Journal: Cell reports

Article Title: Intrinsic antiviral immunity of barrier cells revealed by an iPSC-derived blood-brain barrier cellular model

doi: 10.1016/j.celrep.2022.110885

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Brain Cerebral Cortex Tissue Slides (Adult Normal) , Novus Biologicals , Cat#NBP2-77755.

Techniques: Virus, Recombinant, Modification, Membrane, Knock-Out, Clinical Proteomics, Fluorescence, Plasmid Preparation, Western Blot, Mutagenesis, PCR Cloning, Cloning, Software, Cell Culture, Electroporation

Journal: Journal of Clinical Investigation

Article Title: CCL28-induced RARβ expression inhibits oral squamous cell carcinoma bone invasion

doi: 10.1172/jci125336

Figure Lengend Snippet: Figure 8. Expression levels of CCL28, CCR10, or RARβ are closely associated with overall survival in 117 patients with OSCC. (A) Representative images of IHC staining of CCL28, CCR3, CCR10, and RARβ in normal oral mucosa and OSCC tissues. Scale bars: 100 μm. Magnified images of the boxed area are shown in the insets. Scale bars: 20 μm. (B) Frequency of histoscores in normal oral mucosa and OSCC tissues. (C) Kaplan-Meier survival curve of patients with OSCC stratified based on CCL28, CCR3, CCR10, or RARβ expres- sion by the log-rank test.

Article Snippet: CCL28, RANKL, or OPG levels in cell culture media were measured with commercially available kits for CCL28 (BioLegend), RANKL (EIAab), or OPG (Boster) according to the manufacturer’s instructions.

Techniques: Expressing, Immunohistochemistry

Journal: Stem Cells (Dayton, Ohio)

Article Title: Hes1 regulates anagen initiation and hair follicle regeneration through modulation of hedgehog signaling

doi: 10.1002/stem.3117

Figure Lengend Snippet: Hes1 deletion results in delayed anagen initiation and shortened hair follicle (HF) growth phase. A, In situ hybridization of Hes1 (arrows) in back skin sections at P22 and P24 with hematoxylin counterstain. The dotted lines demarcate the bulge and the solid lines demarcate the boundary between DP and HG when visible. B, Back skin sections were immunostained for Hes1 at P22 and P24. C, Back skin sections were immunostained for HG marker P‐Cadherin (P‐Cad, arrows) at P22. D, Quantification of P‐Cad + cells in the HF at P22 (mean ± SD, n > 30 HFs per genotype from three independent control and mutant pairs, n.s., nonsignificant). E, Back skin sections were double immunostained for P‐Cad and proliferative marker Ki67 (arrows) at P24. F, Quantification of Ki67+ cells in the P‐Cad + cells at P24 (mean ± SD, n > 30 HFs per genotype from three independent control and mutant pairs, *** P < .001). G, Back skin sections at P24 were immunostained for β‐catenin. The arrows mark the nuclear β‐catenin staining. The dotted lines denote the boundary between DP and HG when visible. H, Back skin sections immunostained for phospho‐Smad1/5/8 (arrows). The dotted line marks the HF and solid line marks the DP. I, Double immunostaining of AE13 and KI67 in back skin sections at P29 (full anagen) and P35 (late anagen/early catagen). The dotted lines depict the line of Auber. J, Quantification of the bulb size (Ki67+ area below the line of Auber) (mean ± SD, >40 HFs from three biological replicates per genotype per stage, *** P < .001). K, Back skin sections immunostained for cell mitotic marker phospho‐histone H3 (p‐H3) at P29 and P35. L, Quantification of p‐H3+ cells in the hair matrix (mean ± SD, >40 HFs from three biological replicates per genotype per stage, *** P < .001). DAPI counterstaining in blue. Bu, bulge; HG, hair germ; DP, derma papillae; Bb, hair bulb. M, Bright field images of club hair of four different hair types at P60. N, Quantification of club hair length of each HF type (mean ± SD, 20 club hairs for each hair types per mouse, n = 3 biological replicates per genotype, *** P < .001 determined by analysis of variance). Scale bar, 50 μm except (M), where it is 1 mm

Article Snippet: The sources and dilutions of primary antibodies were Hes1 (1:100, Santa Cruz or Cell Signaling, Danvers, MA), K6 (1:100, Thermo Fisher, Waltham, MA), AE15 (1:100, Santa Cruz), AE13 (1:100, Abcam, Cambridge, MA), K73 (1:150, Biorbyt, San Francisco, CA), K82 (1:100, Abnova, Taiwan), Ki67 (1:100, Thermo Fisher), CD34 (1:100, eBioscience, Waltham, MA), Sox9 (1:100, Santa Cruz), NFATc1 (1:150, Santa Cruz), β‐catenin (1:100, BD, San Jose, CA), P‐cadherin (1:250, R&D), p‐Smad 1/5/8 (1:1000, Santa Cruz), phospho‐histone H3 (1:100, Cell Signaling), Igfbp3 (1:100, R&D), Arl13b (1:200, Abcam), Pericentrin (1:500, Convance, Cambridge, MA), Smo (1:300, Abcam), K14 (1:250, Thermo Fisher), K15 (1:200, Thermo Fisher), Versican (1:50, Chemicon, Temecula, CA), and Vimentin (1:200, Abcam).

Techniques: In Situ Hybridization, Marker, Control, Mutagenesis, Staining, Double Immunostaining