Journal: PLoS ONE

Article Title: Pro-Inflammatory Action of MIF in Acute Myocardial Infarction via Activation of Peripheral Blood Mononuclear Cells

doi: 10.1371/journal.pone.0076206

Figure Lengend Snippet: A . Representative images showing a temporal changes of macrophages (CD68+ cells, purple colour) by immunohistochemical staining in mice treated with isotype control IgG or anti-MIF polyclonal antibody (MIF Ab) post MI. Bar=100 μm. B , C . Grouped data showing that neutralizing MIF by anti-MIF Ab, i.p. given immediately after MI, significantly reduced density of macrophages ( B , CD68 positive cells) and leukocytes ( C , CD45+ cells) at 24 h, but had no effect on macrophage density at 7 days. n=3 for sham-operated groups (SH) and n=6-7 for each time point of MI groups. * P<0 . 05 vs. respective SH, † P<0.05 vs. respective 24 h MI, # P <0.05. D . Representative immunoblotting images for monocyte chemoattractant protein 1 (MCP-1) and CD74 in hearts from sham-operated or MI (24 h) mice treated with isotype control IgG or MIF Ab. E , F . Quantitative analysis of MCP-1 ( E ) and CD74 ( F ) expression. n=3/per sham group, n=5/per MI group. * P<0 . 05 vs. sham, # P<0.05 . G . Effects of anti-MIF Ab and isotype control IgG (CTL) treatment on healing parameters, i.e. size of residual necrotic myocardium and collagen content in the infarct area, and infarct wall thickness at 7 days post MI. n=4-6/group. H . Representative photos of ruptured hearts that occurred at 3-4 days after MI. Arrows indicate the rupture site around the border zone. I . Treatment with the MIF antagonist, COR100140, in the first 3 days post MI significantly reduced incidence of cardiac rupture. n=25 for untreated and 15 for treated groups.

Article Snippet: To investigate the effect of anti-MIF intervention on inflammatory responses, animals were treated with a single dose of anti-MIF polyclonal antibody (Santa Cruz, sc-20121) or isotype control rabbit IgG (Santa Cruz, sc-2027), at 5 mg/kg i.p. immediately after CAO.

Techniques: Immunohistochemical staining, Staining, Control, Western Blot, Expressing

Journal: Scientific Reports

Article Title: Conservation of Cdc14 phosphatase specificity in plant fungal pathogens: implications for antifungal development

doi: 10.1038/s41598-020-68921-3

Figure Lengend Snippet: Fungal Cdc14 homologs can be specifically inhibited by a substrate mimetic. ( a ) Structure of the synthetic peptide used for inhibition assays (sequence Glu-Val-pCF 2 Ser-Pro-Thr-Lys-Arg-amide). ( b ) Dose response with the pCF 2 Ser peptide from A and the indicated fungal Cdc14 enzymes using DiFMUP as substrate. Data represent the average of 5 or 6 independent trials. It was not practical to show error bars on the graph, however error values for replicate K i measurements are provided in ( c ). Best fit lines were generated with a standard slope dose response function with plateaus set at 100% and 0% in Graphpad Prism. We did not have enough pCF 2 Ser peptide to perform the full analysis on all 8 plant fungal pathogen homologs. ( c ) Each individual trial from the experiment in ( b ) was fit as described in b to generate IC 50 , from which K i was calculated (see “ ”). Values represent the mean ± standard deviation. ( d ) Comparison of pCF 2 Ser peptide inhibition of human tyrosine phosphatase PTP1B and dual specificity phosphatase VHR to ScCdc14 and human Cdc14A using DiFMUP at the measured K M for each enzyme. Percent activity relative to a no inhibitor control was calculated and plotted. Data are means of 3 independent experiments and error bars are standard deviations. Numbers over the bars are p values from a t- test (unpaired, one-tail) comparing 0 and 200 µM inhibitor data.

Article Snippet: Best fit lines were generated with a standard slope dose response function with plateaus set at 100% and 0% in Graphpad Prism.

Techniques: Inhibition, Sequencing, Generated, Standard Deviation, Comparison, Activity Assay, Control