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Thermo Fisher human anxa1 elisa kit
Human Anxa1 Elisa Kit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+anxa1+elisa+kit/pm40619476-367-12-16?v=Thermo+Fisher
Average 90 stars, based on 1 article reviews

human anxa1 elisa kit - by Bioz Stars, 2026-08

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NRF2 transcriptionally upregulates ANXA1 expression in GSC to promote TAM recruitment and M2 polarization. (a) The umap plot of GSE131928 single cell sequencing. (b) Venn diagram of the intersection of differentially transcribed genes and genes differentially upregulated for protein activity. (c–e) Correlation analysis of NFE2L2 with CD44, TNFRSF1A, ANXA1 in glioma tissues (data from GEPIA2 database). (f) The qPCR results showed the level of ANXA1 mRNA expression in GSC that interfered with NFE2L2. (g) ChIP assay showing the level of ANXA1 transcriptional promoter enrichment after interference with NFE2L2. (h) ELISA assay showing the expression level of ANXA1 protein in cell supernatants after interference with NFE2L2. (i) Western blot assay showing the expression level of ANXA1 protein in cells after interference with NFE2L2. (j) Schematic representation of the DNA binding motif of NFE2L2. (k) Schematic representation of the ANXA1 promoter mutation. (l) Dual luciferase reporter gene assay interferes with ANXA1 transcriptional activity after NFE2L2.

Journal: CNS Neuroscience & Therapeutics

Article Title: CircMAN1A2 Levels Determine GBM Susceptibility to TMZ in a Pathway Involving TEP1‐ and KEAP1 ‐Mediated NRF2 Degradation Leading to Ferroptosis

doi: 10.1111/cns.70489

Figure Lengend Snippet: NRF2 transcriptionally upregulates ANXA1 expression in GSC to promote TAM recruitment and M2 polarization. (a) The umap plot of GSE131928 single cell sequencing. (b) Venn diagram of the intersection of differentially transcribed genes and genes differentially upregulated for protein activity. (c–e) Correlation analysis of NFE2L2 with CD44, TNFRSF1A, ANXA1 in glioma tissues (data from GEPIA2 database). (f) The qPCR results showed the level of ANXA1 mRNA expression in GSC that interfered with NFE2L2. (g) ChIP assay showing the level of ANXA1 transcriptional promoter enrichment after interference with NFE2L2. (h) ELISA assay showing the expression level of ANXA1 protein in cell supernatants after interference with NFE2L2. (i) Western blot assay showing the expression level of ANXA1 protein in cells after interference with NFE2L2. (j) Schematic representation of the DNA binding motif of NFE2L2. (k) Schematic representation of the ANXA1 promoter mutation. (l) Dual luciferase reporter gene assay interferes with ANXA1 transcriptional activity after NFE2L2.

Article Snippet: Chemerin and ANXA1 concentration in healthy donors' and glioma patients' serum or in the 24 h supernatant of cultured GBM cells were measured by commercial Human Chemerin ELISA Kits (DCHM00, R&D Systems) and Human ANXA1 Quantikine ELISA Kit (DTA00D, R&D Systems), respectively.

Techniques: Expressing, Sequencing, Activity Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Binding Assay, Mutagenesis, Luciferase, Reporter Gene Assay

CircMAN1A2 suppresses glioma progression and promotes TMZ sensitive in vivo. (a) HE staining of brain gliomas in nude mice with circMAN1A2 knockdown or overexpression, and with circMAN1A2 overexpression followed by regulation of TEP1 expression. (b) Differences in intracranial tumor size of tumor‐forming tumors plotted for different treatment scenarios. (c) IHC staining plots for tumor detection of Ki67, NRF2, and ANXA1 under different treatments. (d) HE staining shows the growth of gliomas in the brain of hormonal mice in response to TMZ treatment under different treatment conditions. (e) Effect of TMZ treatment on tumor size and survival in hormonal mice under different treatment scenarios. (f) Schematic representation of the mechanism by which circMAN1A2 regulates GSC progression.

Journal: CNS Neuroscience & Therapeutics

Article Title: CircMAN1A2 Levels Determine GBM Susceptibility to TMZ in a Pathway Involving TEP1‐ and KEAP1 ‐Mediated NRF2 Degradation Leading to Ferroptosis

doi: 10.1111/cns.70489

Figure Lengend Snippet: CircMAN1A2 suppresses glioma progression and promotes TMZ sensitive in vivo. (a) HE staining of brain gliomas in nude mice with circMAN1A2 knockdown or overexpression, and with circMAN1A2 overexpression followed by regulation of TEP1 expression. (b) Differences in intracranial tumor size of tumor‐forming tumors plotted for different treatment scenarios. (c) IHC staining plots for tumor detection of Ki67, NRF2, and ANXA1 under different treatments. (d) HE staining shows the growth of gliomas in the brain of hormonal mice in response to TMZ treatment under different treatment conditions. (e) Effect of TMZ treatment on tumor size and survival in hormonal mice under different treatment scenarios. (f) Schematic representation of the mechanism by which circMAN1A2 regulates GSC progression.

Techniques: In Vivo, Staining, Knockdown, Over Expression, Expressing, Immunohistochemistry

Average biomarker concentrations of participant cohort pre- and post- Bariatric surgery. ( a ) The average body mass index (BMI) (kg/m 2 ) was significantly reduced at post-opt compared to pre-opt ( p < 0.0001). ( b ) The average plasma concentration of C-reactive protein (CRP) (μg/mL) were significantly decreased at post-opt compared to pre-opt ( p = 0.020). ( c ) The average plasma of concentration of leptin (ng/mL) were significantly decreased at post-opt compared to pre-opt ( p = 0.0001). ( d ) The average plasma concentration of interleukin-10 (IL-10) (pg/mL) were significantly increased at post-opt compared to pre-opt ( p = 0.018). ( e ) The average plasma concentration of annexin A1 (ng/mL) were significantly increased at post-opt compared to pre-opt ( p = 0.009). ( f ) The average plasma concentration of adiponectin were significantly increased at post-opt compared to pre-opt ( p = 0.002). One-tailed unpaired t -test was used to statistically analyse the data. Data presented as Mean ± SEM, p value was set at p < 0.05 and is denoted by * = p = 0.05, ** = p = 0.001 or *** = p < 0.0001. Pre-opt = Pre-operatively and Post-opt = Post-operatively.

Journal: Nutrients

Article Title: Suppression of Anti-Inflammatory Mediators in Metabolic Disease May Be Driven by Overwhelming Pro-Inflammatory Drivers

doi: 10.3390/nu14112360

Figure Lengend Snippet: Average biomarker concentrations of participant cohort pre- and post- Bariatric surgery. ( a ) The average body mass index (BMI) (kg/m 2 ) was significantly reduced at post-opt compared to pre-opt ( p < 0.0001). ( b ) The average plasma concentration of C-reactive protein (CRP) (μg/mL) were significantly decreased at post-opt compared to pre-opt ( p = 0.020). ( c ) The average plasma of concentration of leptin (ng/mL) were significantly decreased at post-opt compared to pre-opt ( p = 0.0001). ( d ) The average plasma concentration of interleukin-10 (IL-10) (pg/mL) were significantly increased at post-opt compared to pre-opt ( p = 0.018). ( e ) The average plasma concentration of annexin A1 (ng/mL) were significantly increased at post-opt compared to pre-opt ( p = 0.009). ( f ) The average plasma concentration of adiponectin were significantly increased at post-opt compared to pre-opt ( p = 0.002). One-tailed unpaired t -test was used to statistically analyse the data. Data presented as Mean ± SEM, p value was set at p < 0.05 and is denoted by * = p = 0.05, ** = p = 0.001 or *** = p < 0.0001. Pre-opt = Pre-operatively and Post-opt = Post-operatively.

Article Snippet: Plasma biomarkers including Human C-Reactive Protein (CRP) (R&D, Minneapolis, MN, USA, #DCRP00), Human Annexin A1 (ANXA1) (Cusabio, Houston, TX, USA, #CSB-E12155h), Human Interleukin-10 (IL-10) (R&D #D1000B), Human Leptin (R&D #DLP00) and Human Adiponectin (R&D #DRP300) were quantified using enzyme linked immunosorbent assays following the manufacturers protocols.

Techniques: Biomarker Discovery, Clinical Proteomics, Concentration Assay, One-tailed Test

Correlation between plasma concentration of annexin A1 (ng/mL) and biomarkers in bariatric surgery patients. ( a ) Plasma concentration of Annexin A1 significantly inversely correlated with body mass index (BMI) (kg/m 2 ) ( p = 0.039, r = −0.340), ( b ) significantly positively correlated with plasma concentration of high-density lipoprotein (HDL) (mmol/L) ( p = 0.020, r = 0.398) and ( c ) significantly positively correlated with plasma adiponectin concentration ( p = 0.009, r = 0.468). One-tailed Pearson correlation coefficient was used to statistically analyse the data.

Journal: Nutrients

Article Title: Suppression of Anti-Inflammatory Mediators in Metabolic Disease May Be Driven by Overwhelming Pro-Inflammatory Drivers

doi: 10.3390/nu14112360

Figure Lengend Snippet: Correlation between plasma concentration of annexin A1 (ng/mL) and biomarkers in bariatric surgery patients. ( a ) Plasma concentration of Annexin A1 significantly inversely correlated with body mass index (BMI) (kg/m 2 ) ( p = 0.039, r = −0.340), ( b ) significantly positively correlated with plasma concentration of high-density lipoprotein (HDL) (mmol/L) ( p = 0.020, r = 0.398) and ( c ) significantly positively correlated with plasma adiponectin concentration ( p = 0.009, r = 0.468). One-tailed Pearson correlation coefficient was used to statistically analyse the data.

Techniques: Clinical Proteomics, Concentration Assay, One-tailed Test

Average biomarker concentrations in lipodystrophy patients and matched controls. ( a ) No significant difference between the body mass index (BMI) (kg/m 2 ) of lipodystrophy patients and control was observed ( p = 0.324). ( b ) The average plasma concentration of C-reactive protein (CRP) (μg/mL) were significantly increased ( p = 0.0074) and ( c ) the average plasma concentration of annexin A1 (ng/mL) were significantly reduced ( p = 0.0008) in lipodystrophy patients compared to controls. One-tailed unpaired t -test was used to statistically analyse the data. Data presented as Mean ± SEM, p value was set as p < 0.05 and is denoted by ** = p = 0.001 or *** = p < 0.0001.

Journal: Nutrients

Article Title: Suppression of Anti-Inflammatory Mediators in Metabolic Disease May Be Driven by Overwhelming Pro-Inflammatory Drivers

doi: 10.3390/nu14112360

Figure Lengend Snippet: Average biomarker concentrations in lipodystrophy patients and matched controls. ( a ) No significant difference between the body mass index (BMI) (kg/m 2 ) of lipodystrophy patients and control was observed ( p = 0.324). ( b ) The average plasma concentration of C-reactive protein (CRP) (μg/mL) were significantly increased ( p = 0.0074) and ( c ) the average plasma concentration of annexin A1 (ng/mL) were significantly reduced ( p = 0.0008) in lipodystrophy patients compared to controls. One-tailed unpaired t -test was used to statistically analyse the data. Data presented as Mean ± SEM, p value was set as p < 0.05 and is denoted by ** = p = 0.001 or *** = p < 0.0001.

Techniques: Biomarker Discovery, Control, Clinical Proteomics, Concentration Assay, One-tailed Test

Proposed relationship between CRP and ANXA1 plasma concentrations and BMI/body fat (%) based on the current and previous research.

Journal: Nutrients

Article Title: Suppression of Anti-Inflammatory Mediators in Metabolic Disease May Be Driven by Overwhelming Pro-Inflammatory Drivers

doi: 10.3390/nu14112360

Figure Lengend Snippet: Proposed relationship between CRP and ANXA1 plasma concentrations and BMI/body fat (%) based on the current and previous research.

Techniques: Clinical Proteomics

Fig. 1 ANXA1 expression and secretion from ARPE-19 cells are upregulated by hypoxia. ARPE-19 cells were grown in a hypoxic environment for 0 h, 8 h, 16 h, 24 h or 32 h. A ANXA1 protein level in ARPE-19 cells was measured by Western blot. GAPDH was used as the loading control. B The relative protein level of ANXA1 was analyzed. C The protein level of ANXA1 in ARPE-19 cell culture supernatant was measured by ELISA. In Fig. 1B and C, *P < 0.05 and **P < 0.01 versus the 0 h hypoxia group. n = 4/each group.

Journal: Inflammation

Article Title: Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.

doi: 10.1007/s10753-021-01555-3

Figure Lengend Snippet: Fig. 1 ANXA1 expression and secretion from ARPE-19 cells are upregulated by hypoxia. ARPE-19 cells were grown in a hypoxic environment for 0 h, 8 h, 16 h, 24 h or 32 h. A ANXA1 protein level in ARPE-19 cells was measured by Western blot. GAPDH was used as the loading control. B The relative protein level of ANXA1 was analyzed. C The protein level of ANXA1 in ARPE-19 cell culture supernatant was measured by ELISA. In Fig. 1B and C, *P < 0.05 and **P < 0.01 versus the 0 h hypoxia group. n = 4/each group.

Article Snippet: Enzyme‐Linked Immunosorbent Assay (ELISA) The levels of ANXA1 were measured using a human ANXA1 ELISA kit (NBP2-60,538, Novus Biologicals, USA) according to the manufacturer’s instructions.

Techniques: Expressing, Western Blot, Control, Cell Culture, Enzyme-linked Immunosorbent Assay

Fig. 3 ANXA1 secreted by ARPE-19 cells inhibits NLRP3 inflammasome activation in HCECs by activating the FPR2/SHP2 axis. HCECs were allocated into the normal, hypoxia, human recombinant ANXA1 protein, ANXA1 + WRW4, ANXA1 + SHP099, ARPE-19 cell conditioned culture medium (CCM), CCM + ANXA1 neutralizing antibody, CCM + WRW4, and CCM + SHP099 groups. A The protein levels of NLRP3 inflammasome- associated molecules, including p-SHP, SHP2, ASC, NLRP3, pro-IL-1β, and IL-1β, were measured by Western blot. B–D The relative protein level of each molecule was analyzed. **P < 0.01 versus the normal group. #P < 0.05 and ##P < 0.01 versus the ANXA1 group. %P < 0.05 versus the CCM group. n = 4/each group.

Journal: Inflammation

Article Title: Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.

doi: 10.1007/s10753-021-01555-3

Figure Lengend Snippet: Fig. 3 ANXA1 secreted by ARPE-19 cells inhibits NLRP3 inflammasome activation in HCECs by activating the FPR2/SHP2 axis. HCECs were allocated into the normal, hypoxia, human recombinant ANXA1 protein, ANXA1 + WRW4, ANXA1 + SHP099, ARPE-19 cell conditioned culture medium (CCM), CCM + ANXA1 neutralizing antibody, CCM + WRW4, and CCM + SHP099 groups. A The protein levels of NLRP3 inflammasome- associated molecules, including p-SHP, SHP2, ASC, NLRP3, pro-IL-1β, and IL-1β, were measured by Western blot. B–D The relative protein level of each molecule was analyzed. **P < 0.01 versus the normal group. #P < 0.05 and ##P < 0.01 versus the ANXA1 group. %P < 0.05 versus the CCM group. n = 4/each group.

Techniques: Activation Assay, Recombinant, Western Blot

Fig. 4 ANXA1 secreted by ARPE-19 cells inhibits NLRP3 inflammasome-mediated pyroptosis in HCECs by activating the FPR2/SHP2 axis. HCECs were allocated into the normal, hypoxia, human recombinant ANXA1 protein, ANXA1 + WRW4, ANXA1 + SHP099, ANXA1 + ATP, ANXA1 + caspase-1 CRISPR activation plasmid, ARPE-19 cell CCM, CCM + ANXA1 neutralizing antibody, CCM + WRW4, CCM + SHP099, CCM + ATP, and CCM + caspase-1 CRISPR activation plasmid groups. A N-GSDMD, GSDMD, caspase-1, and cleaved caspase-1 protein levels in HCECs were measured by Western blot. GAPDH was used as the loading control. B–C The mean ratios of N-GSDMD/GSDMD and cleaved caspase-1/caspase-1 were analyzed. *P < 0.05 versus the normal group. #P < 0.05 versus the ANXA1 group. %P < 0.05 versus the CCM group. D Rep- resentative images of TUNEL-stained HCECs are shown. E The mean ratio of TUNEL-positive cells was determined. **P < 0.01 versus the normal group. #P < 0.05 versus the ANXA1 group. %P < 0.05 versus the CCM group. n = 4/each group.

Journal: Inflammation

Article Title: Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.

doi: 10.1007/s10753-021-01555-3

Figure Lengend Snippet: Fig. 4 ANXA1 secreted by ARPE-19 cells inhibits NLRP3 inflammasome-mediated pyroptosis in HCECs by activating the FPR2/SHP2 axis. HCECs were allocated into the normal, hypoxia, human recombinant ANXA1 protein, ANXA1 + WRW4, ANXA1 + SHP099, ANXA1 + ATP, ANXA1 + caspase-1 CRISPR activation plasmid, ARPE-19 cell CCM, CCM + ANXA1 neutralizing antibody, CCM + WRW4, CCM + SHP099, CCM + ATP, and CCM + caspase-1 CRISPR activation plasmid groups. A N-GSDMD, GSDMD, caspase-1, and cleaved caspase-1 protein levels in HCECs were measured by Western blot. GAPDH was used as the loading control. B–C The mean ratios of N-GSDMD/GSDMD and cleaved caspase-1/caspase-1 were analyzed. *P < 0.05 versus the normal group. #P < 0.05 versus the ANXA1 group. %P < 0.05 versus the CCM group. D Rep- resentative images of TUNEL-stained HCECs are shown. E The mean ratio of TUNEL-positive cells was determined. **P < 0.01 versus the normal group. #P < 0.05 versus the ANXA1 group. %P < 0.05 versus the CCM group. n = 4/each group.

Techniques: Recombinant, CRISPR, Activation Assay, Plasmid Preparation, Western Blot, Control, TUNEL Assay, Staining

Fig. 5 ANXA1 secreted by ARPE-19 cells promotes the proliferation, migration, and tube formation of HCECs by activating the FPR2/SHP2 axis and inhibiting NLRP3 inflammasome-mediated pyroptosis. HCECs were allocated into the normal, hypoxia, human recombinant ANXA1 protein, ANXA1 + WRW4, ANXA1 + SHP099, ANXA1 + ATP, ANXA1 + caspase-1 CRISPR activation plasmid, ARPE-19 cell CCM, CCM + ANXA1 neutralizing antibody, CCM + WRW4, CCM + SHP099, CCM + ATP, and CCM + caspase-1 plasmid groups. A The proliferation of HCECs was examined by EdU incorporation assay. Scale bar = 100 µm. B The ratio of EdU-positive cells to DAPI-positive cells was analyzed. C The migration of HCECs was examined by wound healing assay. Scale bar = 50 µm. D The migration distance was analyzed. E Tube formation assay was used to examine the tube formation capability of HCECs. Scale bar = 200 µm. F The tube length (μm) was analyzed. In Fig. 5B, 5D, and 5F, **P < 0.01 the hypoxia group versus the normal group; #P < 0.05 versus the ANXA1 group; %P < 0.05 versus the CCM group. n = 4/each group.

Journal: Inflammation

Article Title: Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.

doi: 10.1007/s10753-021-01555-3

Figure Lengend Snippet: Fig. 5 ANXA1 secreted by ARPE-19 cells promotes the proliferation, migration, and tube formation of HCECs by activating the FPR2/SHP2 axis and inhibiting NLRP3 inflammasome-mediated pyroptosis. HCECs were allocated into the normal, hypoxia, human recombinant ANXA1 protein, ANXA1 + WRW4, ANXA1 + SHP099, ANXA1 + ATP, ANXA1 + caspase-1 CRISPR activation plasmid, ARPE-19 cell CCM, CCM + ANXA1 neutralizing antibody, CCM + WRW4, CCM + SHP099, CCM + ATP, and CCM + caspase-1 plasmid groups. A The proliferation of HCECs was examined by EdU incorporation assay. Scale bar = 100 µm. B The ratio of EdU-positive cells to DAPI-positive cells was analyzed. C The migration of HCECs was examined by wound healing assay. Scale bar = 50 µm. D The migration distance was analyzed. E Tube formation assay was used to examine the tube formation capability of HCECs. Scale bar = 200 µm. F The tube length (μm) was analyzed. In Fig. 5B, 5D, and 5F, **P < 0.01 the hypoxia group versus the normal group; #P < 0.05 versus the ANXA1 group; %P < 0.05 versus the CCM group. n = 4/each group.

Techniques: Migration, Recombinant, CRISPR, Activation Assay, Plasmid Preparation, Wound Healing Assay, Tube Formation Assay

Fig. 6 The ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis is upregulated in laser-induced CNV mice. The mice were allocated into nor- mal and CNV 7 d groups. A ANXA1 was stained on the retina-RPE-choroid complexes. B FPR2 was stained on the retina-RPE-choroid complexes. C P-SHP2 was stained on the retina-RPE-choroid complexes. D NLRP3 was stained on the retina-RPE-choroid complexes. E Cleaved caspase-1 was stained on the retina-RPE-choroid complexes.

Journal: Inflammation

Article Title: Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.

doi: 10.1007/s10753-021-01555-3

Figure Lengend Snippet: Fig. 6 The ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis is upregulated in laser-induced CNV mice. The mice were allocated into nor- mal and CNV 7 d groups. A ANXA1 was stained on the retina-RPE-choroid complexes. B FPR2 was stained on the retina-RPE-choroid complexes. C P-SHP2 was stained on the retina-RPE-choroid complexes. D NLRP3 was stained on the retina-RPE-choroid complexes. E Cleaved caspase-1 was stained on the retina-RPE-choroid complexes.

Techniques: Staining

Fig. 7 Inhibition of the ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis decreases the volume of CNV. The mice were allocated into the normal, CNV 7 d, CNV 7 d + PBS, CNV 7 d + rabbit IgG isotype control, CNV 7 d + control CRISPR activation plasmid, CNV 7 d + ANXA1 neutralizing antibody, CNV 7 d + WRW4, CNV 7 d + SHP099, CNV 7 d + ATP, and CNV + caspase-1 plasmid groups. A IB4 (green) and collagen IV (red) were analyzed on mouse choroidal flat mounts. B The volume of CNV was shown. *P < 0.05 versus the CNV 7 d group. C Diagram depict- ing the mechanisms of the ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis in CNV. After hypoxia, Annexin A1 (ANXA1) secretion from RPE cells increases. ANXA1 binds to FPR2 on the surface of CECs to activate SHP2. SHP2 inhibits the activation of NLRP3 inflammasome and subsequent pyroptosis. Thereafter, proliferation, migration, and tube formation of CECs are enhanced. Inhibition of the ANXA1/FPR2/NLRP3 inflammasome/pyroptosis axis mitigates laser-induced CNV in mice.

Journal: Inflammation

Article Title: Crosstalk Between RPE Cells and Choroidal Endothelial Cells via the ANXA1/FPR2/SHP2/NLRP3 Inflammasome/Pyroptosis Axis Promotes Choroidal Neovascularization.

doi: 10.1007/s10753-021-01555-3

Figure Lengend Snippet: Fig. 7 Inhibition of the ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis decreases the volume of CNV. The mice were allocated into the normal, CNV 7 d, CNV 7 d + PBS, CNV 7 d + rabbit IgG isotype control, CNV 7 d + control CRISPR activation plasmid, CNV 7 d + ANXA1 neutralizing antibody, CNV 7 d + WRW4, CNV 7 d + SHP099, CNV 7 d + ATP, and CNV + caspase-1 plasmid groups. A IB4 (green) and collagen IV (red) were analyzed on mouse choroidal flat mounts. B The volume of CNV was shown. *P < 0.05 versus the CNV 7 d group. C Diagram depict- ing the mechanisms of the ANXA1/FPR2/SHP2/NLRP3 inflammasome/pyroptosis axis in CNV. After hypoxia, Annexin A1 (ANXA1) secretion from RPE cells increases. ANXA1 binds to FPR2 on the surface of CECs to activate SHP2. SHP2 inhibits the activation of NLRP3 inflammasome and subsequent pyroptosis. Thereafter, proliferation, migration, and tube formation of CECs are enhanced. Inhibition of the ANXA1/FPR2/NLRP3 inflammasome/pyroptosis axis mitigates laser-induced CNV in mice.

Techniques: Inhibition, Control, CRISPR, Activation Assay, Plasmid Preparation, Migration

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