Journal: Tissue Engineering Part A

Article Title: The Human Tissue–Biomaterial Interface: A Role for PPARγ-Dependent Glucocorticoid Receptor Activation in Regulating the CD163+ M2 Macrophage Phenotype

doi: 10.1089/ten.tea.2013.0628

Figure Lengend Snippet: FIG. 4. (A) De novo expression of CD163 by THP-1 cells when differentiated into adherent macro- phage-like cells by PMA and fur- ther enhancement in response to the GR agonist dexamethasone (250 nM) treatment for 48 h. b-Actin was used as a loading control. (B) Human peripheral blood monocyte–derived macro- phages at day 6 in either the presence of 250 nM dexamethasone or the DMSO vehicle control. Scale bar represents 100 mm. GR, gluco- corticoid receptor; PMA, phorbol 12-myristate 13-acetate. Color images available online at www.liebertpub.com/tea

Article Snippet: The agonists used were as follows: 250 nM dexamethasone (1126; Tocris), 100 nM phorbol 12-myristate 13-acetate (PMA; Sigma), and 1mM troglitazone (T2573; Sigma-Aldrich).

Techniques: Expressing, Control, Derivative Assay

Journal: Tissue Engineering Part A

Article Title: The Human Tissue–Biomaterial Interface: A Role for PPARγ-Dependent Glucocorticoid Receptor Activation in Regulating the CD163+ M2 Macrophage Phenotype

doi: 10.1089/ten.tea.2013.0628

Figure Lengend Snippet: FIG. 5. (A) The regulation of CD163 expression by PPARg. As observed previously, a subpopulation of monocyte- derived macrophages expressed CD163 in the presence of the DMSO vehicle control. Inhibition of PPARg by culture of monocyte-derived macrophages in the presence of 5 mM T0070907 for 11 days showed an absence of CD163 + subpopu- lation. Activation of PPARg by culture of the monocyte-derived macrophages in the presence of the PPARg agonist troglitazone at 1 mM for 48 h, followed by culture in the DMSO vehicle control medium for 9 days, showed an increase in the CD163 + subpopulation. Scale bar represents 100 mm. (B) Flow cytometric analysis of monocyte-derived macrophages activated with troglitazone for 48 h followed by culture in control medium for a further 9 days. Cells were harvested and immunolabeled with anti-CD163-FITC and anti-CD11b-APC. Regions (R3, R4, R5, R6) of analysis were assigned based on isotype control labeling. Percentage of CD163 + CD11b + monocyte-derived macrophages is shown. (C) Monocyte-derived macrophages were cultured in the presence of 250 nM dexamethasone or 250 nM dexamethasone and 5 mM T0070907. Inhibition of PPARg by T0070907 completely ablated dexamethasone-induced CD163 expression. Scale bar represents 100 mm. PPARg, peroxisome proliferator activated receptor gamma. Color images available online at www.liebertpub.com/tea

Article Snippet: The agonists used were as follows: 250 nM dexamethasone (1126; Tocris), 100 nM phorbol 12-myristate 13-acetate (PMA; Sigma), and 1mM troglitazone (T2573; Sigma-Aldrich).

Techniques: Expressing, Derivative Assay, Control, Inhibition, Activation Assay, Immunolabeling, Labeling, Cell Culture

Journal: STAR Protocols

Article Title: Chronic Cranial Window for Imaging Cortical Activity in Head-Fixed Mice

doi: 10.1016/j.xpro.2020.100194

Figure Lengend Snippet:

Article Snippet: Dexamethasone sodium phosphate , Alfa Aesar , AAJ6408303.

Techniques: Virus, Recombinant, Injection, Ointment, Saline, Adhesive, Microscopy, Sterility, Mutagenesis

Journal: EMBO Molecular Medicine

Article Title: Modulating phosphatase DUSP22 with BML-260 ameliorates skeletal muscle wasting via Akt independent JNK-FOXO3a repression

doi: 10.1038/s44321-025-00234-2

Figure Lengend Snippet: ( A ) DUSP22 expression in aged individuals (over 70 years, n = 15) and aged individuals diagnosed with sarcopenia (over 70 years, n = 18), p = 0.0009 (obtained from the Singapore Sarcopenia Study; (GEO accession no. GSE111016 (Migliavacca et al, )). ( B ) DUSP22 expression in C2C12 murine myotubes treated with vehicle or dexamethasone (Dex) to induce atrophy ( n = 3 each) Custer 1 ( p = 0.024), Cluster 2 ( p = 0.13), Cluster 3 ( p = 0.0246). Expression was measured using RNA Seq. TPM=transcript per million. ( C ) qPCR analysis of DUSP22 expression in four models of muscle atrophy: (1) C2C12 myotubes treated with Dex ( n = 5), p = 7.67E−05, (2) the TA muscle of C57BL/6 mice treated with Dex ( n = 4), p = 0.09, (3) the TA muscle of young (5 months-old, n = 9) and geriatric (27 months-old, n = 8) C57BL/6 mice, p = 0.0324, (4) the TA of C57BL/6 mice after hind limb immobilization ( n = 3), p = 0.018. ( D ) qPCR of DUSP22 expression in C2C12 myoblasts transfected with a DUSP22 CRISPR activation plasmid (DUSP22 endo OE) or control plasmid (CON endo OE) ( n = 3), p = 0.0022. ( E ) Fast myosin (MYH2) immunocytochemistry of CON endo OE and DUSP22 endo OE myoblasts after 96 h culture in DM (scale bar = 100 µm). ( F ) Fusion index ( n = 6). ( G ) Differentiation index ( n = 6), p = 9.91E−09. ( H – L ) qPCR analysis of gene expression related to the following: ( H ) Mitochondrial homeostasis (PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha, p = 1.44E−05), UCP-3 (mitochondrial uncoupling protein 3, p = 4.61E−05), Acly (ATP citrate lyase, p = 0.5141)) ( n = 4). ( I ) Autophagy (LC-3B (microtubule-associated proteins 1 A/1B light chain 3B, p = 0.0152), CtsL (cathepsin L, p = 4.76E−05)) ( n = 4). ( J ) Ubiquitin-proteasome system (UPS) (UBR2 (ubiquitin protein ligase E3, p = 0.0031), Psmd11 (proteasome 26S subunit, non-ATPase 11, p = 0.1718) ( n = 4). ( K ) Myosin heavy chain levels (slow myosin MYH7, p = 7.23E−06, fast myosin MYH1, p = 0.0171) ( n = 4), and ( L ) FoxO3a-related signaling (FoxO3a ( p = 0.0004), MurF-1 ( p = 0.0019), atrogin-1 ( p = 0.001), p62 ( p = 8.67E−08), TGIF (TGFB induced factor homeobox 1, p = 0.0001), ATF4 (activating transcription factor 4, p = 0.3974), Bnip3 (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3, p = 0.0887); Gadd45a (growth arrest and DNA damage inducible alpha, p = 4.19E−06), SMART (specific of muscle atrophy and regulated by transcription, p = 0.0006), MUSA1 (muscle ubiquitin ligase of SCF complex in atrophy-1, p = 0.2357)) ( n = 4). Box plots represent the distribution of DUSP22 expression levels. The center line indicates the median (50th percentile, Q2), representing the middle value of the dataset. The box bounds correspond to the interquartile range (IQR), extending from the 25th percentile (Q1, lower bound) to the 75th percentile (Q3, upper bound). Whiskers extend to the smallest and largest values within 1.5 × IQR from Q1 and Q3, representing the minimum (lower whisker) and maximum (upper whisker) values within this range. Data points that fall beyond this range are considered outliers and are displayed as individual points outside the whiskers. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 indicate significantly increased or decreased. n represents biological replicates. Error bars represent the standard error of the mean (SEM). .

Article Snippet: Dexamethasone , Santa Cruz , SC-204715A.

Techniques: Expressing, RNA Sequencing, Transfection, CRISPR, Activation Assay, Plasmid Preparation, Control, Immunocytochemistry, Gene Expression, Ubiquitin Proteomics, Whisker Assay

Journal: Journal of Virology

Article Title: Human Herpesvirus 8 (HHV-8)-Encoded Cytokines Induce Expression of and Autocrine Signaling by Vascular Endothelial Growth Factor (VEGF) in HHV-8-Infected Primary-Effusion Lymphoma Cell Lines and Mediate VEGF-Independent Antiapoptotic Effects

doi: 10.1128/jvi.75.22.10933-10940.2001

Figure Lengend Snippet: FIG. 5. Confirmation of antiapoptotic effects of viral chemokines. (A) Induction of apoptosis in a representative PEL cell line, BC-3, by dexamethasone (Dex.) was confirmed by using FITC-conjugated an- nexin V. An example of a positively staining cell (observed under UV light) with apparent altered nuclear morphology (observed under white light) is shown, together with healthy cells in the same popula- tion. (B) At different time points, annexin V-staining (apoptotic) cells in untreated cultures or dexamethasone-treated cultures containing vMIP-1A or vMIP-1B peptide (50 ng/ml) or no chemokine were counted and expressed as a percentage of the total number of cells (three fields were counted; n 200 to 300).

Article Snippet: Dexamethasone-induced apoptosis of BC-3 cells and antiapoptotic effects of vMIP-1A and vMIP-1B were confirmed by using fluorescein isothiocyanate (FITC)-conjugated annexin V (catalog no. sc-4252FL; Santa Cruz Biotechnology, Santa Cruz, Calif.).

Techniques: Staining