acetate (PMA) and treated with LPS to induce inflammation. THP-1 cells were transfected with wnt1siRNA and overexpression plasmid to explore the relationship among wnt1, SRA, and NF-KB. Inhibitor of β-catenin and siRNA of FZD1were used to investigate the signaling events involved in SRA activation induced by wnt1. Levels of NF-kB protein and inflammatory cytokines were assessed followingwnt1 siRNA and LPS treatment. PMA activation and LPS treatment of THP-1 cells increased wnt1 protein levels. Wnt1 promoted SRA expression through activation of canonical wnt pathway. Wnt1 increased NF-kB protein levels and enhanced the secretion of IL-6, TNF-α, and iNOS through binding to SRA. These findings suggest that wnt1 increased SRA and NF-kB protein levels and participated in the inflammatory response.

No MeSH data available.


Related in: MedlinePlus