Journal: Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

Article Title: Expression microarray analysis identifies novel epithelial-derived protein markers in eosinophilic esophagitis.

doi: 10.1038/modpathol.2013.41

Figure Lengend Snippet: Figure 2 Real-time reverse transcription-PCR results. Relative expression of ALOX15 (a), TNFAIP6 (b), FLG (c), SLURP1 (d) and CRISP3 (e) in paired samples of eosinophilic esophagitis before (BT) and after therapy (AT).

Article Snippet: The Dako Envision Plus Kit (Dako North America, Carpinteria, CA, USA) was used to perform the polymer-horseradish peroxidase-based IHC using the following antibodies: SLURP1 (Clone 569317; R&D Systems, Minneapolis, MN, USA; 1:100 dilution), CRISP3 (clone 295203, R&D Systems; 1:100 dilution), FLG (SPM181, Abcam, Cambridge, MA, USA; 1:25 dilution), ALOX15 (11-K, Santa Cruz Biotechnology, Santa Cruz, CA, USA; 1:100 dilution) and TNFAIP6 (FL-277, Santa Cruz Biotechnology; 1:200 dilution).

Techniques: Reverse Transcription, Expressing

Journal: Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

Article Title: Expression microarray analysis identifies novel epithelial-derived protein markers in eosinophilic esophagitis.

doi: 10.1038/modpathol.2013.41

Figure Lengend Snippet: Figure 4 Immunohistochemistry results of FLG, SLURP1 and CRISP3. (a) Normal controls; (b) eosinophilic esophagitis; (c) eosinophilic esophagitis after treatment; (d) reflux. FLG expression was present in the cytoplasm of maturing squamous cells of control samples. Eosinophilic esophagitis biopsies show loss of FLG expression with partial recovery after treatment. Reflux biopsies do not show loss of FLG expression. SLURP1 staining was present in cytoplasm of intermediate and mature squamous epithelial cells of control cases. Expression of SLURP1 is minimal in eosinophilic esophagitis and decreased in reflux cases. CRISP3 expression is strong in the cytoplasm of basal cells and peripapillary cells and in mature superficial squamous cells of control samples. Expression of CRISP3 is decreased in eosinophilic esophagitis. Eosinophilic esophagitis after treatment and reflux cases show CRISP3 expression limited to the basal cells and peripapillary cells but with no expression in cytoplasm of mature squamous cells.

Article Snippet: The Dako Envision Plus Kit (Dako North America, Carpinteria, CA, USA) was used to perform the polymer-horseradish peroxidase-based IHC using the following antibodies: SLURP1 (Clone 569317; R&D Systems, Minneapolis, MN, USA; 1:100 dilution), CRISP3 (clone 295203, R&D Systems; 1:100 dilution), FLG (SPM181, Abcam, Cambridge, MA, USA; 1:25 dilution), ALOX15 (11-K, Santa Cruz Biotechnology, Santa Cruz, CA, USA; 1:100 dilution) and TNFAIP6 (FL-277, Santa Cruz Biotechnology; 1:200 dilution).

Techniques: Immunohistochemistry, Reflux, Expressing, Control, Staining

Journal: Oncotarget

Article Title: Endogenous CHRNA7-ligand SLURP1 as a potential tumor suppressor and anti-nicotinic factor in pancreatic cancer

doi: 10.18632/oncotarget.24312

Figure Lengend Snippet: ( A ) The measurement of pancreatic SLURP1 mRNA expression with qRT-PCR in 66 pancreatic samples revealed the lack of expression in non-malignant pancreatic tissues and most PDAC lesions. ( B ) The concentration of SLURP1 was measured in 106 human serum samples using a commercial EIA kit produced by CUSABIO. Multiple comparison testing revealed a lack of difference between the analyzed groups ( p = 0.643). ( C ) Circulating SLURP1 levels correlated with the grade of differentiation but not with any of the TNM parameters. ( D ) Dividing the PDAC patients with resected tumors into SLURP1 high/low groups according to the preoperative level of circulating SLURP1 for the Kaplan-Meier survival analysis revealed significantly longer survival of SLURP1 high patients (cut-off = 16 ng/ml; log-rank test p = 0.007), MS: median survival. ( E ) The concentration of SLURP1 was re-measured in 67 human serum samples using a commercial EIA kit produced by USCN and confirmed the lack of difference between the analyzed groups ( p = 0.951). ( F ) Nevertheless, the USCN-EIA recognized the CUSABIO standard but not vice versa, and the USCN values for SLURP1 were three-fold lower and lacked any correlation with the CUSABIO values. Additional information is presented in Table . ( G ) Clustering analysis of the RNAseq data obtained for the PDAC specimens corresponding to the serum samples with low and high SLURP1 content.

Article Snippet: To determine the exact physiological concentrations of SLURP1 in blood, we used commercially available EIA kits manufactured by CUSABIO Biotech Co., Ltd. (Wuhan, P.R.

Techniques: Expressing, Quantitative RT-PCR, Concentration Assay, Produced, Comparison

Journal: Oncotarget

Article Title: Endogenous CHRNA7-ligand SLURP1 as a potential tumor suppressor and anti-nicotinic factor in pancreatic cancer

doi: 10.18632/oncotarget.24312

Figure Lengend Snippet: Measurement of SLURP1 in human serum by EIA

Article Snippet: To determine the exact physiological concentrations of SLURP1 in blood, we used commercially available EIA kits manufactured by CUSABIO Biotech Co., Ltd. (Wuhan, P.R.

Techniques: Bacteria, Recombinant, Avidin-Biotin Assay

Journal: Oncotarget

Article Title: Endogenous CHRNA7-ligand SLURP1 as a potential tumor suppressor and anti-nicotinic factor in pancreatic cancer

doi: 10.18632/oncotarget.24312

Figure Lengend Snippet: ( A ) Simultaneous FACS and qRT-PCR analyses revealed CHRNA7-positivity of all eight tested PDAC cell lines, whereby membranous CHRNA7-staining showed significant inter-experimental variability and lack of correlation with RNA levels. The graph summarizes the data of two independent experiments shown below and measuring CHRNA7 mRNA (qRT-PCR; log10-transformed number of transcripts/10k PPIB) and surface protein expression (log10-transformed mean fluorescence intensity/MFI values) in unrelated passages of each cell line. ( B ) Individual FACS histograms illustrating intra- and inter-experimental variability are shown as an overlap of anti-CHRNA7-IgG (gray tinted area) and rabbit IgG (bold black line; isotype control) profiles; the difference in their geometric MFIs was used to calculate final MFI value for each culture. ( C ) qRT-PCR data demonstrating the inter-experimental stability of CHRNA7 mRNA expression also revealed the existence of the two groups, whereby CHRNA7 high -group but not CHRNA7 neg/low -group showed RNA-agreeable, stable pattern of protein expression. ( D – F ) The siRNA-based depletion of CHRNA7 confirmed the specificity of the reagents such as primers (qRT-PCR, D) and antibodies (Western blot, E, and FACS, F). As illustrated for COLO357 cultures, transfection with three commercially available CHRNA7-specific siRNA sets (si#1, si#2, si#3) eliminated over 75% of CHRNA7 mRNA and protein compared to the transfection of cells with negative control siRNA set (neg.si) or left untreated (control). ( G ) siRNA-based depletion of CHRNA7 indicated the preferential binding of SLURP1 to this receptor on PDAC cells. For comparison, FITC-conjugated SLURP1 was added to COLO357 and PANC-1 cells transfected with three different CHRNA7-siRNA sets (‘CHRNA7-depletion’ group depicted by grey-, green- and rose-colored profiles for si#1, si#2 and si#3, respectively) and to cells remaining intact or transfected with negative siRNA (‘controls’ group depicted by blue and lilac-colored profiles).

Article Snippet: To determine the exact physiological concentrations of SLURP1 in blood, we used commercially available EIA kits manufactured by CUSABIO Biotech Co., Ltd. (Wuhan, P.R.

Techniques: Quantitative RT-PCR, Staining, Transformation Assay, Expressing, Fluorescence, Control, Western Blot, Transfection, Negative Control, Binding Assay, Comparison

Journal: Oncotarget

Article Title: Endogenous CHRNA7-ligand SLURP1 as a potential tumor suppressor and anti-nicotinic factor in pancreatic cancer

doi: 10.18632/oncotarget.24312

Figure Lengend Snippet: ( A ) The wound healing (scratch) assay, ( B ) The Matrigel-based invasion assay and ( C ) MTT-based growth assay revealed that without affecting proliferation of the PDAC cells, SLURP1 significantly reduced their migration and invasion ( p < 0.01), whereas nicotine tended to promote these ( p = 0.05–0.11). Co-application abolished these opposite effects ( p < 0.05). CHRNA7-depletion abolished the action of the ligands ( p -values < 0.0003 in controls vs. p -values > 0.36 upon CHRNA7-depletion), whereby this effect was evident for SLURP1, it was much weaker for nicotine. Upper panels: representative images from one experiment; lower panels: quantification of data obtained from four to eight independent experiments with control cultures (grey bars: pooled samples which have been left intact or transfected with negative control siRNA) and CHRNA7-depleted cultures (white bars: pooled samples which have been separately transfected with siRNA sets si#1, si#2 and si#3). The effect observed in the non-treated/non-transfected culture was set as control = 100% and served as a reference for normalization of the raw data in each experiment. The detailed description of the data processing and the exact numbers of the values per analyzed group are given in the Materials and Methods. The overall impact of the ligands treatment was determined with one-way ANOVA test separately for control and CHRNA7-depleted cohorts. Two-groups comparisons estimating effects of ligands or knockdowns have been performed with Welch’s t -test. Significant level shown as * = p < 0.05; ** = p < 0.01; *** = p < 0.001.

Article Snippet: To determine the exact physiological concentrations of SLURP1 in blood, we used commercially available EIA kits manufactured by CUSABIO Biotech Co., Ltd. (Wuhan, P.R.

Techniques: Wound Healing Assay, Invasion Assay, Growth Assay, Migration, Control, Transfection, Negative Control

Journal: Oncotarget

Article Title: Endogenous CHRNA7-ligand SLURP1 as a potential tumor suppressor and anti-nicotinic factor in pancreatic cancer

doi: 10.18632/oncotarget.24312

Figure Lengend Snippet: ( A ) FACS analysis of the PDAC cells showed no difference in binding of FITC-labeled SLURP1 in the absence (green line) or presence (blue line) of nicotine. ( B ) Radioligand assay showed no difference in binding of 3 H-labeled nicotine in the absence (red bars) or presence (blue bars) of SLURP1, whereas exposure to a competitive CHRNA7-antagonist methyllycaconitine citrate (MLA) eliminated 80% of the binding. dpm : disintegrations per minute. ( C ) Both, SLURP1 and nicotine, induced MLA-sensitive Ca 2+ influxes in COLO357 and PANC-1 cells. ( D ) Concurrent addition of SLURP1 and nicotine augmented Ca 2+ influx in COLO357 ( p = 0.01) and did no alter it in PANC-1 cultures. ( E ) Western blot analysis of the cellular lysates using the PathScan antibody cocktail showed that SLURP1 significantly inhibited basal phosphorylation of pAKT, pERK1/2, and p90RSK, but not of pRPS6 in COLO357, and this deactivation of potentially oncogenic signaling was maintained with concurrent exposure to nicotine. Nicotine alone showed no significant impact on the phosphorylation of these molecules. The lower panel summarizes data from four independent experiments and presents the quantification of the Western blot bands normalized to the RAB11 signal expressed as fold change over the untreated control. ( F ) TransAM-EIA assay, measuring the concentration of nuclear NF-κB in COLO357 cells, revealed that SLURP1 and nicotine significantly reduced the nuclear translocation of NF-κB when delivered alone but not together. The graphs summarize data from 5 to 14 independent experiments in duplicate or quadruplicate for each treatment. Significance level * = p < 0.05.

Article Snippet: To determine the exact physiological concentrations of SLURP1 in blood, we used commercially available EIA kits manufactured by CUSABIO Biotech Co., Ltd. (Wuhan, P.R.

Techniques: Binding Assay, Labeling, Radioligand Assay, Western Blot, Phospho-proteomics, Control, Enzyme Immunoassay, Concentration Assay, Translocation Assay

Journal: Frontiers in Immunology

Article Title: Endogenous α7 nAChR Agonist SLURP1 Facilitates Escherichia coli K1 Crossing the Blood-Brain Barrier

doi: 10.3389/fimmu.2021.745854

Figure Lengend Snippet: The effect of SLURP1 on E coli K1 penetration and PMN transmigration across the BBB in vitro . (A) The invasion of E coli K1 into HBMEC which pretreated with indicated doses of BSA or SLURP1. Data are presented as percent of the control values. (B) Transwell-cultured HBMEC monolayers were pre treatment with indicated doses of BSA or SLURP1 for 2 h, followed by incubated with E coli K1 in the bottom and PMN in the top of filter successively. PMN in the bottom of filter were harvested and counted. (C) The growth curve of E coli K1 in medium containing indicated doses of SLURP1. (D) The upregulation effect of SLURP1 in HBMEC which had been transfected with pCNDA3.1+-SLURP1. (E) The invasion of E coli K1 into HBMEC which had been transfected with pCNDA3.1+-SLURP1. Data are presented as percent of the control values. (F) Effect of SLURP1 upregulation on E coli K1-induced PMN transmigration across the HBMEC monolayers. Data are presented as percent of the control values. (G) The knockdown effect of SLURP1 in HBMEC transfected with siRNA. (H) The invasion of E coli K1 into HBMEC which had been transfected with siRNA. Data are presented as percent of the control values. (I) Effect of SLURP1 knockdown on E coli K1-induced PMN transmigration across the HBMEC monolayers. Data are presented as percent of the control values. Over., overexpression; Kno., knockdown. The immunoblots results are representative of three independent experiments (D, G) . The data are displayed as the mean ± SEM from three independent experiments (A–I) . * p < 0.05; ** p < 0.01 by one-way ANOVA followed by Bonferroni post-hoc test (A, B, F, I) and Student’s t -test (D, E, G, H) . ns, not significant.

Article Snippet: In brief, predesigned siRNA specific for SLURP1 and nontargeting scrambled siRNA (control) were obtained from Santa Cruz Biotechnology (CA, USA).

Techniques: Transmigration Assay, In Vitro, Control, Cell Culture, Incubation, Transfection, Knockdown, Over Expression, Western Blot

Journal: PLoS ONE

Article Title: IL-22/STAT3-Induced Increases in SLURP1 Expression within Psoriatic Lesions Exerts Antimicrobial Effects against Staphylococcus aureus

doi: 10.1371/journal.pone.0140750

Figure Lengend Snippet: IMQ or control cream was applied daily to the shaved backs for BALB/c mice. (A) Phenotypical presentation of mouse back skin after 2 or 4 days of IMQ treatment. (B) Immunofluorescent staining of vehicle or IMQ cream-treated mouse skin using an anti-SLURP1 antibody. Dashed lines indicate the border between the epidermis and dermis. Scale bars = 50 μm. The experiments were repeated six times with similar results. (C) Quantification of IL-22 and SLURP1 mRNA expression in skin from mice treated for 2 days with IMQ. Bars depict the mean ± S.D. (n = 6) of fold-changes in mRNA copy number normalized to GPADH and quantified relative to control. *p < 0.05, **p < 0.01 vs. control (Student’s t-test).

Article Snippet: The antibodies used in this study were monoclonal anti-human SLURP1 (1:1000 dilution; Abnova, Taipei, Taiwan), polyclonal anti-human STAT-3 (1:1000 dilution; Santa Cruz Biotechnology, Dallas, TX, USA), and monoclonal anti-human STAT-5 (1:1000 dilution; Santa Cruz Biotechnology).

Techniques: Control, Cream, Staining, Expressing

Journal: PLoS ONE

Article Title: IL-22/STAT3-Induced Increases in SLURP1 Expression within Psoriatic Lesions Exerts Antimicrobial Effects against Staphylococcus aureus

doi: 10.1371/journal.pone.0140750

Figure Lengend Snippet: (A, B) NHEKs were stimulated 24 h with the indicated panel of cytokines (50 ng/ml) (A) or with 0.5, 5, 50, 500 and 1000 ng/ml IL-22 (B), after which SLURP1 mRNA levels were measured using quantitative real-time PCR. (C) NHEKs were stimulated with IL-22 or left untreated for 24 h in the presence of actinomycin D (Act. D), cycloheximide (CHX) or the control solvent (DMSO), after which SLURP1 expression was analyzed using real-time PCR. (D, E) NHEKs were stimulated for 24 h with IL-22 or a combination of IL-22 plus IL-17A, TNF-α or IFN-γ. SLURP1 expression was then analyzed using real-time PCR (D) and western blotting (E). Bars depict the mean ± S.D. (n = 6). *p < 0.05, ***p < 0.001 (one-way ANOVA).

Article Snippet: The antibodies used in this study were monoclonal anti-human SLURP1 (1:1000 dilution; Abnova, Taipei, Taiwan), polyclonal anti-human STAT-3 (1:1000 dilution; Santa Cruz Biotechnology, Dallas, TX, USA), and monoclonal anti-human STAT-5 (1:1000 dilution; Santa Cruz Biotechnology).

Techniques: Real-time Polymerase Chain Reaction, Control, Solvent, Expressing, Western Blot

Journal: PLoS ONE

Article Title: IL-22/STAT3-Induced Increases in SLURP1 Expression within Psoriatic Lesions Exerts Antimicrobial Effects against Staphylococcus aureus

doi: 10.1371/journal.pone.0140750

Figure Lengend Snippet: (A) NHEKs were incubated for 24 h with IL-22 (50 ng/ml) in the presence or absence of the MAP kinase kinase inhibitor PD98059 (30 μM), the STAT3 inhibitor S3I-201 (50 μM) or the STAT5 inhibitor 573108 (100) μM), after which SLURP1 expression was analyzed using real-time PCR. As a control, 0.1% (v/v) DMSO was used. Bars depict the mean ± S.D. (n = 6). (B, C) NHEKs were transfected with 100 nM scrambled control, STAT3 or STAT5 siRNA. After incubating the transfectants for 48 h, IL-22 was added to a final concentration of 50 ng/ml, and the cells were harvested 24 h later. (B) Cell lysates (30 μg of total protein/lane) were subjected to SDS-PAGE, and immunoblots were probed with anti-STAT3, anti-STAT5 or anti-β-actin antibody. The experiments were repeated six times with similar results. (C) Quantitative real-time PCR analysis of SLURP1 mRNA. Bars depict the mean ± S.D. (n = 6). ***p < 0.001 (one-way ANOVA).

Article Snippet: The antibodies used in this study were monoclonal anti-human SLURP1 (1:1000 dilution; Abnova, Taipei, Taiwan), polyclonal anti-human STAT-3 (1:1000 dilution; Santa Cruz Biotechnology, Dallas, TX, USA), and monoclonal anti-human STAT-5 (1:1000 dilution; Santa Cruz Biotechnology).

Techniques: Incubation, Expressing, Real-time Polymerase Chain Reaction, Control, Transfection, Concentration Assay, SDS Page, Western Blot

Journal: Biomedicines

Article Title: Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures

doi: 10.3390/biomedicines12102289

Figure Lengend Snippet: Primer sequences used in RT-qPCR reaction.

Article Snippet: The following antibodies were used for the ELISA test: anti-TGFβ1 (TGFB1 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ2 (TGFB2 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ3 (TGFB3 ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL1B (Human IL-1 beta ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL15 (IL15 ELISA Kit; MyBiosource, San Diego, CA, USA), anti-VEGFA (VEGFA ELISA Kit; MyBiosource, San Diego, CA, USA), anti-IHNB (IHNB ELISA Kit; MyBiosource, San Diego, CA, USA), anti-SLURP1 (SLURP1 ELISA Kit; MyBiosource, San Diego, CA, USA), and anti-GAPDH (Thermo Fisher Scientific, Waltham, MA, USA).

Techniques:

Journal: Biomedicines

Article Title: Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures

doi: 10.3390/biomedicines12102289

Figure Lengend Snippet: Changes in gene expression in tears of patients who underwent PRK, FS-LASIK, and SMILE over 180 days of observation.

Article Snippet: The following antibodies were used for the ELISA test: anti-TGFβ1 (TGFB1 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ2 (TGFB2 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ3 (TGFB3 ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL1B (Human IL-1 beta ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL15 (IL15 ELISA Kit; MyBiosource, San Diego, CA, USA), anti-VEGFA (VEGFA ELISA Kit; MyBiosource, San Diego, CA, USA), anti-IHNB (IHNB ELISA Kit; MyBiosource, San Diego, CA, USA), anti-SLURP1 (SLURP1 ELISA Kit; MyBiosource, San Diego, CA, USA), and anti-GAPDH (Thermo Fisher Scientific, Waltham, MA, USA).

Techniques: Gene Expression

Journal: Biomedicines

Article Title: Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures

doi: 10.3390/biomedicines12102289

Figure Lengend Snippet: Changes in concentration profiles of analyzed proteins over a 180-day observation period in patients who underwent PRK procedure. TGF-β1–3 , transforming growth factor beta 1–3; IL-1β , interleukin-1 beta; IL-15 , interleukin-15; IHNBA , inhibin beta A chain; VEGFA , vascular endothelial growth factor A; SLURP1 , secreted Ly-6_uPAR-related protein 1.

Article Snippet: The following antibodies were used for the ELISA test: anti-TGFβ1 (TGFB1 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ2 (TGFB2 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ3 (TGFB3 ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL1B (Human IL-1 beta ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL15 (IL15 ELISA Kit; MyBiosource, San Diego, CA, USA), anti-VEGFA (VEGFA ELISA Kit; MyBiosource, San Diego, CA, USA), anti-IHNB (IHNB ELISA Kit; MyBiosource, San Diego, CA, USA), anti-SLURP1 (SLURP1 ELISA Kit; MyBiosource, San Diego, CA, USA), and anti-GAPDH (Thermo Fisher Scientific, Waltham, MA, USA).

Techniques: Concentration Assay

Journal: Biomedicines

Article Title: Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures

doi: 10.3390/biomedicines12102289

Figure Lengend Snippet: Changes in concentration profiles of analyzed proteins over a 180-day observation period in patients who underwent FS-LASIK procedure. TGF-β1–3 , transforming growth factor beta 1–3; IL-1β , interleukin-1 beta; IL-15 , interleukin-15; IHNBA , inhibin beta A chain; VEGFA , vascular endothelial growth factor A; SLURP1 , secreted Ly-6_uPAR-related protein 1.

Article Snippet: The following antibodies were used for the ELISA test: anti-TGFβ1 (TGFB1 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ2 (TGFB2 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ3 (TGFB3 ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL1B (Human IL-1 beta ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL15 (IL15 ELISA Kit; MyBiosource, San Diego, CA, USA), anti-VEGFA (VEGFA ELISA Kit; MyBiosource, San Diego, CA, USA), anti-IHNB (IHNB ELISA Kit; MyBiosource, San Diego, CA, USA), anti-SLURP1 (SLURP1 ELISA Kit; MyBiosource, San Diego, CA, USA), and anti-GAPDH (Thermo Fisher Scientific, Waltham, MA, USA).

Techniques: Concentration Assay

Journal: Biomedicines

Article Title: Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures

doi: 10.3390/biomedicines12102289

Figure Lengend Snippet: Changes in concentration profiles of analyzed proteins over a 180-day observation period in patients who underwent SMILE procedure. TGF-β1–3 , transforming growth factor beta 1–3; IL-1β , interleukin-1 beta; IL-15 , interleukin-15; IHNBA , inhibin beta A chain; VEGFA , vascular endothelial growth factor A; SLURP1 , secreted Ly-6_uPAR-related protein 1.

Article Snippet: The following antibodies were used for the ELISA test: anti-TGFβ1 (TGFB1 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ2 (TGFB2 ELISA kit; MyBiosource, San Diego, CA, USA), anti-TGFβ3 (TGFB3 ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL1B (Human IL-1 beta ELISA kit; MyBiosource, San Diego, CA, USA), anti-IL15 (IL15 ELISA Kit; MyBiosource, San Diego, CA, USA), anti-VEGFA (VEGFA ELISA Kit; MyBiosource, San Diego, CA, USA), anti-IHNB (IHNB ELISA Kit; MyBiosource, San Diego, CA, USA), anti-SLURP1 (SLURP1 ELISA Kit; MyBiosource, San Diego, CA, USA), and anti-GAPDH (Thermo Fisher Scientific, Waltham, MA, USA).

Techniques: Concentration Assay