Journal: Disease Models & Mechanisms

Article Title: Comparison of the pathogenesis of SARS-CoV-2 infection in K18-hACE2 mouse and Syrian golden hamster models

doi: 10.1242/dmm.049632

Figure Lengend Snippet: Identification of SARS-CoV-2-infected cells in the lungs of K18-hACE2 mice and Syrian golden hamsters. (A) Representative immunofluorescence images for N protein, AGER (type 1 alveolar cell marker), LAMP3 (type 2 alveolar cell marker) and 4′,6-diamidino-2-phenylindole (DAPI; nuclear marker) in the lungs of K18-hACE2 mice 2 days after SARS-CoV-2 infection. Scale bars: 40 µm. (B) Percentage of infected cells (N protein + ) per total positive cells in the alveolar lineage (AGER + or LAMP3 + ) in SARS-CoV-2-infected K18-hACE2 mice at a 40× HPF ( n =6 per group). All data are presented as the mean±s.e.m. P -values were obtained by two-tailed unpaired Student's t -test (*** P <0.001). (C) Representative immunofluorescence images for N protein, SCGB1A1 (club cell marker), acetylated TUBA1A (Ac-TUBA1A; ciliated cell marker) and DAPI in the lungs of Syrian golden hamsters 2 days after SARS-CoV-2 infection. Scale bars: 40 µm. (D) Percentage of infected cells (N protein + ) per total number of positive cells in the bronchus lineage (SCGB1A1 + or Ac-TUBA1A + or MUC5AC + or CHGA + ) in SARS-CoV-2-infected Syrian golden hamsters in a 40× HPF ( n =6 per group). All data are presented as the mean±s.e.m. P -values were obtained by two-tailed unpaired Student's t -test (*** P <0.001, versus goblet cells; ### P <0.001, versus neuroendocrine cells). (E) Representative in situ hybridization images of human ACE2 (h ACE2 ) in the lungs of non-infected K18-hACE2 mice and Syrian golden hamsters. Scale bars: 50 µm. (F) Co-staining images of in situ hybridization for S gene and immunohistochemical images of TUNEL in the lungs of K18-hACE2 mice and Syrian golden hamsters 2 days after SARS-CoV-2 infection. The black arrows indicate TUNEL + / S gene + cells. Scale bars: 50 µm. (G) Percentage of TUNEL + / S gene + cells relative to total S gene + cells in SARS-CoV-2-infected K18-hACE2 mice and Syrian golden hamsters in a 40× HPF ( n =6 per group). All data are presented as the mean±s.e.m. P -values were obtained by two-tailed unpaired Student's t -test (*** P <0.001).

Article Snippet: The sections were incubated with the following primary antibodies overnight at 4°C in a humidity chamber: anti-N protein (NB100-56576, Novus, 1:1000 and 40143-MM08, Sino Biological, 1:1000), anti-LAMP3 (DDX0190P, Novus, 1:500), anti-AGER (MAB1179, R&D Systems, 1:200), anti-SCGB1A1 (ABS1673, Millipore, 1:200), anti-acetylated TUBA1A (T7451, Sigma-Aldrich, 1:1000), anti-MUC5AC (MA5-12178, Thermo Fisher Scientific, 1:1000), anti-PTPRC (ab64100, Abcam, 1:1000), anti-CD3D (ab5690, Abcam, 1:200), anti-Ly-6G/Ly-6C (ab2557, Abcam, 1:250), anti-p-AKT (9271S, Cell Signaling Technology, 1:500), anti-CHGA (ab15160, Abcam, 1:1000), anti-CD4 (25229S, Cell Signaling Technology, 1:200) and anti-CD8 (14-0808-82, Thermo Fisher Scientific, 1:200).

Techniques: Infection, Immunofluorescence, Marker, Two Tailed Test, In Situ Hybridization, Staining, Immunohistochemical staining, TUNEL Assay

Journal: Molecular immunology

Article Title: S100A11 regulates nasal epithelial cell remodeling and inflammation in CRSwNPs via the RAGE-mediated AMPK-STAT3 pathway.

doi: 10.1016/j.molimm.2021.09.014

Figure Lengend Snippet: Fig. 5. S100A11 depends on RAGE-mediated can activate AMPK and inhibit STAT3 signaling pathway. A. The phosphorylation levels of AMPK and STAT3 were detected by Western blot after S100A11 was overexpressed. B. The histogram shows the phosphorylation ratio of AMPK and STAT3 (pAMPK/ AMPK and pSTAT3/ STAT3). C. Western blot showed the expression of cleaved-PARP, CCND1, CCNE, Bcl-2, AMPK and STAT3 phosphorylated proteins after treatment of cells with different concentrations of rh-S100A11 protein (0~10000ug/mL) for 24 h. D. Cell immunofluorescence staining detected the expression of STAT3 phosphorylated protein after treatment with 1000ug/mL rh-S100A11 protein for 24 h (bar = 20um). E. The relative mRNA levels of Fas, Stk35, Tsc2 and Socs3 after cells were treated with 1000ug/mL rh-S100A11 protein or transfected for 24 h. F. RAGE protein inhibitors affect the phosphorylation levels of AMPK and STAT3 caused by rhS100A11. The bar graphs show quantification of the results, with each value represents the mean ± SD of three independent experiments. Statistical significance is shown using the Student’s t-test analysis, *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: Rabbit polyclonal anti− CCND1 antibody (Cat. No. 60,186-1-Ig, 1:2000 diluted), anti-RAGE antibody (Cat. No. 66,833-1-Ig, 1:2000 diluted) and anti− CCNE antibody (Cat. No. 11554− 1-AP, 1:2000 diluted for WB) were purchased from Proteintech.

Techniques: Phospho-proteomics, Western Blot, Expressing, Immunofluorescence, Staining, Transfection

Journal: bioRxiv

Article Title: Aerosolized ApoA1 Nanoparticles Synthesized by Microfluidics Cross the Lung Barrier and Modulate Inflammation

doi: 10.1101/2025.07.09.663869

Figure Lengend Snippet: Cellular localization of A1NPs after aerosolization. Immunofluorescence of lung sections from mice 6 hours after A1NP administration. ApoA1 appears in green and cell nuclei are stained with DAPI (blue). (A) AGER (red), specific to type I pneumocytes. (B) SFTPC (orange), marker for type II pneumocytes. (C) EMCN (red), characteristic of pulmonary endothelial cells. Representative illustration of 10 mice with A1NPs-DilC18.

Article Snippet: In parallel, specific antibodies were applied: a mouse anti-AGER rat antibody diluted 1:100 for type I pneumocytes (MAB 1179-500; R&D Systems), a mouse anti-SFTPC rabbit antibody diluted 1:200 for type II pneumocytes (10774-1AP; Proteintech), and a mouse anti-EMCN goat antibody diluted 1:100 for endothelial cells (AF4666-SP; R&D Systems).

Techniques: Immunofluorescence, Staining, Marker