Journal: Journal of Cell Science

Article Title: Epithelial plasticity in COPD results in cellular unjamming due to an increase in polymerized actin

doi: 10.1242/jcs.258513

Figure Lengend Snippet: Inhibitors of actin polymerization improve monolayer integrity and reverse plasticity. (A–C) LatA (an actin polymerization inhibitor) and U0126 (a MAPK inhibitor) are the only drugs which reduced cellular velocity (A), TEER (B) and correlation length (C) on the CS-exposed epithelia [cells treated with pathway modulators such as LatA, the actin-polymerizing agent JaspA, U0126, the TGFβ1 neutralizer (1D11), or an antagonist of Wnt signaling pathway (DKK1) and compared to vehicle control]. Data is representative of two donors (three to six inserts per donor). (D) None of the inhibitors restored the CS-induced decrease in basal mRNA expression of the epithelial marker CDH1 . (E–J) The levels of the mesenchymal markers ( CDH2 , VIM , SNAI1 , SNAI2 , ZEB1 and ZEB2 ) were significantly reduced relative to GAPDH in CS-exposed epithelia treated with several pathway modulators (LatA, U0126, 1D11 and DKK1) as analyzed by qPCR. (K) LatA and U0126 treatment reduced mean square displacement (MSD) in CS exposed epithelia. Data is representative of three to six inserts from two donors. (L–O) LatA and U0126 treatment improved TEER in CHBE cells (L), LatA and U0126 treatment decreased cellular velocity in COPD epithelia (CHBE) (M), LatA and U0126 treatment reduced correlation length in CHBE cells (N), and LatA and U0126 treatment improved the height of pseudostratified epithelia on COPD epithelia (CHBE) (O). (P) Representative DIC image from three inserts from one donor taken with a 40× oil objective of CHBE treated with or without LatA or U0126 showing improved monolayer height. Scale bars: 25 µm. (Q) LatA and U0126 treatment reduced the MSD with time in CHBE cells approaching levels similar to that of NHBE. Of note, there is not a significant increase in MSD with time in pEMT-induced NHBE. Data is representative of nine inserts, except for cellular velocity and correlation length (six inserts) and height of pseudostratified epithelia (three inserts) from one donor of CHBE. Graphs are shown with median bars. Statistics determined by Kruskal–Wallis test followed by Dunn's multiple comparison test, with P <0.05 considered statistically significant.

Article Snippet: The NHBE cells at the ALI were exposed to CS for 10 days and simultaneously basolaterally treated with an antagonist of Wnt signaling pathway (recombinant human DKK1 protein, 50 ng/ml, R&D Systems), TGFβ1 neutralizer [TGFβ-1,2,3 monoclonal antibody (1D11), 1.25 μg/ml, Thermo Fisher Scientific], MAPK inhibitor (U0126, 15 μM, Cell Signaling Technology ® ), an inhibitor of actin polymerization (Latrunculin A, 0.625 μM, Sigma-Aldrich) or the actin filament-polymerizing and stabilizing agent (Jasplakinolide A, 0.25 μM, Sigma-Aldrich).

Techniques: Control, Expressing, Marker, Comparison

Journal: The Journal of allergy and clinical immunology

Article Title: Activin A and TGF-β promote T H 9 cell–mediated pulmonary allergic pathology

doi: 10.1016/j.jaci.2011.12.965

Figure Lengend Snippet: Induction of TH9 differentiation in vitro by activin A. A, TH9 cells generated in the presence of IL-4 alone or in association with TGF-β1, activin A, and/or IL-25. B, Percentage of TH9 cells plotted in a histogram. C, Phenotype of TH9 cells differentiated in the presence of IL-4 with either TGF-β1 or activin A. D, IL-9 secretion from activin A–derived TH9 cells after 4 days in culture in the presence of 0.1 ng/mL of TGF-β1. Data shown represent means ± SEMs.

Article Snippet: In blocking experiments, mice received 20 μg of neutralizing antibody to murine activin A (R&D Systems, Abingdon, UK) and/or anti-TGF-β (5 mg/kg, clone 1D11 pan neutralizing TGF-β1-3; Genzyme Corporation, Cambridge, Mass) or isotype control intraperitoneally.

Techniques: In Vitro, Generated, Derivative Assay

Journal: The Journal of allergy and clinical immunology

Article Title: Activin A and TGF-β promote T H 9 cell–mediated pulmonary allergic pathology

doi: 10.1016/j.jaci.2011.12.965

Figure Lengend Snippet: Acute blockade of TGF-β and activin A inhibits TH9 differentiation. A, Schematic of experimental protocol. B, TH9 cells recovered from the lung after treatment with either anti–TGF-β and/or anti–activin A in mice challenged with either PBS or HDM. Total cells (C), lung eosinophils (D), and TH2 cells (E) recovered from the lung. Serum mMCP-1 levels (F) and intraepithelial mast cells (G) per lung section. IL-9 (H) and IL-13 (I) levels in supernatants from lymph node cell cultures. J, IL-25 levels in the lungs. Data shown represent means ± SEMs. *P < .05. mMCP-1, Mouse mast cell protease-1.

Article Snippet: In blocking experiments, mice received 20 μg of neutralizing antibody to murine activin A (R&D Systems, Abingdon, UK) and/or anti-TGF-β (5 mg/kg, clone 1D11 pan neutralizing TGF-β1-3; Genzyme Corporation, Cambridge, Mass) or isotype control intraperitoneally.

Techniques:

Journal: The Journal of allergy and clinical immunology

Article Title: Activin A and TGF-β promote T H 9 cell–mediated pulmonary allergic pathology

doi: 10.1016/j.jaci.2011.12.965

Figure Lengend Snippet: Chronic blockade of TGF-β and activin A reduces airway remodeling. A, Schematic of experimental protocol. B, Peribronchial and perivascular cellular infiltrate (H&E), purple-colored mucin-containing cells in the epithelium (PAS), and perivascular and peribronchiolar collagen (sirrius red) and brown stained intraepithelial mast cells. Original magnification ×40. Scale bar = 50 μm. C, Quantification of mucus positive cells. D, Intraepithelial mast cells per lung section. E, Serum mMCP-1 levels. F, Total lung collagen. G, Total cells recovered from BAL and lung. H, IL-25 levels in the lung. I, Airway resistance (RI) following 3-week HDM challenge. Data shown represent means ± SEMs. *P < .05. BAL, Bronchoalveolar lavage; MCPT7, mouse tryptase beta 1; mMCP-1, mouse mast cell protease-1; PAS, periodic acid-Schiff.

Article Snippet: In blocking experiments, mice received 20 μg of neutralizing antibody to murine activin A (R&D Systems, Abingdon, UK) and/or anti-TGF-β (5 mg/kg, clone 1D11 pan neutralizing TGF-β1-3; Genzyme Corporation, Cambridge, Mass) or isotype control intraperitoneally.

Techniques: Staining

Journal: BMC Biology

Article Title: Single-cell transcriptomics reveals the effect of PD-L1/TGF-β blockade on the tumor microenvironment

doi: 10.1186/s12915-021-01034-z

Figure Lengend Snippet: Anti-PD-L1 plus anti-TGF-β leads to tumor regression in mice. a–d Hu-PD-L1 KI mice bearing s.c. Hu-PD-L1-MC38 tumors ( n = 6 per group) were dosed I.P. biweekly for 3 weeks with PBS, aPD-L1 (2 mg/kg; atezolizumab), or aPD-L1 plus aTGF-β (10 mg/kg; 1D11). a Average MC38 tumor volume ± SEM is shown. P values were determined using Wilcoxon rank sum test, comparing tumor sizes on day 18. b Spider plots showing MC38 tumor volume for individual mice over time. c Survival plot for the MC38 study. P values were determined using log-rank test. d CD3 IHC score in MC38 tumors by immunohistochemistry (IHC). Each point is the IHC score representing the density of CD3+ cells from an individual mouse. The horizontal black bars of the box plots indicate median score, while the lower and upper hinges correspond to the first and third quartiles, respectively. P values were determined using Wilcoxon rank sum test. e–h Mice bearing orthotopic EMT6 tumors were treated with PBS, aPD-L1 (10 mg/kg for the first dose with each subsequent dose at 5 mg/kg; atezolizumab), aTGF-β (10 mg/kg; 1D11), or aPD-L1 plus aTGF-β. For all treatments, the first dose was administered I.V. on day 0 and the eight subsequent doses were administered I.P. three times per week. n = 12 mice per group, including 3 mice per group taken down early on day 8 for scRNA-seq analysis. e Average EMT6 tumor volume ± SEM is shown. P values were determined using Wilcoxon rank sum test. Mice removed early for scRNA-seq analysis were not included in the average. f Spider plots showing EMT6 tumor volume for individual mice over time. Mice sacrificed for scRNA-seq ( n = 3 per group) are shown in red. g Survival plot for the EMT6 study. P values were determined using log-rank test. h CD3 IHC score in EMT6 tumors. Each point is the IHC score representing the density of CD3+ cells from an individual mouse. The horizontal black bars of the box plots indicate median score, while the lower and upper hinges correspond to the first and third quartiles, respectively. P values were determined using Wilcoxon rank sum test. Non-significant p values are not shown for all panels

Article Snippet: The mice were dosed I.P. biweekly for 3 weeks with PBS, anti-PD-L1 (atezolizumab, Roche, 2 mg/kg), anti-TGF-β (mouse IgG1 clone 1D11 from BioXCell, 10 mg/kg), or a combination of anti-PD-L1 (2 mg/kg) and anti-TGF-β (10 mg/kg).

Techniques: Immunohistochemistry

Journal:

Article Title: Defective T-Cell Activation Is Associated with Augmented Transforming Growth Factor ? Sensitivity in Mice with Mutations in the Sno Gene

doi: 10.1128/MCB.23.15.5446-5459.2003

Figure Lengend Snippet: T-cell proliferation assays examining functions of unprimed T cells show that Sno5Δ−/− and Snoex1−/− mutant T cells have a T-cell activation defect that is largely compensated for by addition of excess IL-2 or incubation with anti-TGF-β antibody. (A) Spleen cells from littermates of each genotype were seeded at a density of 500 × 103 responder cells per microwell in 96-well plates. The cells were incubated for 66 h at 37°C and then for a final 6 h with 1 μCi of [3H]thymidine and then harvested onto glass fiber filters to determine the [3H]thymidine incorporation. The numbers presented are kilocounts of [3H]thymidine per minute (background samples without stimulator were subtracted) in the average of triplicate wells from a representative experiment. The error bars indicate the calculated standard deviations. For T-cell receptor stimulation of splenocytes, 10 ng of 145-2C11 αCD3 allogeneic major histocompatibility complex anti-T-cell receptor (T-cell receptor) monoclonal antibody was preincubated in each well as indicated (aCD3). Additional antibody or cytokines were added as indicated (TGFb, TGF-β). Control wells had no αCD3 stimulator or other additions to the media and had very low proliferation. The genotypes were wild type (Sno+/+), Sno5Δ−/−, and Snoex1−/−. The asterisks indicate results that were statistically significantly (P < 0.05) different from the wild type. (B) Splenocytes were stimulated with PMA-ionomycin (PMA/io), with added cytokines as indicated. [3H]thymidine incorporation was measured on day 4 after plating. The genotypes were as in panel A. Representative experiments of 5 to 12 repetitions are shown in both panels.

Article Snippet: Anti-TGF-β antibody (MAB1835, clone 1D11 anti-TGF-β1, -β2, -β3; R&D Systems) was used at 2 μg/ml.

Techniques: Mutagenesis, Activation Assay, Incubation

Journal:

Article Title: Defective T-Cell Activation Is Associated with Augmented Transforming Growth Factor ? Sensitivity in Mice with Mutations in the Sno Gene

doi: 10.1128/MCB.23.15.5446-5459.2003

Figure Lengend Snippet: (A and B) Wild-type and mutant MEFs show different DNA synthetic rates (A) and Sno mutant cells are more sensitive to TGF-β (B). MEFs were isolated from litters of embryos derived from intercrossed mice that were either both wild type or both homozygous mutant. The genotype of each MEF preparation was verified by PCR; multiple preparations gave the same results in these experiments. Equal numbers of cells were plated in quadruplicate sets of microwells and untreated or treated with increasing concentrations of TGF-β or panspecific anti-TGF-β antibody at 2 μg/ml for 24 h. The cells were metabolically labeled for the final 3 h with 1 μCi of [3H]thymidine per well and harvested onto glass fiber filters to determine the [3H]thymidine incorporation. The asterisks above the control bars (panel A, control; panel B, 0.0 pM) indicate results that were statistically significantly (P < 0.05) different from the wild-type control. In panel A, the asterisks above the other bars indicate results that were statistically significantly (P < 0.05) different from the corresponding untreated control cells. In panel B, the asterisks at 100 pM TGF-β indicate significant (P < 0.02) difference from the wild type; the other asterisks indicate significant difference (P < 0.009) from the wild type. Incorporation into mutant cells was statistically significantly different from the wild type in the presence of anti-TGF-β antibody (Sno5Δ−/−, P < 0.013; Snoex1−/−, P < 0.001), whereas incorporation in mutants and the wild type was not significantly different in the presence of 5 pM TGF-β. The genotypes were wild type (Sno+/+), Sno5Δ−/−, and Snoex1−/−. Two independent experiments are shown with different absolute [3H]thymidine incorporation levels in the controls.

Article Snippet: Anti-TGF-β antibody (MAB1835, clone 1D11 anti-TGF-β1, -β2, -β3; R&D Systems) was used at 2 μg/ml.

Techniques: Mutagenesis, Isolation, Derivative Assay, Metabolic Labelling, Labeling

Journal:

Article Title: Defective T-Cell Activation Is Associated with Augmented Transforming Growth Factor ? Sensitivity in Mice with Mutations in the Sno Gene

doi: 10.1128/MCB.23.15.5446-5459.2003

Figure Lengend Snippet: MEFs from Snoex1−/− embryos show increased activity of the 3TP-lux and A3-lux TGF-β-responsive promoters, either with or without TGF-β supplementation of the cultures. (A) The activity of a TGF-β-responsive promoter element, 3TP-lux, was tested in transfected MEFs. The genotypes were wild type (Sno+/+), Sno5Δ−/−, and Snoex1−/−. “Control” indicates the level of luciferase activity of transfected 3TP-lux reporter alone. +TGF-b, TGF-β (100 pM) was added; +Sno, pCMV-SnoN expression construct was cotransfected. Sixty-millimeter-diameter dishes were transfected in triplicate, and the relative light units (RLU) emitted by the luciferase reporter were measured in duplicate in a luminometer. The error bars indicate the calculated standard deviations from each group of six values measured. The asterisks above the control bars indicate results that were statistically significantly (P < 0.05) different from the wild type. The asterisks above the other bars indicate results that were statistically significantly (P < 0.05) different from the corresponding untreated control cells. The results for the mutants were significantly different from the corresponding wild-type results under each condition (Snoex1−/−, P < 0.0007; Sno5Δ−/−, P < 0.034). (B) The increase with added TGF-β was plotted for Sno+/+ and Snoex1−/− cells from combined data from five experiments. Sno5Δ−/− cells had the same 2.7-fold increase as Sno+/+ cells and were not plotted. The asterisk indicates that the 3.2-fold increase in luciferase in the presence of TGF-β was statistically significantly (P ≤ 0.016) higher in Snoex1−/− cells than the 2.7-fold increase in the wild type. (C) The activity of a different TGF-β-responsive promoter element, A3-lux, was tested in wild-type and Snoex1−/− MEFs cotransfected with a FAST-2 expression vector. The asterisk indicates that the activity in the presence of TGF-β was statistically significantly higher in Snoex1−/− than in Sno+/+ MEFs (P < 0.005). (D) To confirm that MEFs of the three genotypes were transfected with similar efficiencies, a pSVβgal construct was transfected in parallel in the same experiment, and the dishes were stained and photographed. The transfection efficiencies were similar among the threegenotypes. The Snoex1−/− cells expressed lacZ from the knock-in construct, seen in the nuclear staining in the figure. The transfected pSVβgal gave cytoplasmic staining and was thus distinguishable from the nuclear-staining Snoex1−/− background.

Article Snippet: Anti-TGF-β antibody (MAB1835, clone 1D11 anti-TGF-β1, -β2, -β3; R&D Systems) was used at 2 μg/ml.

Techniques: Activity Assay, Transfection, Luciferase, Expressing, Construct, Plasmid Preparation, Staining, Knock-In

Journal:

Article Title: Defective T-Cell Activation Is Associated with Augmented Transforming Growth Factor ? Sensitivity in Mice with Mutations in the Sno Gene

doi: 10.1128/MCB.23.15.5446-5459.2003

Figure Lengend Snippet: Snoex1−/− MEFs show enhanced activation of endogenous JunB in response to TGF-β. (A) Real-time PCR measured levels of JunB endogenous mRNAs in wild-type and Sno mutant MEFs with (+TGFb) or without (−TGFb) incubation with 100 pM TGF-β for 2 h. The quantified levels calculated for each sample are presented in the histograms. Each sample was measured in quadruplicate and standardized against a dilution curve generated in the same experiment, using the same JunB primers and twofold serial dilutions of template (not shown). The genotypes are indicated below panel B. The asterisks indicate results that were statistically significantly (P < 0.015) different from the corresponding untreated cells. The difference in the presence of added TGF-β between Snoex1−/− and the wild type was significant (P < 0.018). (B) L7 ribosomal protein loading control real-time PCR results are presented as a histogram, showing that the samples contained comparable levels of RT-RNA; the profiles were not normalized. The error bars indicate the calculated standard deviations.

Article Snippet: Anti-TGF-β antibody (MAB1835, clone 1D11 anti-TGF-β1, -β2, -β3; R&D Systems) was used at 2 μg/ml.

Techniques: Activation Assay, Real-time Polymerase Chain Reaction, Mutagenesis, Incubation, Generated

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: A. OCT images of the left (OS) and right (OD) corneas of a cat before and 4 weeks after −10D PRK. Note the greater reflectivity in the sub-ablation stroma of the control eye (arrows) relative to the eye that received anti-TGFβ treatment post-PRK. The rectangles superposed over the corneal images indicate the location and approximate size of the areas analyzed for reflectivity and thickness. These analysis areas were located 1mm nasal to the center of each cornea and well outside the zone of the specular reflex. B. Plot of normalized backscattered light intensity obtained from the rectangular analysis areas in 25 OCT images of the left and right corneas of the cat shown in A versus central stromal depth, expressed as a percentage of the total stromal depth. 0% indicates the stromal/endothelial boundary, while 100% indicates the stromal/epithelial boundary. Reflectivity profiles are shown for both eyes of this cat pre-operatively and 4 weeks post-PRK. Note that the curves are relatively flat for both eyes pre-operatively, but that stromal reflectivity increases post-PRK. However, the eye that received anti-TGFβ treatments exhibits lower anterior stromal reflectivity than the control eye. C. Plot of the area under the reflectivity curve (see examples of these in B) for the anterior 20% of the corneal stroma as a function of time. Eyes that received anti-TGFβ treatment post-PRK exhibited lower mean reflectivity than control eyes at all post-operative time-points. D. Central epithelial thickness for control and anti-TGFβ eyes as a function of time. There was no significant difference between the two treatment groups. E. Central stromal thickness for control and anti-TGFβ eyes as a function of time, illustrating the consistently thinner stromas in anti-TGFβ treated eyes across post-PRK time-points. All graphs show means and standard errors of the mean.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques:

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: A-D. Images of the right eye (OD) of one cat treated with anti-TGFβ/Dexamethasone after PRK. Images were collected pre-operatively, 2, 4 and 12 weeks post-operatively, and demonstrate the radical change in reflectivity in this corneal region over time. E-F. Images of the left eye (OS) of the same cat, which only received vehicle solution following −10D PRK. Images were also collected pre-operatively, and then at 2, 4 and 12 weeks following PRK. Note the well-organized, regular syncitium of quiescent keratocytes pre-operatively and the disrupted, reactive and strongly reflective activated keratocytes and myofibroblasts that replace it postoperatively. Note also that the control eye exhibits much stronger reflectivity and cellularity than the anti TGFβ-treated eye, especially at 2 and 4 weeks post PRK.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques:

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: A-D. Images of the right eye (OD) of the cat in Fig.2, which was treated with −10D PRK and anti-TGFβ/Dexamethasone post-operatively, and demonstrating the radical change in reflectivity in this corneal region over time. E-F. Images of the left eye (OS) of the same cat, which only received vehicle solution following the −10D PRK. Images were also collected preoperatively, and then at 2, 4 and 12 weeks following PRK. Note the well-organized, regular syncitium of quiescent keratocytes pre-operatively, which contrasts with the less regular, reactive and strongly reflective activated keratocytes and myofibroblasts that replace it postoperatively, particularly in the control (left) eye. Indeed, the control eye exhibits much stronger reflectivity and cellularity than the anti-TGFβ-treated eye, especially at 2 and 4 weeks post-PRK. Note the spindle-shaped migratory fibroblasts (arrowed) and the cluster of reflective activated keratocytes in the right eye at 2 weeks post-PRK. Clustering is still present in anti-TGFβ-treated eyes 4 weeks post-PRK and is not seen in control eyes. As is evident in this set of images, control eyes exhibited greater cell density and greater reflectivity at this corneal depth than eyes treated with anti-TGFβ/Dexamethasone, at all post-operative time points.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques:

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: Photomicrographs of corneal sections from a normal, unoperated cat and pairs of cat eyes that underwent PRK and received either vehicle or anti-TGFβ treatment post-operatively. These cats were sacrificed at 2, 4 and 12 weeks post-PRK and sections of their corneas were double-labeled with antibodies against αSMA to label myofibroblasts and with propidium iodide (PI) to label cell nuclei. Note the absence of αSMA staining in the operated cat cornea, in contrast with the significant αSMA expression in the sub-ablation stroma of eyes that underwent PRK. The band of αSMA expression was significantly thicker and more continuous in control eyes than in contralateral eyes treated with anti-TGFβ. It was also most intense at 2 and 4 weeks post-PRK, becoming almost absent in the stroma by 12 weeks-post-PRK. PI staining also revealed an area of increased cellularity under the ablation zone in all post-operative eyes, although cell density appeared consistently higher in control eyes relative to eyes treated with anti-TGFβ.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques: Labeling, Staining, Expressing

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: A. Spherical equivalent M. B. 0°/90° astigmatic component J0. C. 45°/135° astigmatic component J45. All graphs are plotting values expressed as dioptric power vectors M, J0 and J45 for a 6 mm pupil diameter as a function of post-operative time. All values are means and standard errors of the mean. On the horizontal axis, P=pre-operative time. Note that lack of significant effect of anti-TGFβ treatment on changes in lower order aberrations induced by PRK.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques:

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: A. Total higher order aberration (HOA) RMS. B. Coma RMS (RMS of all Cn±1). C. Spherical aberration (SA) RMS (RMS of all Cn0). D. Residual HOA RMS (RMS of all Cn≥|±2|). All graphs are plotting means ± standard errors of the mean as a function of post-operative time, with P=pre-operative time. * = significantly greater change from pre-op in controls than eyes that received anti-TGFβ treatment at that particular time-point (P<0.05). Note the peak in HOA, coma, spherical aberration and residual HOA exhibited by control eyes 2 weeks post-PRK. Except for spherical aberration RMS, anti-TGFβ treated eyes maintained pre-operative levels of higher order aberrations after PRK.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques:

Journal:

Article Title: Optical effects of anti-TGF? treatment after photorefractive keratectomy in a cat model

doi: 10.1167/iovs.08-2277

Figure Lengend Snippet: Wavefront error maps (for a 9mm pupil diameter) in the right and left eye of the same cat at 8 weeks post-PRK, demonstrating the greater spatial irregularity of the wavefront in the control eye (bottom) compared to the eye treated with anti-TGFβ after PRK. While this effect was greatest at 2 weeks post-PRK, it was also maintained over the longer term.

Article Snippet: Anti-TGFβ treatment Following PRK, 13 eyes received a topical administration of anti-TGFβ antibody (Clone 1D11, R&D Systems, Minneapolis, Minn.).

Techniques: