Limits...
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

wnt1 promotes SRA expression through the canonical wnt pathway. a–b SRA protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with siRNA-FZD1 or VAX939 (β-catenin inhibitor) (p < 0.05). c Co-immunoprecipitation experiments showed an interaction between wnt1 and SRA (p < 0.05). LPS treatment strengthened it (p < 0.05). d THP-1 cells were cultured in the presence or absence of LPS (40 ug/ml) for 24 h. Confocal microscopy imaging of wnt1 (green), SRA (red), and optical microscopic view (gray) were shown. Results were normalized against levels of GAPDH protein.
© Copyright Policy - OpenAccess
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4495710&req=5

Fig4: wnt1 promotes SRA expression through the canonical wnt pathway. a–b SRA protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with siRNA-FZD1 or VAX939 (β-catenin inhibitor) (p < 0.05). c Co-immunoprecipitation experiments showed an interaction between wnt1 and SRA (p < 0.05). LPS treatment strengthened it (p < 0.05). d THP-1 cells were cultured in the presence or absence of LPS (40 ug/ml) for 24 h. Confocal microscopy imaging of wnt1 (green), SRA (red), and optical microscopic view (gray) were shown. Results were normalized against levels of GAPDH protein.

Mentions: The levels of SRA protein were decreased in LPS-stimulated THP-1 cells transfected with FZD1 siRNA compared to negative control (Fig. 4a). The levels of SRA protein were also decreased in LPS-stimulated THP-1 cells treated with VAX939 (inhibitor of β-catenin) compared to untreated cells (Fig. 4b). Co-immunoprecipitation (IP) experiments were performed, and data showed that there was an interaction between wnt1 and SRA, and LPS stimulation strengthened it (Fig. 4c). Confocal image systems were also used to further assure there is the complex of wnt1 and SRA. More importantly, optical microscopy view show that the complex maybe localized in cell surface (Fig. 4d).Fig. 4


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)

wnt1 promotes SRA expression through the canonical wnt pathway. a–b SRA protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with siRNA-FZD1 or VAX939 (β-catenin inhibitor) (p < 0.05). c Co-immunoprecipitation experiments showed an interaction between wnt1 and SRA (p < 0.05). LPS treatment strengthened it (p < 0.05). d THP-1 cells were cultured in the presence or absence of LPS (40 ug/ml) for 24 h. Confocal microscopy imaging of wnt1 (green), SRA (red), and optical microscopic view (gray) were shown. Results were normalized against levels of GAPDH protein.
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4495710&req=5

Fig4: wnt1 promotes SRA expression through the canonical wnt pathway. a–b SRA protein level was decreased in wnt1 overexpression-transfected THP-1 cells treated with siRNA-FZD1 or VAX939 (β-catenin inhibitor) (p < 0.05). c Co-immunoprecipitation experiments showed an interaction between wnt1 and SRA (p < 0.05). LPS treatment strengthened it (p < 0.05). d THP-1 cells were cultured in the presence or absence of LPS (40 ug/ml) for 24 h. Confocal microscopy imaging of wnt1 (green), SRA (red), and optical microscopic view (gray) were shown. Results were normalized against levels of GAPDH protein.
Mentions: The levels of SRA protein were decreased in LPS-stimulated THP-1 cells transfected with FZD1 siRNA compared to negative control (Fig. 4a). The levels of SRA protein were also decreased in LPS-stimulated THP-1 cells treated with VAX939 (inhibitor of β-catenin) compared to untreated cells (Fig. 4b). Co-immunoprecipitation (IP) experiments were performed, and data showed that there was an interaction between wnt1 and SRA, and LPS stimulation strengthened it (Fig. 4c). Confocal image systems were also used to further assure there is the complex of wnt1 and SRA. More importantly, optical microscopy view show that the complex maybe localized in cell surface (Fig. 4d).Fig. 4

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