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MedChemExpress c5ar antagonist w54011 mice
C5ar Antagonist W54011 Mice, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c5ar+antagonist+w54011/W-54011/pm41299858-68-2-28
Average 93 stars, based on 8 article reviews

c5ar antagonist w54011 mice - by Bioz Stars, 2026-10

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Article Title: Complement C5a receptor antagonist in the treatment of experimental periodontitis in mice.
Article Snippet: .. Treatment with C5aR antagonist W54011 Mice with successful periodontitis model construction were subsequently allocated to one of three groups (n = 5/group) receiving injection with C5aR antagonist W54011 (MedChemExpress) corresponding to total delivered doses of 1, 2, and 5 μg per injection session, respectively. .. Treatment with C5aR antagonist W54011 Mice with successful periodontitis model construction were subsequently allocated to one of three groups (n = 5/group) receiving injection with C5aR antagonist W54011 (MedChemExpress) corresponding to total delivered doses of 1, 2, and 5 μg per injection session, respectively.

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DPSCs express BDNF and NGF. Cultured cells were treated with C5aR-agonist or antagonist for 48 h and then stimulated with LPS for 1 h, and fixed and stained accordingly. Immunofluorescence double staining was used to analyze the expression of BDNF and NGF. Anti-BDNF (green) and anti-NGF (red) were found co-localized in the cytoplasm of DPSCs in C5aR-agonist treated cells after 48 h of treatment. Intense staining was observed in C5aR-agonist and LPS + C5aR-agonist treated cells. For each condition, negative controls, performed by replacement of the BDNF and NGF primary antibodies and secondary antibody used to detect BDNF was Alexa-488 (green) and NGF through Alexa-594 (red); nuclei were counterstained with DAPI (blue). Scale bar: 100 µm.

Journal: Scientific Reports

Article Title: Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

doi: 10.1038/s41598-022-06110-0

Figure Lengend Snippet: DPSCs express BDNF and NGF. Cultured cells were treated with C5aR-agonist or antagonist for 48 h and then stimulated with LPS for 1 h, and fixed and stained accordingly. Immunofluorescence double staining was used to analyze the expression of BDNF and NGF. Anti-BDNF (green) and anti-NGF (red) were found co-localized in the cytoplasm of DPSCs in C5aR-agonist treated cells after 48 h of treatment. Intense staining was observed in C5aR-agonist and LPS + C5aR-agonist treated cells. For each condition, negative controls, performed by replacement of the BDNF and NGF primary antibodies and secondary antibody used to detect BDNF was Alexa-488 (green) and NGF through Alexa-594 (red); nuclei were counterstained with DAPI (blue). Scale bar: 100 µm.

Article Snippet: C5aR antagonist—W54011 was acquired from Calbiochem (San Diego, CA, USA) and C5aR agonist from Anaspec (Fremont, CA, USA).

Techniques: Cell Culture, Staining, Immunofluorescence, Double Staining, Expressing

BDNF and NGF are weakly expressed in BM-MSCs. Cultured cells were treated with C5aR-agonist or antagonist for 48 h and then stimulated with LPS for 1 h, and fixed and stained accordingly. Immunofluorescence double staining was used to analyze the expression of BDNF and NGF. Anti-BDNF (green) and anti-NGF (red) were found weakly co-localized in the cytoplasm of BM-MSCs in C5aR-agonist treated cells after 48 h of treatment. Staining was observed in C5aR-agonist and LPS + C5aR-agonist treated cells. For each condition, negative controls, performed by replacement of the BDNF and NGF primary antibodies and secondary antibody used to detect BDNF was Alexa-488 (green) and NGF through Alexa-594 (red); nuclei were counterstained with DAPI (blue). Scale bar: 100 µm.

Journal: Scientific Reports

Article Title: Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

doi: 10.1038/s41598-022-06110-0

Figure Lengend Snippet: BDNF and NGF are weakly expressed in BM-MSCs. Cultured cells were treated with C5aR-agonist or antagonist for 48 h and then stimulated with LPS for 1 h, and fixed and stained accordingly. Immunofluorescence double staining was used to analyze the expression of BDNF and NGF. Anti-BDNF (green) and anti-NGF (red) were found weakly co-localized in the cytoplasm of BM-MSCs in C5aR-agonist treated cells after 48 h of treatment. Staining was observed in C5aR-agonist and LPS + C5aR-agonist treated cells. For each condition, negative controls, performed by replacement of the BDNF and NGF primary antibodies and secondary antibody used to detect BDNF was Alexa-488 (green) and NGF through Alexa-594 (red); nuclei were counterstained with DAPI (blue). Scale bar: 100 µm.

Article Snippet: C5aR antagonist—W54011 was acquired from Calbiochem (San Diego, CA, USA) and C5aR agonist from Anaspec (Fremont, CA, USA).

Techniques: Cell Culture, Staining, Immunofluorescence, Double Staining, Expressing

DPSCs produce higher levels of BDNF than BM-MSCs. BDNF in supernatants ( A ) and cell lysate ( B ) was measured by enzyme-linked immunosorbent assay after 48 h of treatment. For each experiment/ condition, the BDNF quantity was normalized to cell viability. Stimulation with C5aR-agonist or co-stimulation with LPS significantly increased the BDNF secretion in supernatants of DPSCs compared to BM-MSCs. BDNF secretion in the cell lysate of DPSCs was also significantly higher than BM-MSCs cell lysate. * p < 0.05, ** p < 0.01 and *** p < 0.001 versus untreated control of resting cells (n = 3).

Journal: Scientific Reports

Article Title: Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

doi: 10.1038/s41598-022-06110-0

Figure Lengend Snippet: DPSCs produce higher levels of BDNF than BM-MSCs. BDNF in supernatants ( A ) and cell lysate ( B ) was measured by enzyme-linked immunosorbent assay after 48 h of treatment. For each experiment/ condition, the BDNF quantity was normalized to cell viability. Stimulation with C5aR-agonist or co-stimulation with LPS significantly increased the BDNF secretion in supernatants of DPSCs compared to BM-MSCs. BDNF secretion in the cell lysate of DPSCs was also significantly higher than BM-MSCs cell lysate. * p < 0.05, ** p < 0.01 and *** p < 0.001 versus untreated control of resting cells (n = 3).

Article Snippet: C5aR antagonist—W54011 was acquired from Calbiochem (San Diego, CA, USA) and C5aR agonist from Anaspec (Fremont, CA, USA).

Techniques: Enzyme-linked Immunosorbent Assay

C5aR or LPS-stimulated DPSCs express more BDNF than BM-MSCs. ( A – L ) Magnified pictures from the respective boxes of Figs. and in subsequent order. Groups: Resting ( A , G ), C5aR agonist ( B , H ), C5aR antagonist ( C , I ), LPS ( D , J ), LPS + C5aR agonist ( E , K ), LPS + C5aR antagonist ( F , L ). Double fluorescence immunohistochemistry with anti-BDNF (green) and anti-NGF (red) deposit’s reaction product in punctae of both stem cells. BDNF and NGF immune intensities are significantly higher in the C5aR agonist or LPS + C5aR-agonist treatment group ( B , E & H , K ) compared to resting ( A , G ) and C5aR antagonist treatment ( C , I ) groups. ( M , N ) Bar graphs showing the fluorescence intensity of BDNF and NGF in various treatment groups normalized to untreated control of resting cells. C5aR stimulation by C5aR-agonist or co-stimulation with LPS specifically increases BDNF and NGF (E) expression in DPSCs undergoing differentiation. (D1) DPSCs negative control. (M1) BM-MSCs negative control. Values for resting control were set at 100 as a reference. * p < 0.05, ** p < 0.01 and *** p < 0.001 vs untreated control of resting cells (n = 3). Scale bar: 50 μm.

Journal: Scientific Reports

Article Title: Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

doi: 10.1038/s41598-022-06110-0

Figure Lengend Snippet: C5aR or LPS-stimulated DPSCs express more BDNF than BM-MSCs. ( A – L ) Magnified pictures from the respective boxes of Figs. and in subsequent order. Groups: Resting ( A , G ), C5aR agonist ( B , H ), C5aR antagonist ( C , I ), LPS ( D , J ), LPS + C5aR agonist ( E , K ), LPS + C5aR antagonist ( F , L ). Double fluorescence immunohistochemistry with anti-BDNF (green) and anti-NGF (red) deposit’s reaction product in punctae of both stem cells. BDNF and NGF immune intensities are significantly higher in the C5aR agonist or LPS + C5aR-agonist treatment group ( B , E & H , K ) compared to resting ( A , G ) and C5aR antagonist treatment ( C , I ) groups. ( M , N ) Bar graphs showing the fluorescence intensity of BDNF and NGF in various treatment groups normalized to untreated control of resting cells. C5aR stimulation by C5aR-agonist or co-stimulation with LPS specifically increases BDNF and NGF (E) expression in DPSCs undergoing differentiation. (D1) DPSCs negative control. (M1) BM-MSCs negative control. Values for resting control were set at 100 as a reference. * p < 0.05, ** p < 0.01 and *** p < 0.001 vs untreated control of resting cells (n = 3). Scale bar: 50 μm.

Article Snippet: C5aR antagonist—W54011 was acquired from Calbiochem (San Diego, CA, USA) and C5aR agonist from Anaspec (Fremont, CA, USA).

Techniques: Fluorescence, Immunohistochemistry, Expressing, Negative Control

C5aR and pp38 expression in DPSCs and BM-MSCs. Cells were cultured for 3 days and then stimulated with LPS for 1 h, and fixed and stained accordingly. Immunofluorescence double staining was used to analyze the expression of C5aR and pp38. Anti-C5aR (green) and anti-pp38 (red) were found highly co-localized in the cytoplasm of DPSCs ( A – J ) and BM-MSCs ( K – T ) in LPS-stimulated cells. For each condition, negative controls, performed by replacement of the C5aR and pp38 primary antibodies and secondary antibody used to detect C5aR were Alexa-488 (green) and pp38 through Alexa-594 (red); nuclei were counterstained with DAPI (blue). ( U , V ) Bar graphs showing the fluorescence intensity of C5aR and pp38 in resting and LPS-stimulated DPSCs and BM-MSCs. ( E , J , O , T ) are higher magnification views of the areas indicated in ( D , I , N , S ). ** p < 0.01 and *** p < 0.001 versus untreated control of resting cells (n = 3). Scale bars: 50 μm.

Journal: Scientific Reports

Article Title: Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

doi: 10.1038/s41598-022-06110-0

Figure Lengend Snippet: C5aR and pp38 expression in DPSCs and BM-MSCs. Cells were cultured for 3 days and then stimulated with LPS for 1 h, and fixed and stained accordingly. Immunofluorescence double staining was used to analyze the expression of C5aR and pp38. Anti-C5aR (green) and anti-pp38 (red) were found highly co-localized in the cytoplasm of DPSCs ( A – J ) and BM-MSCs ( K – T ) in LPS-stimulated cells. For each condition, negative controls, performed by replacement of the C5aR and pp38 primary antibodies and secondary antibody used to detect C5aR were Alexa-488 (green) and pp38 through Alexa-594 (red); nuclei were counterstained with DAPI (blue). ( U , V ) Bar graphs showing the fluorescence intensity of C5aR and pp38 in resting and LPS-stimulated DPSCs and BM-MSCs. ( E , J , O , T ) are higher magnification views of the areas indicated in ( D , I , N , S ). ** p < 0.01 and *** p < 0.001 versus untreated control of resting cells (n = 3). Scale bars: 50 μm.

Article Snippet: C5aR antagonist—W54011 was acquired from Calbiochem (San Diego, CA, USA) and C5aR agonist from Anaspec (Fremont, CA, USA).

Techniques: Expressing, Cell Culture, Staining, Immunofluorescence, Double Staining, Fluorescence

Effect of C5aR or LPS on cell proliferation of DPSCs and BM-MSCs. Cultured DPSCs ( A–F ) and MSCs ( G – L ) under a light microscope. Groups: Resting ( A , G ), C5aR agonist ( B , H ), C5aR antagonist ( C , I ), LPS ( D , J ), LPS + C5aR agonist ( E , K ), LPS + C5aR antagonist ( F , L ). ( M , N ) Bar graph showing statistical analysis—number of cells normalized as cell proliferation. Generally, C5aR modulation and LPS treatment do not affect DPSCs and BM-MSCs proliferation. Note : a slight increase in cell proliferation was observed in DPSCs stimulated with LPS + C5aR-agonist. Scale bar: 100 µm. * p < 0.05 versus untreated control of resting cells (n = 5).

Journal: Scientific Reports

Article Title: Complement C5aR/LPS-induced BDNF and NGF modulation in human dental pulp stem cells

doi: 10.1038/s41598-022-06110-0

Figure Lengend Snippet: Effect of C5aR or LPS on cell proliferation of DPSCs and BM-MSCs. Cultured DPSCs ( A–F ) and MSCs ( G – L ) under a light microscope. Groups: Resting ( A , G ), C5aR agonist ( B , H ), C5aR antagonist ( C , I ), LPS ( D , J ), LPS + C5aR agonist ( E , K ), LPS + C5aR antagonist ( F , L ). ( M , N ) Bar graph showing statistical analysis—number of cells normalized as cell proliferation. Generally, C5aR modulation and LPS treatment do not affect DPSCs and BM-MSCs proliferation. Note : a slight increase in cell proliferation was observed in DPSCs stimulated with LPS + C5aR-agonist. Scale bar: 100 µm. * p < 0.05 versus untreated control of resting cells (n = 5).

Article Snippet: C5aR antagonist—W54011 was acquired from Calbiochem (San Diego, CA, USA) and C5aR agonist from Anaspec (Fremont, CA, USA).

Techniques: Cell Culture, Light Microscopy

A schematic timeline representation of odontogenic DPSCs differentiation. Commercially available DPSCs were acquired and confluent DPSCs were cultured in a regular growth media for 4 days. 2–4 passage of DPSCs were cultured at 5 × 10 4 cells per well concentration. Subsequently, cells were cultured in dentinogenic media and treated with a C5aR agonist or antagonist from the differentiation day 4 to day 24. The medium was replaced every 3 days. Representative images of differentiating DPSCs at day 4 ( a ) and day 24 ( b – d ). e – h Double-immunofluorescence staining with anti-STRO-1 (red channel) and C5aR (green channel) in DPSCs at day 4 confirms that C5a receptor-positive cells also express STRO-1. i Bar graph showing no. of differentiated cells as cell proliferation. Differentiated DAPI stained cells were counted using ImageJ software. Scale bars: 100 μm ( a – d ), and 50 μm ( e – h )

Journal: International Journal of Oral Science

Article Title: The role of complement C5a receptor in DPSC odontoblastic differentiation and in vivo reparative dentin formation

doi: 10.1038/s41368-022-00158-4

Figure Lengend Snippet: A schematic timeline representation of odontogenic DPSCs differentiation. Commercially available DPSCs were acquired and confluent DPSCs were cultured in a regular growth media for 4 days. 2–4 passage of DPSCs were cultured at 5 × 10 4 cells per well concentration. Subsequently, cells were cultured in dentinogenic media and treated with a C5aR agonist or antagonist from the differentiation day 4 to day 24. The medium was replaced every 3 days. Representative images of differentiating DPSCs at day 4 ( a ) and day 24 ( b – d ). e – h Double-immunofluorescence staining with anti-STRO-1 (red channel) and C5aR (green channel) in DPSCs at day 4 confirms that C5a receptor-positive cells also express STRO-1. i Bar graph showing no. of differentiated cells as cell proliferation. Differentiated DAPI stained cells were counted using ImageJ software. Scale bars: 100 μm ( a – d ), and 50 μm ( e – h )

Article Snippet: C5aR antagonist – W54011 was acquired from MilliporeSigma (Cat. # 234415; Billerica, MA, USA) and C5aR agonist from Anaspec (Cat. # AS-65121; Fremont, CA, USA).

Techniques: Cell Culture, Concentration Assay, Double Immunofluorescence Staining, Staining, Software

Complement C5a receptor-mediated DSPP and DMP-1 expression after DPSCs odontoblastic differentiation. Immunofluorescence double staining was used to analyze DSPP and DMP-1 expression in C5aR-mediated DPSC differentiation. Anti-DSPP (green) and DMP-1 (red) were found co-localized in cytoplasm of DPSCs in C5aR-agonist-treated cells after 21 days of treatment ( b , e , and k ). An intense staining was observed in C5aR-agonist-treated cells. For each condition, negative controls, performed by replacement of the DSPP and DMP-1 primary antibodies and secondary antibody used to detect DSPP was Alexa-488 (green; a - c ) and DMP-1 through Alexa-594 (red; d − f ); nuclei were counterstained with DAPI (blue; g − i ). ( j − l ) Merged figures showing colocalization of DSPP and DMP-1 among resting, C5aR-agonist and C5aR-antagonist treated DPSCs.

Journal: International Journal of Oral Science

Article Title: The role of complement C5a receptor in DPSC odontoblastic differentiation and in vivo reparative dentin formation

doi: 10.1038/s41368-022-00158-4

Figure Lengend Snippet: Complement C5a receptor-mediated DSPP and DMP-1 expression after DPSCs odontoblastic differentiation. Immunofluorescence double staining was used to analyze DSPP and DMP-1 expression in C5aR-mediated DPSC differentiation. Anti-DSPP (green) and DMP-1 (red) were found co-localized in cytoplasm of DPSCs in C5aR-agonist-treated cells after 21 days of treatment ( b , e , and k ). An intense staining was observed in C5aR-agonist-treated cells. For each condition, negative controls, performed by replacement of the DSPP and DMP-1 primary antibodies and secondary antibody used to detect DSPP was Alexa-488 (green; a - c ) and DMP-1 through Alexa-594 (red; d − f ); nuclei were counterstained with DAPI (blue; g − i ). ( j − l ) Merged figures showing colocalization of DSPP and DMP-1 among resting, C5aR-agonist and C5aR-antagonist treated DPSCs.

Article Snippet: C5aR antagonist – W54011 was acquired from MilliporeSigma (Cat. # 234415; Billerica, MA, USA) and C5aR agonist from Anaspec (Cat. # AS-65121; Fremont, CA, USA).

Techniques: Expressing, Immunofluorescence, Double Staining, Staining

DPSC-derived odontoblastic cells express more DSPP and DMP-1 under C5aR agonist treatment. a – c Magnified pictures ( a – c ) from the respective boxes of Fig. . Anti-DSPP (green) and DMP-1 (red) immune intensities are significantly higher in the C5aR agonist treatment group ( b ) compared to resting ( a ) and C5aR antagonist treatment ( c ) groups. d , e Bar graphs showing the fluorescence intensity of DSPP and DMP-1 in various treatment groups. C5aR stimulation by C5aR agonist specifically increases DSPP ( d ) and DMP-1 ( e ) expression in DPSCs undergoing odontoblastic differentiation (gray versus red lines). *** P < 0.001 vs untreated control of resting cells ( n = 3).

Journal: International Journal of Oral Science

Article Title: The role of complement C5a receptor in DPSC odontoblastic differentiation and in vivo reparative dentin formation

doi: 10.1038/s41368-022-00158-4

Figure Lengend Snippet: DPSC-derived odontoblastic cells express more DSPP and DMP-1 under C5aR agonist treatment. a – c Magnified pictures ( a – c ) from the respective boxes of Fig. . Anti-DSPP (green) and DMP-1 (red) immune intensities are significantly higher in the C5aR agonist treatment group ( b ) compared to resting ( a ) and C5aR antagonist treatment ( c ) groups. d , e Bar graphs showing the fluorescence intensity of DSPP and DMP-1 in various treatment groups. C5aR stimulation by C5aR agonist specifically increases DSPP ( d ) and DMP-1 ( e ) expression in DPSCs undergoing odontoblastic differentiation (gray versus red lines). *** P < 0.001 vs untreated control of resting cells ( n = 3).

Article Snippet: C5aR antagonist – W54011 was acquired from MilliporeSigma (Cat. # 234415; Billerica, MA, USA) and C5aR agonist from Anaspec (Cat. # AS-65121; Fremont, CA, USA).

Techniques: Derivative Assay, Fluorescence, Expressing, Control

Effect of exogenous C5a on DSPP and DMP-1 expression and PCR analysis of DPSC-derived odontoblast-like cells. a – f Immunofluorescence double staining was used to analyze DSPP and DMP-1 expression in exogenous C5a-mediated DPSCs at day 10. Anti-DSPP (red) and DMP-1 (green) were found weakly co-localized in the cytoplasm of DPSCs in C5a-treated cells without any significant difference compared with resting control. Scale bar: 25 μm. g , h Real-time PCR analysis of DSPP and DMP-1 in the C5aR agonist, C5aR antagonist, and C5a recombinant protein treatment groups compared to control (calculated ‘1’ value of respective genes expression). The analysis reveals a significant upregulation of DSPP and DMP-1 mRNA expression in the C5aR agonist treatment group. Treatment of DPSCs using the recombinant human C5a protein does not affect the basal level of DSPP expression. i C5aR mRNA expression between resting cells and C5aR-agonist or antagonist-treated cells. C5aR-agonist or antagonist treatment do not induce a C5aR mRNA expression change

Journal: International Journal of Oral Science

Article Title: The role of complement C5a receptor in DPSC odontoblastic differentiation and in vivo reparative dentin formation

doi: 10.1038/s41368-022-00158-4

Figure Lengend Snippet: Effect of exogenous C5a on DSPP and DMP-1 expression and PCR analysis of DPSC-derived odontoblast-like cells. a – f Immunofluorescence double staining was used to analyze DSPP and DMP-1 expression in exogenous C5a-mediated DPSCs at day 10. Anti-DSPP (red) and DMP-1 (green) were found weakly co-localized in the cytoplasm of DPSCs in C5a-treated cells without any significant difference compared with resting control. Scale bar: 25 μm. g , h Real-time PCR analysis of DSPP and DMP-1 in the C5aR agonist, C5aR antagonist, and C5a recombinant protein treatment groups compared to control (calculated ‘1’ value of respective genes expression). The analysis reveals a significant upregulation of DSPP and DMP-1 mRNA expression in the C5aR agonist treatment group. Treatment of DPSCs using the recombinant human C5a protein does not affect the basal level of DSPP expression. i C5aR mRNA expression between resting cells and C5aR-agonist or antagonist-treated cells. C5aR-agonist or antagonist treatment do not induce a C5aR mRNA expression change

Article Snippet: C5aR antagonist – W54011 was acquired from MilliporeSigma (Cat. # 234415; Billerica, MA, USA) and C5aR agonist from Anaspec (Cat. # AS-65121; Fremont, CA, USA).

Techniques: Expressing, Derivative Assay, Immunofluorescence, Double Staining, Control, Real-time Polymerase Chain Reaction, Recombinant

C5aR expression increased in injured teeth of wild-type mice. a , b 0.3 mm drill tip was used to puncture the dentin until the upper surface of the pulp, and shortly after, the injured area was capped with MTA. Scale bar: 5 mm. c , d Hematoxylin and eosin staining showed a reparative dentin formation in the control mice (red arrows) after 4 weeks of recovery. Scale bar: 250 μm. e – g Immunofluorescence labeling for C5aR (green) reveals that after 24 h of the injury, C5aR expression is significantly increased in the injured area ( f ; Scale bar: 250 μm, g ; Scale bar: 50 μm.) compared to control ( e )

Journal: International Journal of Oral Science

Article Title: The role of complement C5a receptor in DPSC odontoblastic differentiation and in vivo reparative dentin formation

doi: 10.1038/s41368-022-00158-4

Figure Lengend Snippet: C5aR expression increased in injured teeth of wild-type mice. a , b 0.3 mm drill tip was used to puncture the dentin until the upper surface of the pulp, and shortly after, the injured area was capped with MTA. Scale bar: 5 mm. c , d Hematoxylin and eosin staining showed a reparative dentin formation in the control mice (red arrows) after 4 weeks of recovery. Scale bar: 250 μm. e – g Immunofluorescence labeling for C5aR (green) reveals that after 24 h of the injury, C5aR expression is significantly increased in the injured area ( f ; Scale bar: 250 μm, g ; Scale bar: 50 μm.) compared to control ( e )

Article Snippet: C5aR antagonist – W54011 was acquired from MilliporeSigma (Cat. # 234415; Billerica, MA, USA) and C5aR agonist from Anaspec (Cat. # AS-65121; Fremont, CA, USA).

Techniques: Expressing, Staining, Control, Immunofluorescence, Labeling

Transcriptome sequencing of NSCLC tissues, the expression of KLF5, GCN5, GDF15, C5aR in tumor tissues and the content of C5a in plasma of NSCLC patients. a Venn diagram showed that a total of 944 genes were upregulated (≥2-fold) by RNA-seq of 12 pairs of NSCLC tissues and 86 genes were in the overlap of all three sequencing results. b Gene ontology (GO) analysis for the 86 genes displayed that represented biological processes included cell proliferation, growth and maintenance. c , d Representative images of IHC staining for KLF5, GCN5, and GDF15 in paraffin-embedded sections of NSCLC patients ( c ) and statistical analysis of IHC staining intensity and area ( d ). The expression of KLF5, GCN5, and GDF15 in NSCLC tumor tissues were increased compared to adjacent tissues ( N = 185). e Quantification of plasma C5a in 40 NSCLC patients and 40 healthy volunteers by ELISA. Plasma C5a level of NSCLC patients was higher than control donors (** P < 0.01). f , g Representative result ( f ) and statistical analysis ( g ) for C5aR expression in NSCLC tissues by IHC. The C5aR expression was upregulated in NSCLC tumor tissues in comparison with adjacent tissues ( N = 185)

Journal: Oncogene

Article Title: C5a induces A549 cell proliferation of non-small cell lung cancer via GDF15 gene activation mediated by GCN5-dependent KLF5 acetylation

doi: 10.1038/s41388-018-0298-9

Figure Lengend Snippet: Transcriptome sequencing of NSCLC tissues, the expression of KLF5, GCN5, GDF15, C5aR in tumor tissues and the content of C5a in plasma of NSCLC patients. a Venn diagram showed that a total of 944 genes were upregulated (≥2-fold) by RNA-seq of 12 pairs of NSCLC tissues and 86 genes were in the overlap of all three sequencing results. b Gene ontology (GO) analysis for the 86 genes displayed that represented biological processes included cell proliferation, growth and maintenance. c , d Representative images of IHC staining for KLF5, GCN5, and GDF15 in paraffin-embedded sections of NSCLC patients ( c ) and statistical analysis of IHC staining intensity and area ( d ). The expression of KLF5, GCN5, and GDF15 in NSCLC tumor tissues were increased compared to adjacent tissues ( N = 185). e Quantification of plasma C5a in 40 NSCLC patients and 40 healthy volunteers by ELISA. Plasma C5a level of NSCLC patients was higher than control donors (** P < 0.01). f , g Representative result ( f ) and statistical analysis ( g ) for C5aR expression in NSCLC tissues by IHC. The C5aR expression was upregulated in NSCLC tumor tissues in comparison with adjacent tissues ( N = 185)

Article Snippet: The recombinant human C5a was from R&D systems (Tustin, CA, USA), and C5aR antagonist W54011 was provided by Merck Millipore (Darmstadt, Germany).

Techniques: Sequencing, Expressing, Clinical Proteomics, RNA Sequencing, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Control, Comparison

C5aR expression in human NSCLC cell lines as well as cell proliferation and KLF5, GCN5, GDF15 expression upon C5a stimulation. a IB assay showed that human C5aR was highly expressed in A549 and PC9 cell lines. b – d The proliferation of A549 and PC9 cells exposed to C5a (25 ng/ml and 250 ng/ml, especially 25 ng/ml) was notably increased by CCK8 (72 h, b ), cell counting (7 days, c ), and colony-forming assays (14 days, d ). e , f Real-time PCR ( e ) and IB ( f ) exhibited that mRNA and protein of KLF5, GCN5, and GDF15 in A549 cells following 25 ng/ml C5a incubation started to increase from 1 h, and peaked at 2 h and 3 h (GCN5 peaked at 6 h). Representative photographs are manifested. Data are expressed as means ± S.E.M. from three independent experiments, * P < 0.05, ** P < 0.01 vs. 0 ng/ml C5a

Journal: Oncogene

Article Title: C5a induces A549 cell proliferation of non-small cell lung cancer via GDF15 gene activation mediated by GCN5-dependent KLF5 acetylation

doi: 10.1038/s41388-018-0298-9

Figure Lengend Snippet: C5aR expression in human NSCLC cell lines as well as cell proliferation and KLF5, GCN5, GDF15 expression upon C5a stimulation. a IB assay showed that human C5aR was highly expressed in A549 and PC9 cell lines. b – d The proliferation of A549 and PC9 cells exposed to C5a (25 ng/ml and 250 ng/ml, especially 25 ng/ml) was notably increased by CCK8 (72 h, b ), cell counting (7 days, c ), and colony-forming assays (14 days, d ). e , f Real-time PCR ( e ) and IB ( f ) exhibited that mRNA and protein of KLF5, GCN5, and GDF15 in A549 cells following 25 ng/ml C5a incubation started to increase from 1 h, and peaked at 2 h and 3 h (GCN5 peaked at 6 h). Representative photographs are manifested. Data are expressed as means ± S.E.M. from three independent experiments, * P < 0.05, ** P < 0.01 vs. 0 ng/ml C5a

Article Snippet: The recombinant human C5a was from R&D systems (Tustin, CA, USA), and C5aR antagonist W54011 was provided by Merck Millipore (Darmstadt, Germany).

Techniques: Expressing, Cell Counting, Real-time Polymerase Chain Reaction, Incubation

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