human airway epithelial cells Search Results


human normal colon epithelial cell  (ATCC)
97
ATCC human normal colon epithelial cell
FIGURE 7 | Compound 5a decreases HT29 and SW620 cell viability without affecting the viability of normal colon <t>epithelial</t> CCD 841 cells and enhances irinotecan (IRI), 5-fluorouracil (5-FU), and oxaliplatin (OXA) cytotoxic effects on HT29 and SW620 cells. (A) HT29, SW620, and the normal colon epithelial CCD 841 cell lines were exposed to different concentrations (5-10-20 μM) of Compound 5a for 24 h. Cell viability was measured by the MTT assay at 540 nm regarding the cellular metabolic activity. Bar graph showing the cell viability percentage and the data are expressed as mean ± SD (n = 3). ***p < 0.001 and ****p < 0.0001 vs. Control. Half-maximal inhibitory concentrations (IC50) of Compound 5a on HT29 and SW620 cell viability were determined. HT29 (B,C) and SW620 (D,E) cells were treated with different concentrations of the chemotherapeutic drugs IRI, 5-FU, and OXA for 24 h in the presence (C,E) or absence (B,D) of various concentrations (5-10-20 μM) of Compound 5a. Cell cytotoxicity was measured by the MTT assay at 540 nm. Bar graph showing the cell viability percentage and the data are expressed as mean ± SD (n = 3). Half- maximal inhibitory concentrations (IC50) of each chemotherapeutic drug on HT29 and SW620 cell viability were also determined.
Human Normal Colon Epithelial Cell, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Primary+Small+Airway+Epithelial+Cells%3B+Normal%2C+Human/pm36046830-49-0-18
Average 97 stars, based on 1 article reviews
human normal colon epithelial cell - by Bioz Stars, 2026-11
97/100 stars
  Buy from Supplier
human small airway epithelial cells hsaepcs  (PromoCell)
94
PromoCell human small airway epithelial cells hsaepcs
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Human Small Airway Epithelial Cells Hsaepcs, supplied by PromoCell, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Human+Small+Airway+Epithelial+Cells/pmc12441582-49-0-18
Average 94 stars, based on 1 article reviews
human small airway epithelial cells hsaepcs - by Bioz Stars, 2026-11
94/100 stars
  Buy from Supplier
human bronchial epithelial cells  (ATCC)
96
ATCC human bronchial epithelial cells
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Human Bronchial Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Primary+Small+Airway+Epithelial+Cells%3B+Asthma%2C+Human/pm34193607-46-0-7
Average 96 stars, based on 1 article reviews
human bronchial epithelial cells - by Bioz Stars, 2026-11
96/100 stars
  Buy from Supplier
hsaec1 kt human small airway epithelial cells  (ATCC)
94
ATCC hsaec1 kt human small airway epithelial cells
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Hsaec1 Kt Human Small Airway Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/HSAEC1-KT%3B+Small+Airway+Epithelial+Cells%3B+Human/pmc05870190__SC___009___C7SC03712K___s003-9-0-9
Average 94 stars, based on 1 article reviews
hsaec1 kt human small airway epithelial cells - by Bioz Stars, 2026-11
94/100 stars
  Buy from Supplier
t 75 flasks  (Cell Applications Inc)
96
Cell Applications Inc t 75 flasks
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
T 75 Flasks, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Major+Media/bio_rxiv__64898__2026__04__03__716316-186-4-10
Average 96 stars, based on 1 article reviews
t 75 flasks - by Bioz Stars, 2026-11
96/100 stars
  Buy from Supplier
pcs 301 010  (ATCC)
95
ATCC pcs 301 010
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Pcs 301 010, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Primary+Small+Airway+Epithelial+Cells%3B+Normal%2C+Human/pmc07229915-18-9-8
Average 95 stars, based on 1 article reviews
pcs 301 010 - by Bioz Stars, 2026-11
95/100 stars
  Buy from Supplier
passage 1 human airway epithelial cells hae  (Cell Applications Inc)
90
Cell Applications Inc passage 1 human airway epithelial cells hae
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Passage 1 Human Airway Epithelial Cells Hae, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Human+Small+Airway+Epithelial+Cell+Media/pmc02743663-181-0-10
Average 90 stars, based on 1 article reviews
passage 1 human airway epithelial cells hae - by Bioz Stars, 2026-11
90/100 stars
  Buy from Supplier
airway epithelial cells  (ATCC)
94
ATCC airway epithelial cells
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Airway Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Primary+Small+Airway+Epithelial%3B+Cells%2C+Fibrosis%3BHuman/pm09698598-56-0-10
Average 94 stars, based on 1 article reviews
airway epithelial cells - by Bioz Stars, 2026-11
94/100 stars
  Buy from Supplier
atcc pcs 301 013  (ATCC)
92
ATCC atcc pcs 301 013
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Atcc Pcs 301 013, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Primary+Small+Airway+Epithelial+Cells%3B+COPD%2C+Human/pmc08568944__41467_2021_26637_MOESM2_ESM-354-16-16
Average 92 stars, based on 1 article reviews
atcc pcs 301 013 - by Bioz Stars, 2026-11
92/100 stars
  Buy from Supplier
small airway epithelial cells hsaepc  (Cell Applications Inc)
90
Cell Applications Inc small airway epithelial cells hsaepc
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Small Airway Epithelial Cells Hsaepc, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Human+Small+Airway+Epithelial+Cells%3A+HSAEpC/pmc08463074-532-7-15
Average 90 stars, based on 1 article reviews
small airway epithelial cells hsaepc - by Bioz Stars, 2026-11
90/100 stars
  Buy from Supplier
sv40 immortalized line  (AcceGen Biotechnology)
92
AcceGen Biotechnology sv40 immortalized line
Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial <t>epithelial</t> (BEAS-2B), normal human small airway epithelial cells <t>(HSAEpCs)</t> or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.
Sv40 Immortalized Line, supplied by AcceGen Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/Immortalized+Human+Small+Airway+Epithelial+Cell+Line+-+SV40/pmc10400971-298-10-12
Average 92 stars, based on 1 article reviews
sv40 immortalized line - by Bioz Stars, 2026-11
92/100 stars
  Buy from Supplier
normal human cp epithelial cells  (ScienCell)
90
ScienCell normal human cp epithelial cells
Constitutive Notch 1 signaling leads to CP tumour. (a) Schematic illustration of the strategy for Notch 1 signaling activation in vivo . (b) Brain hemispheres and CPs from postnatal day 7 (P7) mice are shown. Notice that the enlarged CP from Math1-Cre;Rosa26-NICD1;Rosa26-EYFP ( Mcre;NICD1;EYFP ) animal contains many EYFP + cells (arrows), while EYFP + cells (arrowheads) are sparsely found in the CP from Math1-Cre;Rosa26-EYFP ( Mcre;EYFP ) animals. Scale bar: 1 mm. (c) Analysis of gene expression in CP of Math1-Cre;Rosa26-EYFP mice. EYFP expression (green) labels cells derived from Atoh1 + progenitors. The expression of Lmx1a (red), Otx2 (red), cytokeratins (red), and Aqp1 (red) labels CP <t>epithelial</t> cells. Scale bar: 25μm. (d) Quantitation of the percentage of EYFP + cells or NICD1 + /GFP + cells in Otx2 + hindbrain CP epithelium of Mcre;EYFP mice or Math1-Cre;Rosa26-NICD1 ( Mcre;NICD1 ) mice, respectively, at different time points (n=3 tumours from 3 Mcre;NICD1 animals/time point; CPs from Mcre;EYFP mice: n=4 (P0, P14), n=6 (P7, P21), n=5 (P90), data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, **, P<0.01; ***, P <0.001; ns, non-significant). (e) H&E staining of CPs from Mcre;NICD1 and wild type (WT) mice at P0 and P14. Notice that CP epithelium exhibits the “hobnail” configuration (arrowhead), while the enlarged CP in Mcre;NICD1 mice appear “flattened” on ventricular surfaces (arrow). Vesicular sac with accumulated CSF is shown (asterisk). Scale bars: white, 500μm; black, 25μm. (f) H&E staining of human CP papilloma (CPP) and normal CP. Scale bar: 25μm. (g) Quantitative RT-PCR (Q-RT-PCR) analysis of Hes1 and Hes5 expression in CP tumours (black circles) and wild type CPs (white circles) at P0, P7, P14, and P21 (data from technical replicates of each specimen set in a single experiment are shown; experiment was not repeated. Raw data can be found in ). (h) The expression of Ki-67 is shown in CP tumours from Mcre;NICD1 mice, Lmx1a-Cre;Rosa26-NICD1 ( Lcre;NICD1 ) mice, and normal CPs from wild type mice. Dotted lines mark the boundary of lateral ventricles. The expression of Ki-67 in human CPP and normal CP is shown. Scale bar: 50μm.
Normal Human Cp Epithelial Cells, supplied by ScienCell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+airway+epithelial+cells/human+small+airway+epithelial+cells++hsaepics+/pmc04814324-202-14-19
Average 90 stars, based on 1 article reviews
normal human cp epithelial cells - by Bioz Stars, 2026-11
90/100 stars
  Buy from Supplier

Image Search Results


FIGURE 7 | Compound 5a decreases HT29 and SW620 cell viability without affecting the viability of normal colon epithelial CCD 841 cells and enhances irinotecan (IRI), 5-fluorouracil (5-FU), and oxaliplatin (OXA) cytotoxic effects on HT29 and SW620 cells. (A) HT29, SW620, and the normal colon epithelial CCD 841 cell lines were exposed to different concentrations (5-10-20 μM) of Compound 5a for 24 h. Cell viability was measured by the MTT assay at 540 nm regarding the cellular metabolic activity. Bar graph showing the cell viability percentage and the data are expressed as mean ± SD (n = 3). ***p < 0.001 and ****p < 0.0001 vs. Control. Half-maximal inhibitory concentrations (IC50) of Compound 5a on HT29 and SW620 cell viability were determined. HT29 (B,C) and SW620 (D,E) cells were treated with different concentrations of the chemotherapeutic drugs IRI, 5-FU, and OXA for 24 h in the presence (C,E) or absence (B,D) of various concentrations (5-10-20 μM) of Compound 5a. Cell cytotoxicity was measured by the MTT assay at 540 nm. Bar graph showing the cell viability percentage and the data are expressed as mean ± SD (n = 3). Half- maximal inhibitory concentrations (IC50) of each chemotherapeutic drug on HT29 and SW620 cell viability were also determined.

Journal: Frontiers in pharmacology

Article Title: The Anticancer Effects of the Pro-Apoptotic Benzofuran-Isatin Conjugate (5a) Are Associated With p53 Upregulation and Enhancement of Conventional Chemotherapeutic Drug Efficiency in Colorectal Cancer Cell Lines.

doi: 10.3389/fphar.2022.923398

Figure Lengend Snippet: FIGURE 7 | Compound 5a decreases HT29 and SW620 cell viability without affecting the viability of normal colon epithelial CCD 841 cells and enhances irinotecan (IRI), 5-fluorouracil (5-FU), and oxaliplatin (OXA) cytotoxic effects on HT29 and SW620 cells. (A) HT29, SW620, and the normal colon epithelial CCD 841 cell lines were exposed to different concentrations (5-10-20 μM) of Compound 5a for 24 h. Cell viability was measured by the MTT assay at 540 nm regarding the cellular metabolic activity. Bar graph showing the cell viability percentage and the data are expressed as mean ± SD (n = 3). ***p < 0.001 and ****p < 0.0001 vs. Control. Half-maximal inhibitory concentrations (IC50) of Compound 5a on HT29 and SW620 cell viability were determined. HT29 (B,C) and SW620 (D,E) cells were treated with different concentrations of the chemotherapeutic drugs IRI, 5-FU, and OXA for 24 h in the presence (C,E) or absence (B,D) of various concentrations (5-10-20 μM) of Compound 5a. Cell cytotoxicity was measured by the MTT assay at 540 nm. Bar graph showing the cell viability percentage and the data are expressed as mean ± SD (n = 3). Half- maximal inhibitory concentrations (IC50) of each chemotherapeutic drug on HT29 and SW620 cell viability were also determined.

Article Snippet: Human normal colon epithelial cell (CCD841 CoTr), colorectal adenocarcinoma HT29, and mCRC SW620 cell lines were obtained from American Type Culture Collection (ATCC, Manassas, VA, United States) and grown in a complete medium composed of DMEM supplemented with 10% heatinactivated fetal bovine serum (FBS), 100 μg/ml streptomycin, 100 IU/ml penicillin and 2 mmol/l L-glutamine.

Techniques: MTT Assay, Activity Assay, Control

Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial epithelial (BEAS-2B), normal human small airway epithelial cells (HSAEpCs) or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.

Journal: The European Respiratory Journal

Article Title: Particulate matter-related ITIH4 deficiency is associated with an emphysema phenotype of COPD through JNK-dependent and JNK-independent signalling

doi: 10.1183/13993003.01610-2024

Figure Lengend Snippet: Role of reactive oxygen species (ROS) in mediating low-level inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protein expression. a) Secretory ITIH4 levels in bronchial epithelial (BEAS-2B), normal human small airway epithelial cells (HSAEpCs) or COPD HSAEpC cells exposed to irritants, including vehicle control, lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) and hydrogen peroxide (H 2 O 2 ) (100 μM). ITIH4 levels in cells treated with the antioxidant N-acetyl- l -cysteine (NAC; 5 mM). b) Secretory ITIH4 levels in cells subject to 50 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) or vehicle control exposure. c) Levels of normalised ITIH4 gene expression (log 2 FPKM) in lung tissues from 98 patients with COPD ( GSE57148 dataset cohort), compared with the normal group (n=91). d) Histograms comparing ITIH4 expression levels in BEAS-2B cells exposed to irritants, including LPS (20 ng·mL −1 ), IL-1β (10 ng·mL −1 ), 100 μM H 2 O 2 and vehicle control (n=5−8 per group). The gene expression levels were measured using a quantitative real-time reverse transcription (qRT)-PCR assay. The levels of ITIH4 expression were examined in cells subject to 50 μg·mL −1 CB, DEP, UD or vehicle control exposure. e) ITIH4 gene expression levels in normal and COPD HSAEpCs exposed to irritants including LPS, IL-1β, H 2 O 2 and vehicle control. ITIH4 expression levels were measured in normal control and COPD HSAEpCs subject to CB, DEP, UD or vehicle control exposure (n=5−8 per group). f) Effect of 100 μM H 2 O 2 or vehicle with or without 50 μg·mL −1 cycloheximide on ITIH4 in BEAS-2B cells over a duration of 2 h. The half-life (t 1/2 ) of ITIH4 protein in vehicle and H 2 O 2 was analysed (n=5 per group). Relative values are expressed as the fold change calculated by comparison with vehicle control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.

Article Snippet: Human small airway epithelial cells (HSAEpCs) from healthy (aged 53–70 years) and COPD (aged 59–67 years) donors (C-12642, PromoCell, Heidelberg, Germany) were cultured as submerged undifferentiated monolayers in PromoCell cell growth medium and passaged fewer than five times to prevent cell senescence.

Techniques: Expressing, Control, Gene Expression, Reverse Transcription, Quantitative RT-PCR, Comparison

Inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protects epithelial cells from particulate matter with aerodynamic diameter <2.5 µm (PM 2.5 )-induced and reactive oxygen species (ROS)-induced apoptosis. a) Cleaved caspase-3 levels in the airway or alveolar epithelium of normal control participants or patients with COPD. Cleaved caspase-3 levels in lung tissue sections from patients with COPD (n=16) and normal controls (n=20) were analysed through immunohistochemical (IHC) staining. An enlarged view of two rectangular regions in the airway and alveolar epithelium is shown in the right panel. Airway epithelial cells are represented by pink dashed lines. Staining signals were observed under a conventional light microscope. Scale bar=200 μm. Original magnification ×200. The IHC scores of cleaved caspase-3 levels in the airway or alveolar areas in COPD patients were compared with that in normal controls. b) ROS accumulation levels in control and N-acetyl- l -cysteine (NAC)-treated bronchial epithelial cells (BEAS-2B) exposed to 0–100 μg·mL −1 PM 2.5 (n=5−8 per group). Moreover, ROS levels were measured in normal human small airway epithelial cells (HSAEpCs) and COPD HSAEpCs exposed to 0–50 μg·mL −1 PM 2.5 (n=5–9 per group). c) Secreted ITIH4 levels in control and NAC-treated BEAS-2B, normal and COPD HSAEpCs exposed to PM 2.5 (n=5–8 per group). d) Apoptotic cell population (%) in si-ITIH4-knockdown and ITIH4-overexpressing BEAS-2B cells in comparison with scramble si-RNA and pcDNA vector control cells exposed to 20 μg·mL −1 PM 2.5 , respectively. Apoptosis was measured by knockdown and overexpression of ITIH4 in HSAEpCs and COPD HSAEpCs exposed to 20 μg·mL −1 PM 2.5 , respectively (n=5–9 per group). e) Apoptosis was analysed in ITIH4-knockdown and ITIH4-overexpressing cells exposed to hydrogen peroxide (H 2 O 2 ) as indicated (n=5–8 per group). Relative values are expressed as the fold change calculated through comparison with vehicle-treated si-scramble or pcDNA control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.

Journal: The European Respiratory Journal

Article Title: Particulate matter-related ITIH4 deficiency is associated with an emphysema phenotype of COPD through JNK-dependent and JNK-independent signalling

doi: 10.1183/13993003.01610-2024

Figure Lengend Snippet: Inter-α-trypsin inhibitor heavy chain 4 (ITIH4) protects epithelial cells from particulate matter with aerodynamic diameter <2.5 µm (PM 2.5 )-induced and reactive oxygen species (ROS)-induced apoptosis. a) Cleaved caspase-3 levels in the airway or alveolar epithelium of normal control participants or patients with COPD. Cleaved caspase-3 levels in lung tissue sections from patients with COPD (n=16) and normal controls (n=20) were analysed through immunohistochemical (IHC) staining. An enlarged view of two rectangular regions in the airway and alveolar epithelium is shown in the right panel. Airway epithelial cells are represented by pink dashed lines. Staining signals were observed under a conventional light microscope. Scale bar=200 μm. Original magnification ×200. The IHC scores of cleaved caspase-3 levels in the airway or alveolar areas in COPD patients were compared with that in normal controls. b) ROS accumulation levels in control and N-acetyl- l -cysteine (NAC)-treated bronchial epithelial cells (BEAS-2B) exposed to 0–100 μg·mL −1 PM 2.5 (n=5−8 per group). Moreover, ROS levels were measured in normal human small airway epithelial cells (HSAEpCs) and COPD HSAEpCs exposed to 0–50 μg·mL −1 PM 2.5 (n=5–9 per group). c) Secreted ITIH4 levels in control and NAC-treated BEAS-2B, normal and COPD HSAEpCs exposed to PM 2.5 (n=5–8 per group). d) Apoptotic cell population (%) in si-ITIH4-knockdown and ITIH4-overexpressing BEAS-2B cells in comparison with scramble si-RNA and pcDNA vector control cells exposed to 20 μg·mL −1 PM 2.5 , respectively. Apoptosis was measured by knockdown and overexpression of ITIH4 in HSAEpCs and COPD HSAEpCs exposed to 20 μg·mL −1 PM 2.5 , respectively (n=5–9 per group). e) Apoptosis was analysed in ITIH4-knockdown and ITIH4-overexpressing cells exposed to hydrogen peroxide (H 2 O 2 ) as indicated (n=5–8 per group). Relative values are expressed as the fold change calculated through comparison with vehicle-treated si-scramble or pcDNA control cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.

Article Snippet: Human small airway epithelial cells (HSAEpCs) from healthy (aged 53–70 years) and COPD (aged 59–67 years) donors (C-12642, PromoCell, Heidelberg, Germany) were cultured as submerged undifferentiated monolayers in PromoCell cell growth medium and passaged fewer than five times to prevent cell senescence.

Techniques: Control, Immunohistochemical staining, Immunohistochemistry, Staining, Light Microscopy, Knockdown, Comparison, Plasmid Preparation, Over Expression

Overexpression of inter-α-trypsin inhibitor heavy chain 4 (ITIH4) inhibits oxidative-stress-induced activation of c-Jun N-terminal kinase (JNK) signalling and reduction of β-catenin. a) Levels of ITIH4, β-catenin, p-JNK and JNK in bronchial epithelial (BEAS-2B) cells exposed to lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) or hydrogen peroxide (H 2 O 2 ) (100–300 μM), examined through an immunoblot analysis (n=6 per group). b) Levels of ITIH4, β-catenin, p-JNK and JNK in BEAS-2B cells exposed to 50–100 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) and vehicle control (ctrl) were measured. Moreover, levels of ITIH4, β-catenin, p-JNK and JNK were determined in c) bronchial epithelial (BEAS-2B) cells and d) human small airway epithelial cells (HSAEpCs) exposed to 50–100 μg·mL −1 DEP and DEP-derived particulate matter with aerodynamic diameter <2.5 µm (PM 2.5 ) (n=6 per group). e) The effects of exposure to 100 μM H 2 O 2 -mediated expression of ITIH4, β-catenin, p-JNK and JNK proteins were assessed in BEAS-2B cells transfected with ITIH4-overexpression vector or empty vector control (EV) (n=6–7 per group). f) By contrast, the effects of exposure to H 2 O 2 -mediated β-catenin expression and JNK activation were evaluated in BEAS-2B cells transfected with siRNA control or si-ITIH4 (n=6 per group). Levels of p-JNK and JNK were measured in cells exposed to stimuli for 2 h. Levels of ITIH4, β-catenin and actin were measured in cells treated with irritants for 24 h. Relative values are expressed as the fold change calculated through comparison with vehicle-treated cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.

Journal: The European Respiratory Journal

Article Title: Particulate matter-related ITIH4 deficiency is associated with an emphysema phenotype of COPD through JNK-dependent and JNK-independent signalling

doi: 10.1183/13993003.01610-2024

Figure Lengend Snippet: Overexpression of inter-α-trypsin inhibitor heavy chain 4 (ITIH4) inhibits oxidative-stress-induced activation of c-Jun N-terminal kinase (JNK) signalling and reduction of β-catenin. a) Levels of ITIH4, β-catenin, p-JNK and JNK in bronchial epithelial (BEAS-2B) cells exposed to lipopolysaccharide (LPS) (20 ng·mL −1 ), interleukin (IL)-1β (10 ng·mL −1 ) or hydrogen peroxide (H 2 O 2 ) (100–300 μM), examined through an immunoblot analysis (n=6 per group). b) Levels of ITIH4, β-catenin, p-JNK and JNK in BEAS-2B cells exposed to 50–100 μg·mL −1 carbon black (CB), diesel exhaust particles (DEP), urban dust (UD) and vehicle control (ctrl) were measured. Moreover, levels of ITIH4, β-catenin, p-JNK and JNK were determined in c) bronchial epithelial (BEAS-2B) cells and d) human small airway epithelial cells (HSAEpCs) exposed to 50–100 μg·mL −1 DEP and DEP-derived particulate matter with aerodynamic diameter <2.5 µm (PM 2.5 ) (n=6 per group). e) The effects of exposure to 100 μM H 2 O 2 -mediated expression of ITIH4, β-catenin, p-JNK and JNK proteins were assessed in BEAS-2B cells transfected with ITIH4-overexpression vector or empty vector control (EV) (n=6–7 per group). f) By contrast, the effects of exposure to H 2 O 2 -mediated β-catenin expression and JNK activation were evaluated in BEAS-2B cells transfected with siRNA control or si-ITIH4 (n=6 per group). Levels of p-JNK and JNK were measured in cells exposed to stimuli for 2 h. Levels of ITIH4, β-catenin and actin were measured in cells treated with irritants for 24 h. Relative values are expressed as the fold change calculated through comparison with vehicle-treated cells. Data are presented as mean± sd of at least five for each independent group. *: p<0.05; **: p<0.01.

Article Snippet: Human small airway epithelial cells (HSAEpCs) from healthy (aged 53–70 years) and COPD (aged 59–67 years) donors (C-12642, PromoCell, Heidelberg, Germany) were cultured as submerged undifferentiated monolayers in PromoCell cell growth medium and passaged fewer than five times to prevent cell senescence.

Techniques: Over Expression, Activation Assay, Western Blot, Control, Derivative Assay, Expressing, Transfection, Plasmid Preparation, Comparison

Constitutive Notch 1 signaling leads to CP tumour. (a) Schematic illustration of the strategy for Notch 1 signaling activation in vivo . (b) Brain hemispheres and CPs from postnatal day 7 (P7) mice are shown. Notice that the enlarged CP from Math1-Cre;Rosa26-NICD1;Rosa26-EYFP ( Mcre;NICD1;EYFP ) animal contains many EYFP + cells (arrows), while EYFP + cells (arrowheads) are sparsely found in the CP from Math1-Cre;Rosa26-EYFP ( Mcre;EYFP ) animals. Scale bar: 1 mm. (c) Analysis of gene expression in CP of Math1-Cre;Rosa26-EYFP mice. EYFP expression (green) labels cells derived from Atoh1 + progenitors. The expression of Lmx1a (red), Otx2 (red), cytokeratins (red), and Aqp1 (red) labels CP epithelial cells. Scale bar: 25μm. (d) Quantitation of the percentage of EYFP + cells or NICD1 + /GFP + cells in Otx2 + hindbrain CP epithelium of Mcre;EYFP mice or Math1-Cre;Rosa26-NICD1 ( Mcre;NICD1 ) mice, respectively, at different time points (n=3 tumours from 3 Mcre;NICD1 animals/time point; CPs from Mcre;EYFP mice: n=4 (P0, P14), n=6 (P7, P21), n=5 (P90), data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, **, P<0.01; ***, P <0.001; ns, non-significant). (e) H&E staining of CPs from Mcre;NICD1 and wild type (WT) mice at P0 and P14. Notice that CP epithelium exhibits the “hobnail” configuration (arrowhead), while the enlarged CP in Mcre;NICD1 mice appear “flattened” on ventricular surfaces (arrow). Vesicular sac with accumulated CSF is shown (asterisk). Scale bars: white, 500μm; black, 25μm. (f) H&E staining of human CP papilloma (CPP) and normal CP. Scale bar: 25μm. (g) Quantitative RT-PCR (Q-RT-PCR) analysis of Hes1 and Hes5 expression in CP tumours (black circles) and wild type CPs (white circles) at P0, P7, P14, and P21 (data from technical replicates of each specimen set in a single experiment are shown; experiment was not repeated. Raw data can be found in ). (h) The expression of Ki-67 is shown in CP tumours from Mcre;NICD1 mice, Lmx1a-Cre;Rosa26-NICD1 ( Lcre;NICD1 ) mice, and normal CPs from wild type mice. Dotted lines mark the boundary of lateral ventricles. The expression of Ki-67 in human CPP and normal CP is shown. Scale bar: 50μm.

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Constitutive Notch 1 signaling leads to CP tumour. (a) Schematic illustration of the strategy for Notch 1 signaling activation in vivo . (b) Brain hemispheres and CPs from postnatal day 7 (P7) mice are shown. Notice that the enlarged CP from Math1-Cre;Rosa26-NICD1;Rosa26-EYFP ( Mcre;NICD1;EYFP ) animal contains many EYFP + cells (arrows), while EYFP + cells (arrowheads) are sparsely found in the CP from Math1-Cre;Rosa26-EYFP ( Mcre;EYFP ) animals. Scale bar: 1 mm. (c) Analysis of gene expression in CP of Math1-Cre;Rosa26-EYFP mice. EYFP expression (green) labels cells derived from Atoh1 + progenitors. The expression of Lmx1a (red), Otx2 (red), cytokeratins (red), and Aqp1 (red) labels CP epithelial cells. Scale bar: 25μm. (d) Quantitation of the percentage of EYFP + cells or NICD1 + /GFP + cells in Otx2 + hindbrain CP epithelium of Mcre;EYFP mice or Math1-Cre;Rosa26-NICD1 ( Mcre;NICD1 ) mice, respectively, at different time points (n=3 tumours from 3 Mcre;NICD1 animals/time point; CPs from Mcre;EYFP mice: n=4 (P0, P14), n=6 (P7, P21), n=5 (P90), data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, **, P<0.01; ***, P <0.001; ns, non-significant). (e) H&E staining of CPs from Mcre;NICD1 and wild type (WT) mice at P0 and P14. Notice that CP epithelium exhibits the “hobnail” configuration (arrowhead), while the enlarged CP in Mcre;NICD1 mice appear “flattened” on ventricular surfaces (arrow). Vesicular sac with accumulated CSF is shown (asterisk). Scale bars: white, 500μm; black, 25μm. (f) H&E staining of human CP papilloma (CPP) and normal CP. Scale bar: 25μm. (g) Quantitative RT-PCR (Q-RT-PCR) analysis of Hes1 and Hes5 expression in CP tumours (black circles) and wild type CPs (white circles) at P0, P7, P14, and P21 (data from technical replicates of each specimen set in a single experiment are shown; experiment was not repeated. Raw data can be found in ). (h) The expression of Ki-67 is shown in CP tumours from Mcre;NICD1 mice, Lmx1a-Cre;Rosa26-NICD1 ( Lcre;NICD1 ) mice, and normal CPs from wild type mice. Dotted lines mark the boundary of lateral ventricles. The expression of Ki-67 in human CPP and normal CP is shown. Scale bar: 50μm.

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Activation Assay, In Vivo, Gene Expression, Expressing, Derivative Assay, Quantitation Assay, Staining, Quantitative RT-PCR, Reverse Transcription Polymerase Chain Reaction

Notch-induced CP tumours undergo enhanced proliferation and exhibit defects in differentiation. (a) The expression of Ki-67 is shown in CP tumours from Mcre;NICD1 mice at P0, P7, and P14; CPs from P0 wild type (WT) and Mcre;EYFP mice, respectively, serve as control. Ki-67 expression (red) labels proliferating cells, GFP expression (green) marks NICD1 + tumour cells, expression of Lmx1a (green) labels CP epithelium in wild type mice, and EYFP expression (green, arrowheads) detected with a GFP antibody demarcates CP epithelial cells derived from Atoh1 + progenitors in Mcre;EYFP mice. DAPI staining (blue) marks nuclei. Scale bar: 25μm. (b) Quantitation of the percentage of Ki-67 + cells in NICD1 + /GFP + tumour cells from Mcre;NICD1 mice and Lmx1a + wild type CP epithelial cells at different time points (n=3 CPs from 3 animals/genotype/time point, data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, ****, P <0.0001). (c) The expression of Ki-67 and Cdkn1b (p27 Kip1) is shown in tumours from Mcre;NICD1 mice and wild type (WT) CPs at P7. Notice that staining for Ki-67 and p27 is mutually exclusive. And p27 or Ki-67 expression is absent in wild type CP epithelium despite positive staining in the cerebellum (Cb). Scale bar: 25μm. (d) The expression of Lmx1a (red), Otx2 (red), Ttr (red), Aqp1 (red), and cytokeratins (red) is shown in CP tumours. GFP expression (green) labels NICD1 + tumour cells. Dotted lines mark the boundary between GFP + tumour cells and epithelium. DAPI staining (blue) marks nuclei. Scale bar: 25μm. (e) Q-RT-PCR analysis of Ttr and Aqp1 expression in tumours from Mcre;NICD1 mice (black circles) and wild type (WT) CPs (white circles) at different time points (data from technical replicates in a single experiment are shown and available in . Experiment was not repeated for Ttr expression; Aqp1 expression analysis was repeated in one independent experiment). (f) Western blot analysis of Aqp1 and Otx2 expression in CP tumours and wild type (WT) CPs at P14. β-actin serves as loading control. Molecular size marker and representative image of unprocessed blots can be found in .

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Notch-induced CP tumours undergo enhanced proliferation and exhibit defects in differentiation. (a) The expression of Ki-67 is shown in CP tumours from Mcre;NICD1 mice at P0, P7, and P14; CPs from P0 wild type (WT) and Mcre;EYFP mice, respectively, serve as control. Ki-67 expression (red) labels proliferating cells, GFP expression (green) marks NICD1 + tumour cells, expression of Lmx1a (green) labels CP epithelium in wild type mice, and EYFP expression (green, arrowheads) detected with a GFP antibody demarcates CP epithelial cells derived from Atoh1 + progenitors in Mcre;EYFP mice. DAPI staining (blue) marks nuclei. Scale bar: 25μm. (b) Quantitation of the percentage of Ki-67 + cells in NICD1 + /GFP + tumour cells from Mcre;NICD1 mice and Lmx1a + wild type CP epithelial cells at different time points (n=3 CPs from 3 animals/genotype/time point, data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, ****, P <0.0001). (c) The expression of Ki-67 and Cdkn1b (p27 Kip1) is shown in tumours from Mcre;NICD1 mice and wild type (WT) CPs at P7. Notice that staining for Ki-67 and p27 is mutually exclusive. And p27 or Ki-67 expression is absent in wild type CP epithelium despite positive staining in the cerebellum (Cb). Scale bar: 25μm. (d) The expression of Lmx1a (red), Otx2 (red), Ttr (red), Aqp1 (red), and cytokeratins (red) is shown in CP tumours. GFP expression (green) labels NICD1 + tumour cells. Dotted lines mark the boundary between GFP + tumour cells and epithelium. DAPI staining (blue) marks nuclei. Scale bar: 25μm. (e) Q-RT-PCR analysis of Ttr and Aqp1 expression in tumours from Mcre;NICD1 mice (black circles) and wild type (WT) CPs (white circles) at different time points (data from technical replicates in a single experiment are shown and available in . Experiment was not repeated for Ttr expression; Aqp1 expression analysis was repeated in one independent experiment). (f) Western blot analysis of Aqp1 and Otx2 expression in CP tumours and wild type (WT) CPs at P14. β-actin serves as loading control. Molecular size marker and representative image of unprocessed blots can be found in .

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Expressing, Control, Derivative Assay, Staining, Quantitation Assay, Reverse Transcription Polymerase Chain Reaction, Western Blot, Marker

Shh drives the proliferation of Notch-induced CP tumours. Lmx1a (a) (red) and Ki-67 (b) (red) expression is shown in cultured tumour cells from Mcre;NICD1 mice. GFP (green) marks tumour cells, DAPI staining (blue) labels nuclei. Scale bar: 10μm. (c) Images of tumour cells and wild type (WT) epithelial cells. Scale bar: 50μm. (d) Quantitation of tumour cells after 96-hour treatments (n=3 specimens/treatment/time point, raw data are available in ; mean ± SEM, two-way ANOVA, ****, P <0.0001; ns, non-significant). (e) Kaplan-Meier curve depicting the survival of Lcre;NICD1 mice treated with vismodegib (n=22 animals) or vehicle (n=19 animals). (f) Hindbrain CPs from day P7 Lcre;NICD1 mice treated with vismodegib (lower) or vehicle (upper). Scale bar: 1 mm. Quantitation of tumour cells in treated animals is shown (n=7 animals/treatment, raw data are available in ; mean ± SEM, two-tailed unpaired t test, **, P <0.01). (g) H&E staining of tumours from treated Mcre;NICD1 mice. Ki-67 expression (red) labels proliferating cells, while GFP (green) marks tumour cells. DAPI staining (blue) labels nuclei. Scale bar: 25μm. (h) Analysis of tumour cell proliferation in animals shown in (g) (n=10 animals/treatment; mean ± SEM, two-tailed unpaired t test, **, P <0.01). (i) In-situ hybridization analysis of Mycn expression in tumour (arrows) or epithelial cells (arrowheads) in animals shown in (g). Scale bar: 25μm. (j) Principal component analysis of human CPPs (red dots, n=7 tumours from 7 individuals) and normal CPs (blue dots, n=8 CPs from 8 individuals). (k) MetaCore analysis of differential genes in human CPPs. (l) Venn diagram shows the overlap of differential genes (FDR < 0.05) between human CPPs and normal CPs (A), with those between murine tumours and wild type CPs at P21 (B, n=3 specimens/genotype) and P0 (C, n=3 specimens/genotype). (m) MetaCore analysis of overlapping genes between mouse and human CPPs shown in (l). (n) Q-RT-PCR analysis of gene expression in human CP tumours (CPP: n=7 tumours from 7 individuals; CPC: n=2 tumours from 2 individuals). Values represent fold changes relative to human CP epithelium. Data are derived from single experiment shown in and not repeated.

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Shh drives the proliferation of Notch-induced CP tumours. Lmx1a (a) (red) and Ki-67 (b) (red) expression is shown in cultured tumour cells from Mcre;NICD1 mice. GFP (green) marks tumour cells, DAPI staining (blue) labels nuclei. Scale bar: 10μm. (c) Images of tumour cells and wild type (WT) epithelial cells. Scale bar: 50μm. (d) Quantitation of tumour cells after 96-hour treatments (n=3 specimens/treatment/time point, raw data are available in ; mean ± SEM, two-way ANOVA, ****, P <0.0001; ns, non-significant). (e) Kaplan-Meier curve depicting the survival of Lcre;NICD1 mice treated with vismodegib (n=22 animals) or vehicle (n=19 animals). (f) Hindbrain CPs from day P7 Lcre;NICD1 mice treated with vismodegib (lower) or vehicle (upper). Scale bar: 1 mm. Quantitation of tumour cells in treated animals is shown (n=7 animals/treatment, raw data are available in ; mean ± SEM, two-tailed unpaired t test, **, P <0.01). (g) H&E staining of tumours from treated Mcre;NICD1 mice. Ki-67 expression (red) labels proliferating cells, while GFP (green) marks tumour cells. DAPI staining (blue) labels nuclei. Scale bar: 25μm. (h) Analysis of tumour cell proliferation in animals shown in (g) (n=10 animals/treatment; mean ± SEM, two-tailed unpaired t test, **, P <0.01). (i) In-situ hybridization analysis of Mycn expression in tumour (arrows) or epithelial cells (arrowheads) in animals shown in (g). Scale bar: 25μm. (j) Principal component analysis of human CPPs (red dots, n=7 tumours from 7 individuals) and normal CPs (blue dots, n=8 CPs from 8 individuals). (k) MetaCore analysis of differential genes in human CPPs. (l) Venn diagram shows the overlap of differential genes (FDR < 0.05) between human CPPs and normal CPs (A), with those between murine tumours and wild type CPs at P21 (B, n=3 specimens/genotype) and P0 (C, n=3 specimens/genotype). (m) MetaCore analysis of overlapping genes between mouse and human CPPs shown in (l). (n) Q-RT-PCR analysis of gene expression in human CP tumours (CPP: n=7 tumours from 7 individuals; CPC: n=2 tumours from 2 individuals). Values represent fold changes relative to human CP epithelium. Data are derived from single experiment shown in and not repeated.

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Expressing, Cell Culture, Staining, Quantitation Assay, Two Tailed Test, In Situ Hybridization, Reverse Transcription Polymerase Chain Reaction, Gene Expression, Derivative Assay

Notch-induced CP tumours possess solitary primary cilium. (a) Transmission electron micrographs of primary cilia in tumour cells (arrow) from Mcre;NICD1 animals and wild type (WT) CP epithelium (arrowheads). Scale bar: 0.5μm. (b) The expression of cilia markers Arl13b (red) and γ-tubulin (red) in tumour cells is shown. Dotted lines mark the boundary between GFP + (green) tumour cells and Aqp1 + (yellow) epithelium. DAPI staining (blue) labels nuclei. Primary cilia in epithelial (arrowheads, upper) or tumour cells (arrows, lower) are magnified in inset pictures. Scale bar: 10μm. (c) The expression of Arl13b (red), γ-tubulin (red), and acetylated α-tubulin (act-α-tubulin, red) is shown in cultured CP cells. GFP (green) labels tumour cells, while Aqp1 (yellow) labels epithelial cells. DAPI staining (blue) labels nuclei. Scale bar: 5μm. (d) Hierarchical clustering of tumours and normal CPs at P0 based on 147 genes involved in cilia differentiation (n=3 specimens/genotype; one-way ANOVA, FDR < 0.05, fold change is shown). (e) Q-RT-PCR analysis of the expression of Mcidas and Foxj1 in tumours (black circles) and CPs (white circles) at different time points (data from technical replicates of each specimen in a single experiment are shown and available in . Experiment was not repeated for Mcidas expression; Foxj1 expression analysis was repeated in one independent experiment). (f) In-situ hybridization analysis of the expression of Hes1 and Hes5 is shown in hindbrain roof plate (red dotted lines) and tumour cells (arrows) in Mcre;NICD1 or wild type animals at day E14.5. Scale bar: 100μm. (g) Primary cilia are shown for cells in hindbrain roof plate, CP epithelium, and tumours shown in (f). Arl13b (red) and γ-tubulin (red) expression marks primary cilia and basal body, respectively. DAPI staining (blue) labels nuclei. RP: roof plate. Scale bar: 10μm. (h) Representative images show ARL13B expression (red) in human CP tumour cells (arrows) or normal CP epithelium (arrowhead). Primary cilia are magnified in inset pictures. DAPI staining (blue) labels nuclei. Scale bar: 10μm. (i) Summary of cilia pattern in human CPPs (n=17 tumours from 16 individuals), CPCs (n=13 tumours from 13 individuals), and normal CPs (n=6 CPs from 6 disease-free individuals).

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Notch-induced CP tumours possess solitary primary cilium. (a) Transmission electron micrographs of primary cilia in tumour cells (arrow) from Mcre;NICD1 animals and wild type (WT) CP epithelium (arrowheads). Scale bar: 0.5μm. (b) The expression of cilia markers Arl13b (red) and γ-tubulin (red) in tumour cells is shown. Dotted lines mark the boundary between GFP + (green) tumour cells and Aqp1 + (yellow) epithelium. DAPI staining (blue) labels nuclei. Primary cilia in epithelial (arrowheads, upper) or tumour cells (arrows, lower) are magnified in inset pictures. Scale bar: 10μm. (c) The expression of Arl13b (red), γ-tubulin (red), and acetylated α-tubulin (act-α-tubulin, red) is shown in cultured CP cells. GFP (green) labels tumour cells, while Aqp1 (yellow) labels epithelial cells. DAPI staining (blue) labels nuclei. Scale bar: 5μm. (d) Hierarchical clustering of tumours and normal CPs at P0 based on 147 genes involved in cilia differentiation (n=3 specimens/genotype; one-way ANOVA, FDR < 0.05, fold change is shown). (e) Q-RT-PCR analysis of the expression of Mcidas and Foxj1 in tumours (black circles) and CPs (white circles) at different time points (data from technical replicates of each specimen in a single experiment are shown and available in . Experiment was not repeated for Mcidas expression; Foxj1 expression analysis was repeated in one independent experiment). (f) In-situ hybridization analysis of the expression of Hes1 and Hes5 is shown in hindbrain roof plate (red dotted lines) and tumour cells (arrows) in Mcre;NICD1 or wild type animals at day E14.5. Scale bar: 100μm. (g) Primary cilia are shown for cells in hindbrain roof plate, CP epithelium, and tumours shown in (f). Arl13b (red) and γ-tubulin (red) expression marks primary cilia and basal body, respectively. DAPI staining (blue) labels nuclei. RP: roof plate. Scale bar: 10μm. (h) Representative images show ARL13B expression (red) in human CP tumour cells (arrows) or normal CP epithelium (arrowhead). Primary cilia are magnified in inset pictures. DAPI staining (blue) labels nuclei. Scale bar: 10μm. (i) Summary of cilia pattern in human CPPs (n=17 tumours from 16 individuals), CPCs (n=13 tumours from 13 individuals), and normal CPs (n=6 CPs from 6 disease-free individuals).

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Transmission Assay, Expressing, Staining, Cell Culture, Reverse Transcription Polymerase Chain Reaction, In Situ Hybridization

Mono-ciliated CP tumour cells are uniquely capable of transducing Shh signals. (a) Dissociated CP tumour cells from Mcre;NICD1 animals were initially cultured in the presence of 10% fetal bovine serum (FBS). Cultured CP tumour cells were then switched to serum-free conditions for 2 days followed by treatment with ShhN or SAG for 1.5 or 3 days for signaling and proliferation analysis, respectively. (b) The expression of Lmx1a (red) and Ki-67 (red) is shown in CP tumour cells cultured with FBS. GFP (green) labels NICD1 + CP tumour cells, while Aqp1 labels CP epithelial cells. DAPI staining (blue) labels nuclei. Scale bar: 25μm. After treatment with ShhN, SAG, or vehicle, Smo (red) localization is shown in CP tumour (c) or epithelial cells (d). Arl13b expression (green) labels primary cilia, while DAPI staining (blue) labels nuclei. Scale bar: 10μm. (e) Q-RT-PCR analysis of Ptch1 and Smo expression in CP tumours from Mcre;NICD1 animals (black circles) and wild type CPs (WT, while circles) at P7 (data from technical replicates of each set of specimen in a single experiment are shown; experiment was not repeated. Raw data can be found in ). (f) The expression of Ki-67 (green) in CP tumour cells from Mcre;NICD1 animals treated with ShhN for 48 hours treatment is shown. Arl13b expression (red) labels primary cilia, DAPI staining (blue) labels nuclei. Notice that Ki-67 expression is present in mono-ciliated CP tumour cell, while multi-ciliated CP epithelial cell lacks Ki-67 expression. Scale bar: 10μm. (g) The expression of Ki-67 (red) in CP tumour cells from Mcre;NICD1 animals treated as indicated is shown. GFP (green) labels NICD1 + tumour cells. DAPI staining (blue) labels nuclei. Scale bar: 25μm. (h) Quantitation of the percentage of Ki-67 + cells in NICD1 + /GFP + tumour cells after 72-hour treatment as indicated (n=4 specimens/treatment, data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, ***, P< 0.001; ****, P <0.0001).

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Mono-ciliated CP tumour cells are uniquely capable of transducing Shh signals. (a) Dissociated CP tumour cells from Mcre;NICD1 animals were initially cultured in the presence of 10% fetal bovine serum (FBS). Cultured CP tumour cells were then switched to serum-free conditions for 2 days followed by treatment with ShhN or SAG for 1.5 or 3 days for signaling and proliferation analysis, respectively. (b) The expression of Lmx1a (red) and Ki-67 (red) is shown in CP tumour cells cultured with FBS. GFP (green) labels NICD1 + CP tumour cells, while Aqp1 labels CP epithelial cells. DAPI staining (blue) labels nuclei. Scale bar: 25μm. After treatment with ShhN, SAG, or vehicle, Smo (red) localization is shown in CP tumour (c) or epithelial cells (d). Arl13b expression (green) labels primary cilia, while DAPI staining (blue) labels nuclei. Scale bar: 10μm. (e) Q-RT-PCR analysis of Ptch1 and Smo expression in CP tumours from Mcre;NICD1 animals (black circles) and wild type CPs (WT, while circles) at P7 (data from technical replicates of each set of specimen in a single experiment are shown; experiment was not repeated. Raw data can be found in ). (f) The expression of Ki-67 (green) in CP tumour cells from Mcre;NICD1 animals treated with ShhN for 48 hours treatment is shown. Arl13b expression (red) labels primary cilia, DAPI staining (blue) labels nuclei. Notice that Ki-67 expression is present in mono-ciliated CP tumour cell, while multi-ciliated CP epithelial cell lacks Ki-67 expression. Scale bar: 10μm. (g) The expression of Ki-67 (red) in CP tumour cells from Mcre;NICD1 animals treated as indicated is shown. GFP (green) labels NICD1 + tumour cells. DAPI staining (blue) labels nuclei. Scale bar: 25μm. (h) Quantitation of the percentage of Ki-67 + cells in NICD1 + /GFP + tumour cells after 72-hour treatment as indicated (n=4 specimens/treatment, data from a single experiment are shown, raw data are available in ; mean ± SEM, two-way ANOVA, ***, P< 0.001; ****, P <0.0001).

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Cell Culture, Expressing, Staining, Reverse Transcription Polymerase Chain Reaction, Quantitation Assay

Notch-induced CP tumours arise from progenitors in the roof plate. (a) Atoh1:EGFP expression in Math1 M1GFP mice at day E14.5 is detected with a GFP antibody and shown in green signals. Lmx1a expression (red) marks the roof plate (marked by dotted lines), while DAPI staining (blue) labels nuclei. Notice that Atoh1:EGFP + progenitors (arrows) are present only in Lmx1a + upper roof plate. Scale bar: 50μm. (b) Schematic illustration of hindbrain roof plate (RP) and CP at day E12.5. Solid line marks the transverse plane across the roof plate shown in the H&E staining and diagram. Boxed region in the diagram representing the interface of the rhombic lip and roof plate is shown in Mcre:NICD1 mice at day E12.5. GFP (green) marks Atoh1 + rhombic lip progenitors and prospective tumour cells (arrows) in the roof plate and CP. The expression of Lmx1a (red) marks the roof plate/CP lineage. While Ki-67 expression (red) labels proliferating cells, Aqp1 expression (red) marks differentiated epithelial cells. DAPI staining (blue) labels nuclei. Scale bars: black, 1 mm; white, 30μm. (c) Gene expression in the roof plate and CP in Mcre:NICD1 mice at day E14.5. Boxed regions of progenitors within upper (a1, a2) and lower (b1, b2) roof plate as well as tumour cells (c) in CP are shown in higher magnification. GFP expression (green) marks NICD1 + tumour cells in the roof plate and CP. Lmx1a expression (red) labels the roof plate and CP lineage, while DAPI staining (blue) marks nuclei. Scale bar: 300μm.

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Notch-induced CP tumours arise from progenitors in the roof plate. (a) Atoh1:EGFP expression in Math1 M1GFP mice at day E14.5 is detected with a GFP antibody and shown in green signals. Lmx1a expression (red) marks the roof plate (marked by dotted lines), while DAPI staining (blue) labels nuclei. Notice that Atoh1:EGFP + progenitors (arrows) are present only in Lmx1a + upper roof plate. Scale bar: 50μm. (b) Schematic illustration of hindbrain roof plate (RP) and CP at day E12.5. Solid line marks the transverse plane across the roof plate shown in the H&E staining and diagram. Boxed region in the diagram representing the interface of the rhombic lip and roof plate is shown in Mcre:NICD1 mice at day E12.5. GFP (green) marks Atoh1 + rhombic lip progenitors and prospective tumour cells (arrows) in the roof plate and CP. The expression of Lmx1a (red) marks the roof plate/CP lineage. While Ki-67 expression (red) labels proliferating cells, Aqp1 expression (red) marks differentiated epithelial cells. DAPI staining (blue) labels nuclei. Scale bars: black, 1 mm; white, 30μm. (c) Gene expression in the roof plate and CP in Mcre:NICD1 mice at day E14.5. Boxed regions of progenitors within upper (a1, a2) and lower (b1, b2) roof plate as well as tumour cells (c) in CP are shown in higher magnification. GFP expression (green) marks NICD1 + tumour cells in the roof plate and CP. Lmx1a expression (red) labels the roof plate and CP lineage, while DAPI staining (blue) marks nuclei. Scale bar: 300μm.

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Expressing, Staining, Gene Expression

Notch-induced CP tumour cells retain properties of roof plate progenitor. (a) Analysis of gene expression and cell proliferation in tumour cells and progenitors within hindbrain roof plate in Mcre;NICD1 and wild type (WT) animals, respectively, at day E12.5. The expression of Lmx1a (red) marks the roof plate and CP lineage. Ki-67 expression (green) labels proliferating cells, and Aqp1 expression (green) marks differentiated epithelial cells. White dotted lines demarcate domain of progenitors in hindbrain roof plate. Boxed regions of Lmx1a + /Ki-67 + /Aqp1 − progenitors (a, c, e, f), tumour cells (b, d) (arrows), and Lmx1a + /Ki-67 − /Aqp1 + differentiated epithelial cells (b, d) (red bracket lines) are shown in higher magnification. Scale bar: 100μm. (b) Schematic diagram of interaction between Notch and Shh pathways during the roof plate/CP morphogenesis and tumour formation. Epithelial progenitors in the roof plate (RP, yellow) next to the rhombic lip (RL) exhibits active Notch signaling, possess a solitary primary cilium, and proliferate in response to Shh (green dots) secreted from multiciliated epithelial cells (grey). The self-renewal will cease as Notch pathway activity in progenitor cells is attenuated to allow for multiciliate differentiation, thereby abolishing the response of the progenitors to Shh that drives their expansion during development. (c) Epithelial progenitors with constitutive Notch pathway activity (red) remain mono-ciliated and undergo aberrant proliferation to become tumour cells that retain the ability to respond to Shh signals in the local environment and undergo Shh-driven proliferation.

Journal: Nature cell biology

Article Title: Sonic Hedgehog promotes proliferation of Notch-dependent monociliated choroid plexus tumour cells

doi: 10.1038/ncb3327

Figure Lengend Snippet: Notch-induced CP tumour cells retain properties of roof plate progenitor. (a) Analysis of gene expression and cell proliferation in tumour cells and progenitors within hindbrain roof plate in Mcre;NICD1 and wild type (WT) animals, respectively, at day E12.5. The expression of Lmx1a (red) marks the roof plate and CP lineage. Ki-67 expression (green) labels proliferating cells, and Aqp1 expression (green) marks differentiated epithelial cells. White dotted lines demarcate domain of progenitors in hindbrain roof plate. Boxed regions of Lmx1a + /Ki-67 + /Aqp1 − progenitors (a, c, e, f), tumour cells (b, d) (arrows), and Lmx1a + /Ki-67 − /Aqp1 + differentiated epithelial cells (b, d) (red bracket lines) are shown in higher magnification. Scale bar: 100μm. (b) Schematic diagram of interaction between Notch and Shh pathways during the roof plate/CP morphogenesis and tumour formation. Epithelial progenitors in the roof plate (RP, yellow) next to the rhombic lip (RL) exhibits active Notch signaling, possess a solitary primary cilium, and proliferate in response to Shh (green dots) secreted from multiciliated epithelial cells (grey). The self-renewal will cease as Notch pathway activity in progenitor cells is attenuated to allow for multiciliate differentiation, thereby abolishing the response of the progenitors to Shh that drives their expansion during development. (c) Epithelial progenitors with constitutive Notch pathway activity (red) remain mono-ciliated and undergo aberrant proliferation to become tumour cells that retain the ability to respond to Shh signals in the local environment and undergo Shh-driven proliferation.

Article Snippet: For human tissues, seven CPPs from seven individuals, two CPCs from two individuals, and normal human CP epithelial cells (ScienCell) were used ( ).

Techniques: Gene Expression, Expressing, Activity Assay