Journal: Retrovirology

Article Title: Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies Peroxisome Proliferator-Activated Receptor Gamma as an intrinsic negative regulator of viral replication

doi: 10.1186/1742-4690-10-160

Figure Lengend Snippet: Selected genes upregulated in Th1Th17 vs. Th1

Article Snippet: Fluorochrome-conjugated Abs used for polychromatic flow cytometry analysis were CD3-Pacific Blue (UCHT1), CD4-Alexa Fluor 700 (RPA-T4), CD45RA-APC-Cy7 (H1100), CCR4-PE-Cy7 (1G1), CXCR3-PE-Cy5 (1C6), CCR6-PE (11A9), CCR5-PE (2D7) and CEACAM1-FITC (B1.1) (BD Pharmingen), CD56-FITC (MEM188) (eBioscience), CD8-FITC (BW135/80), CD19-FITC (LT19), and MCAM-FITC (541-10B2) (Miltenyi Biotec).

Techniques:

Journal: Nature communications

Article Title: Klf4 and Klf5 differentially inhibit mesoderm and endoderm differentiation in embryonic stem cells.

doi: 10.1038/ncomms4719

Figure Lengend Snippet: Figure 5 | Knockdown of Klf5 increases the yield of definitive mesoderm. (a) FACS profiles of Klf4-KD1, Klf4-KD2, Klf5-KD1, Klf5-KD2 and control cells (Ctrl-KD), after immunostaining for Flk1, PDGFRa and E-cadherin expression, and showing increased differentiation to mesoderm (Flk1 þ E-Cadh

Article Snippet: Antibodies used in this study were previously described27,38: APC-anti-human CD25 mAb (M-A251, Becton-Dickinson & Co; 5 ml 10 6 cells), fluorescein-anti-mouse E-Cadherin mAb (FAB7481F, R&D systems; 2.5 mg ml 1), APC-anti-mouse CD140a (PDGFRa) mAb (17–1401, eBioscience; 5 mg ml 1) and APC-anti-mouse Flk1 mAb (560070, BD pharmingen; 5 mg ml 1).

Techniques: Knockdown, Control, Immunostaining, Expressing

Journal: Stem Cell Research & Therapy

Article Title: Synergism of MSC-secreted HGF and VEGF in stabilising endothelial barrier function upon lipopolysaccharide stimulation via the Rac1 pathway

doi: 10.1186/s13287-015-0257-0

Figure Lengend Snippet: MSC-secreted paracrine HGF upregulated endothelial VE-cadherin protein expression and decreased caveolin-1 protein expression. The results showed that LPS stimulation of HPMECs reduced the expression of VE-cadherin and occludin protein ( p < 0.01; a , b , c ) but increased the expression of caveolin-1 protein ( p < 0.05; a , d ) and that these effects were inhibited by MSCs. However, the effect of MSCs was significantly blocked by anti-HGF antibody ( p < 0.05). Furthermore, the role of MSCs in reducing caveolin-1 protein expression was clearly inhibited by anti-HGF and anti-VEGF antibodies. Adding MSC-CM in all groups except control group and LPS group. n = 3, * p < 0.05, ** p < 0.01 vs. control group; # p < 0.05 vs. LPS group; & p < 0.05 vs. MSC-CM group. CM Conditioned medium, HGF Hepatocyte growth factor, LPS Lipopolysaccharide, MSC Mesenchymal stem cell, VEGF Vascular endothelial growth factor

Article Snippet: Then the membranes were blocked in phosphate-buffered saline-Tween (PBS-T) containing 5 % milk for 2 h at room temperature and incubated at 4 °C overnight with primary antibodies against VE-cadherin (1:1000; Cell Signaling), occludin (1:250; Abcam) or caveolin-1 (1:1000; Epitomics).

Techniques: Expressing, Control

Journal: Stem Cell Research & Therapy

Article Title: Synergism of MSC-secreted HGF and VEGF in stabilising endothelial barrier function upon lipopolysaccharide stimulation via the Rac1 pathway

doi: 10.1186/s13287-015-0257-0

Figure Lengend Snippet: MSC-secreted HGF restored endothelial VE-cadherin remodelling. LPS causes the remodelling of the junctional localisation of VE-cadherin, which causes HPMEC to contract, increasing paracellular permeability. After 24 h of MSC-CM and HPMEC co-culture, the remodelling of the junctional localisation of VE-cadherin was partially restored. However, neutralising HGF from the MSC-CM with anti-HGF antibody caused VE-cadherin to be disrupted again. Adding MSC-CM in all groups except control group and LPS group. CM Conditioned medium, HGF Hepatocyte growth factor, LPS Lipopolysaccharide, MSC Mesenchymal stem cell, VEGF Vascular endothelial growth factor

Article Snippet: Then the membranes were blocked in phosphate-buffered saline-Tween (PBS-T) containing 5 % milk for 2 h at room temperature and incubated at 4 °C overnight with primary antibodies against VE-cadherin (1:1000; Cell Signaling), occludin (1:250; Abcam) or caveolin-1 (1:1000; Epitomics).

Techniques: Permeability, Co-Culture Assay, Control

Journal: Stem Cell Research & Therapy

Article Title: Synergism of MSC-secreted HGF and VEGF in stabilising endothelial barrier function upon lipopolysaccharide stimulation via the Rac1 pathway

doi: 10.1186/s13287-015-0257-0

Figure Lengend Snippet: VEGF/HGF and MSC treatments enhanced VE-cadherin and occludin protein expression and reduced caveolin-1 protein expression in LPS-stimulated HPMECs via the RhoA/Rac1 pathway. The results showed that the effects of MSCs and VEGF/HGF on enhancing VE-cadherin (Fig. 10a and b) and occludin protein expression (Fig. 10a and c) were weakened when injured HPMECs were pretreated with the Rac1 inhibitor NSC23766. However, caveolin-1 protein expression (Fig. 10a and d) increased in HPMECs pretreated with the Rac1 inhibitor NSC23766 or with the RhoA inhibitor C3 transferase. n = 3, * p < 0.05; ** p < 0.01 vs. MSC group; # p < 0.05 vs. VEGF/HGF group. CM Conditioned medium, HGF Hepatocyte growth factor, LPS Lipopolysaccharide, MSC Mesenchymal stem cell, VEGF Vascular endothelial growth factor

Article Snippet: Then the membranes were blocked in phosphate-buffered saline-Tween (PBS-T) containing 5 % milk for 2 h at room temperature and incubated at 4 °C overnight with primary antibodies against VE-cadherin (1:1000; Cell Signaling), occludin (1:250; Abcam) or caveolin-1 (1:1000; Epitomics).

Techniques: Expressing