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93
ATCC human small cell lung carcinoma line nci h1930
Immunohistochemical analysis of SLC35D3 expression in human tumors, normal tissues, and positive-control samples. (A) SLC35D3 staining in human tumors: (a) primary colon tumor; (b) corresponding lymph-node metastasis; (c) normal adjacent tissue (NAT) of a; (d) primary rectal tumor; (e) corresponding lymph-node metastasis; (f) NAT of d; (g–h) small-cell lung carcinoma (SCLC); (i) pancreatic neuroendocrine neoplasm; (j) pancreatic islet tumor. (B) SLC35D3 staining in human normal tissues: (a) cerebrum; (b) bone marrow; (c) lung; (d) heart; (e) liver; (f) kidney; (g) eye; (h) colon; (i) adrenal gland; (j) pancreas; (k) hypophysis; (l) stomach; (m) small intestine; (n) prostate. Arrowheads indicate SLC35D3-positive cells. (C) SLC35D3 staining of negative and positive control cell lines: (a) HCT 116-mock (negative control); (b) HCT 116-hSLC35D3 (engineered overexpression); <t>(c)</t> <t>NCI–H1930</t> (endogenously SLC35D3-expressing).
Human Small Cell Lung Carcinoma Line Nci H1930, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC human lung carcinoma a 549 cells
Immunohistochemical analysis of SLC35D3 expression in human tumors, normal tissues, and positive-control samples. (A) SLC35D3 staining in human tumors: (a) primary colon tumor; (b) corresponding lymph-node metastasis; (c) normal adjacent tissue (NAT) of a; (d) primary rectal tumor; (e) corresponding lymph-node metastasis; (f) NAT of d; (g–h) small-cell lung carcinoma (SCLC); (i) pancreatic neuroendocrine neoplasm; (j) pancreatic islet tumor. (B) SLC35D3 staining in human normal tissues: (a) cerebrum; (b) bone marrow; (c) lung; (d) heart; (e) liver; (f) kidney; (g) eye; (h) colon; (i) adrenal gland; (j) pancreas; (k) hypophysis; (l) stomach; (m) small intestine; (n) prostate. Arrowheads indicate SLC35D3-positive cells. (C) SLC35D3 staining of negative and positive control cell lines: (a) HCT 116-mock (negative control); (b) HCT 116-hSLC35D3 (engineered overexpression); <t>(c)</t> <t>NCI–H1930</t> (endogenously SLC35D3-expressing).
Human Lung Carcinoma A 549 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human lung carcinoma a 549 cells - by Bioz Stars, 2026-05
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99
ATCC human lung adenocarcinoma a549 cells
ALDH3A1 and NQO1 as guardians of epithelial survival and barrier function upon smoke exposure (A) <t>A549</t> epithelial cell death upon 4 h of exposure to 0%–100% cigarette smoke extract in ALDH3A1 and NQO1 CRISPR-Cas9 knockout cells. Epithelial cell barrier function change in response to 0%–20% cigarette smoke extract exposure for 24 h, which was measured in real-time monitoring of electrical resistance and capacitance during and upon the establishment of epithelial monolayers using electric cell-substrate impedance sensing (ECIS) in ALDH3A1- (B) and NQO1-knockout (C) A549 cells. ∗ p value <0.05.
Human Lung Adenocarcinoma A549 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC w138 human lung cells
ALDH3A1 and NQO1 as guardians of epithelial survival and barrier function upon smoke exposure (A) <t>A549</t> epithelial cell death upon 4 h of exposure to 0%–100% cigarette smoke extract in ALDH3A1 and NQO1 CRISPR-Cas9 knockout cells. Epithelial cell barrier function change in response to 0%–20% cigarette smoke extract exposure for 24 h, which was measured in real-time monitoring of electrical resistance and capacitance during and upon the establishment of epithelial monolayers using electric cell-substrate impedance sensing (ECIS) in ALDH3A1- (B) and NQO1-knockout (C) A549 cells. ∗ p value <0.05.
W138 Human Lung Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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w138 human lung cells - by Bioz Stars, 2026-05
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99
ATCC human lung cells
ALDH3A1 and NQO1 as guardians of epithelial survival and barrier function upon smoke exposure (A) <t>A549</t> epithelial cell death upon 4 h of exposure to 0%–100% cigarette smoke extract in ALDH3A1 and NQO1 CRISPR-Cas9 knockout cells. Epithelial cell barrier function change in response to 0%–20% cigarette smoke extract exposure for 24 h, which was measured in real-time monitoring of electrical resistance and capacitance during and upon the establishment of epithelial monolayers using electric cell-substrate impedance sensing (ECIS) in ALDH3A1- (B) and NQO1-knockout (C) A549 cells. ∗ p value <0.05.
Human Lung Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
ATCC human egfr mutant lung adenocarcinoma cell lines
ALDH3A1 and NQO1 as guardians of epithelial survival and barrier function upon smoke exposure (A) <t>A549</t> epithelial cell death upon 4 h of exposure to 0%–100% cigarette smoke extract in ALDH3A1 and NQO1 CRISPR-Cas9 knockout cells. Epithelial cell barrier function change in response to 0%–20% cigarette smoke extract exposure for 24 h, which was measured in real-time monitoring of electrical resistance and capacitance during and upon the establishment of epithelial monolayers using electric cell-substrate impedance sensing (ECIS) in ALDH3A1- (B) and NQO1-knockout (C) A549 cells. ∗ p value <0.05.
Human Egfr Mutant Lung Adenocarcinoma Cell Lines, 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
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99
ATCC primary human lung smooth muscle cells
A <t>Human</t> <t>lung</t> <t>smooth</t> <t>muscle</t> <t>cells</t> (HLSMCs), lung fibroblasts (HLFs), and small airway epithelial cells (HSAECs) were treated with TFP at the indicated concentrations for 24 h. Human peripheral blood eosinophils and neutrophils were treated with TFP for 2 h. Cell viability was assessed by staining the cells with Annexin V (AnnV) and DRAQ7. Viable cells, AnnV − DRAQ7 − ; apoptotic cells, AnnV + DRAQ7 − ; necrotic/late apoptotic cells, AnnV + DRAQ7 + . HSAECs, n = 6 from three independent experiments; HLSMCs, eosinophils, neutrophils, n = 4 from four independent experiments; HLFs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA for HLSMCs, HLFs; Kruskal-Wallis for HSAECs; Friedman test for eosinophils, neutrophils). B – C Bone marrow-derived MCs (BMMCs) and peritoneal cell-derived MCs (PCMCs) treated under the same conditions as in ( A ) for 24 h. BMMCs, n = 5 from two independent experiments; PCMCs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA). Untreated (control) cells were used for statistical comparisons to all other groups in all figures. The bar charts show mean values + SEM or median + interquartile range. * P < 0.05; ** P < 0 .01; **** P < 0.0001. D Effect of TFP on DNA degradation. MCs were preincubated with bafilomycin A1 (Baf A1) (20 nM) for 2 h followed by treatment with TFP (10 μΜ) for 2 h. DNA was extracted from MCs and fragmentation was assessed by agarose gel electrophoresis. St standard marker.
Primary Human Lung Smooth Muscle Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC primary human lung fibroblasts hlfs
A Human lung smooth muscle cells (HLSMCs), lung <t>fibroblasts</t> <t>(HLFs),</t> and small airway epithelial cells (HSAECs) were treated with TFP at the indicated concentrations for 24 h. Human peripheral blood eosinophils and neutrophils were treated with TFP for 2 h. Cell viability was assessed by staining the cells with Annexin V (AnnV) and DRAQ7. Viable cells, AnnV − DRAQ7 − ; apoptotic cells, AnnV + DRAQ7 − ; necrotic/late apoptotic cells, AnnV + DRAQ7 + . HSAECs, n = 6 from three independent experiments; HLSMCs, eosinophils, neutrophils, n = 4 from four independent experiments; HLFs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA for HLSMCs, HLFs; Kruskal-Wallis for HSAECs; Friedman test for eosinophils, neutrophils). B – C Bone marrow-derived MCs (BMMCs) and peritoneal cell-derived MCs (PCMCs) treated under the same conditions as in ( A ) for 24 h. BMMCs, n = 5 from two independent experiments; PCMCs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA). Untreated (control) cells were used for statistical comparisons to all other groups in all figures. The bar charts show mean values + SEM or median + interquartile range. * P < 0.05; ** P < 0 .01; **** P < 0.0001. D Effect of TFP on DNA degradation. MCs were preincubated with bafilomycin A1 (Baf A1) (20 nM) for 2 h followed by treatment with TFP (10 μΜ) for 2 h. DNA was extracted from MCs and fragmentation was assessed by agarose gel electrophoresis. St standard marker.
Primary Human Lung Fibroblasts Hlfs, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Immunohistochemical analysis of SLC35D3 expression in human tumors, normal tissues, and positive-control samples. (A) SLC35D3 staining in human tumors: (a) primary colon tumor; (b) corresponding lymph-node metastasis; (c) normal adjacent tissue (NAT) of a; (d) primary rectal tumor; (e) corresponding lymph-node metastasis; (f) NAT of d; (g–h) small-cell lung carcinoma (SCLC); (i) pancreatic neuroendocrine neoplasm; (j) pancreatic islet tumor. (B) SLC35D3 staining in human normal tissues: (a) cerebrum; (b) bone marrow; (c) lung; (d) heart; (e) liver; (f) kidney; (g) eye; (h) colon; (i) adrenal gland; (j) pancreas; (k) hypophysis; (l) stomach; (m) small intestine; (n) prostate. Arrowheads indicate SLC35D3-positive cells. (C) SLC35D3 staining of negative and positive control cell lines: (a) HCT 116-mock (negative control); (b) HCT 116-hSLC35D3 (engineered overexpression); (c) NCI–H1930 (endogenously SLC35D3-expressing).

Journal: Biochemistry and Biophysics Reports

Article Title: Integrated transcriptomic and proteomic validation identifies SLC35D3 as a tumor-selective surface antigen for colorectal and neuroendocrine carcinomas

doi: 10.1016/j.bbrep.2026.102587

Figure Lengend Snippet: Immunohistochemical analysis of SLC35D3 expression in human tumors, normal tissues, and positive-control samples. (A) SLC35D3 staining in human tumors: (a) primary colon tumor; (b) corresponding lymph-node metastasis; (c) normal adjacent tissue (NAT) of a; (d) primary rectal tumor; (e) corresponding lymph-node metastasis; (f) NAT of d; (g–h) small-cell lung carcinoma (SCLC); (i) pancreatic neuroendocrine neoplasm; (j) pancreatic islet tumor. (B) SLC35D3 staining in human normal tissues: (a) cerebrum; (b) bone marrow; (c) lung; (d) heart; (e) liver; (f) kidney; (g) eye; (h) colon; (i) adrenal gland; (j) pancreas; (k) hypophysis; (l) stomach; (m) small intestine; (n) prostate. Arrowheads indicate SLC35D3-positive cells. (C) SLC35D3 staining of negative and positive control cell lines: (a) HCT 116-mock (negative control); (b) HCT 116-hSLC35D3 (engineered overexpression); (c) NCI–H1930 (endogenously SLC35D3-expressing).

Article Snippet: The human pancreatic islet cell carcinoma line QGP-1 (Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan; Cat. No. JCRB0183), human small-cell lung carcinoma line NCI–H1930 (American Type Culture Collection (ATCC), Manassas, VA, USA; Cat. No. CRL-5906), human colorectal carcinoma line LoVo (ATCC; Cat. No. CCL-229), human gastric carcinoma line SNU-16 (ATCC; Cat. No. CRL-5974), and human colorectal carcinoma line HCT 116 (ATCC; Cat. No. CCL-247) were used.

Techniques: Immunohistochemical staining, Expressing, Positive Control, Staining, Negative Control, Over Expression

Validation of cell-surface SLC35D3 expression in cancer cell lines by flow cytometry and comparison with CCLE transcriptomic data. Flow cytometry histograms of cell-surface SLC35D3 staining in human cancer cell lines (HCT 116, LoVo, QGP-1, NCI–H1930, and SNU-16). For each cell line, the MFI ratio (anti-SLC35D3/isotype) and the corresponding mRNA expression level (log2[TPM+1]) from the CCLE are indicated below the histogram. HCT 116 served as a negative control and showed minimal surface staining, consistent with a CCLE value of log2[TPM+1] = 0.0.

Journal: Biochemistry and Biophysics Reports

Article Title: Integrated transcriptomic and proteomic validation identifies SLC35D3 as a tumor-selective surface antigen for colorectal and neuroendocrine carcinomas

doi: 10.1016/j.bbrep.2026.102587

Figure Lengend Snippet: Validation of cell-surface SLC35D3 expression in cancer cell lines by flow cytometry and comparison with CCLE transcriptomic data. Flow cytometry histograms of cell-surface SLC35D3 staining in human cancer cell lines (HCT 116, LoVo, QGP-1, NCI–H1930, and SNU-16). For each cell line, the MFI ratio (anti-SLC35D3/isotype) and the corresponding mRNA expression level (log2[TPM+1]) from the CCLE are indicated below the histogram. HCT 116 served as a negative control and showed minimal surface staining, consistent with a CCLE value of log2[TPM+1] = 0.0.

Article Snippet: The human pancreatic islet cell carcinoma line QGP-1 (Japanese Collection of Research Bioresources Cell Bank, Osaka, Japan; Cat. No. JCRB0183), human small-cell lung carcinoma line NCI–H1930 (American Type Culture Collection (ATCC), Manassas, VA, USA; Cat. No. CRL-5906), human colorectal carcinoma line LoVo (ATCC; Cat. No. CCL-229), human gastric carcinoma line SNU-16 (ATCC; Cat. No. CRL-5974), and human colorectal carcinoma line HCT 116 (ATCC; Cat. No. CCL-247) were used.

Techniques: Biomarker Discovery, Expressing, Flow Cytometry, Comparison, Staining, Negative Control

ALDH3A1 and NQO1 as guardians of epithelial survival and barrier function upon smoke exposure (A) A549 epithelial cell death upon 4 h of exposure to 0%–100% cigarette smoke extract in ALDH3A1 and NQO1 CRISPR-Cas9 knockout cells. Epithelial cell barrier function change in response to 0%–20% cigarette smoke extract exposure for 24 h, which was measured in real-time monitoring of electrical resistance and capacitance during and upon the establishment of epithelial monolayers using electric cell-substrate impedance sensing (ECIS) in ALDH3A1- (B) and NQO1-knockout (C) A549 cells. ∗ p value <0.05.

Journal: iScience

Article Title: A comprehensive multi-omics and functional study of evolutionary adaptive responses to smoke

doi: 10.1016/j.isci.2026.115547

Figure Lengend Snippet: ALDH3A1 and NQO1 as guardians of epithelial survival and barrier function upon smoke exposure (A) A549 epithelial cell death upon 4 h of exposure to 0%–100% cigarette smoke extract in ALDH3A1 and NQO1 CRISPR-Cas9 knockout cells. Epithelial cell barrier function change in response to 0%–20% cigarette smoke extract exposure for 24 h, which was measured in real-time monitoring of electrical resistance and capacitance during and upon the establishment of epithelial monolayers using electric cell-substrate impedance sensing (ECIS) in ALDH3A1- (B) and NQO1-knockout (C) A549 cells. ∗ p value <0.05.

Article Snippet: For in vitro experiments human lung adenocarcinoma A549 cells were used (CCL-185, ATCC).

Techniques: CRISPR, Knock-Out, Electric Cell-substrate Impedance Sensing

A Human lung smooth muscle cells (HLSMCs), lung fibroblasts (HLFs), and small airway epithelial cells (HSAECs) were treated with TFP at the indicated concentrations for 24 h. Human peripheral blood eosinophils and neutrophils were treated with TFP for 2 h. Cell viability was assessed by staining the cells with Annexin V (AnnV) and DRAQ7. Viable cells, AnnV − DRAQ7 − ; apoptotic cells, AnnV + DRAQ7 − ; necrotic/late apoptotic cells, AnnV + DRAQ7 + . HSAECs, n = 6 from three independent experiments; HLSMCs, eosinophils, neutrophils, n = 4 from four independent experiments; HLFs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA for HLSMCs, HLFs; Kruskal-Wallis for HSAECs; Friedman test for eosinophils, neutrophils). B – C Bone marrow-derived MCs (BMMCs) and peritoneal cell-derived MCs (PCMCs) treated under the same conditions as in ( A ) for 24 h. BMMCs, n = 5 from two independent experiments; PCMCs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA). Untreated (control) cells were used for statistical comparisons to all other groups in all figures. The bar charts show mean values + SEM or median + interquartile range. * P < 0.05; ** P < 0 .01; **** P < 0.0001. D Effect of TFP on DNA degradation. MCs were preincubated with bafilomycin A1 (Baf A1) (20 nM) for 2 h followed by treatment with TFP (10 μΜ) for 2 h. DNA was extracted from MCs and fragmentation was assessed by agarose gel electrophoresis. St standard marker.

Journal: Cell Death Discovery

Article Title: Trifluoperazine causes mast cell apoptosis through a secretory granule-mediated pathway

doi: 10.1038/s41420-026-03122-x

Figure Lengend Snippet: A Human lung smooth muscle cells (HLSMCs), lung fibroblasts (HLFs), and small airway epithelial cells (HSAECs) were treated with TFP at the indicated concentrations for 24 h. Human peripheral blood eosinophils and neutrophils were treated with TFP for 2 h. Cell viability was assessed by staining the cells with Annexin V (AnnV) and DRAQ7. Viable cells, AnnV − DRAQ7 − ; apoptotic cells, AnnV + DRAQ7 − ; necrotic/late apoptotic cells, AnnV + DRAQ7 + . HSAECs, n = 6 from three independent experiments; HLSMCs, eosinophils, neutrophils, n = 4 from four independent experiments; HLFs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA for HLSMCs, HLFs; Kruskal-Wallis for HSAECs; Friedman test for eosinophils, neutrophils). B – C Bone marrow-derived MCs (BMMCs) and peritoneal cell-derived MCs (PCMCs) treated under the same conditions as in ( A ) for 24 h. BMMCs, n = 5 from two independent experiments; PCMCs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA). Untreated (control) cells were used for statistical comparisons to all other groups in all figures. The bar charts show mean values + SEM or median + interquartile range. * P < 0.05; ** P < 0 .01; **** P < 0.0001. D Effect of TFP on DNA degradation. MCs were preincubated with bafilomycin A1 (Baf A1) (20 nM) for 2 h followed by treatment with TFP (10 μΜ) for 2 h. DNA was extracted from MCs and fragmentation was assessed by agarose gel electrophoresis. St standard marker.

Article Snippet: Primary human lung fibroblasts (HLFs) (PCS-201-013) and primary human lung smooth muscle cells (HLSMCs)(PCS-130-010) were obtained from American Type Culture Collection (ATCC, Manassas, VA) and cultured following the manufacturer’s instructions.

Techniques: Staining, Derivative Assay, Control, Agarose Gel Electrophoresis, Marker

A Human lung smooth muscle cells (HLSMCs), lung fibroblasts (HLFs), and small airway epithelial cells (HSAECs) were treated with TFP at the indicated concentrations for 24 h. Human peripheral blood eosinophils and neutrophils were treated with TFP for 2 h. Cell viability was assessed by staining the cells with Annexin V (AnnV) and DRAQ7. Viable cells, AnnV − DRAQ7 − ; apoptotic cells, AnnV + DRAQ7 − ; necrotic/late apoptotic cells, AnnV + DRAQ7 + . HSAECs, n = 6 from three independent experiments; HLSMCs, eosinophils, neutrophils, n = 4 from four independent experiments; HLFs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA for HLSMCs, HLFs; Kruskal-Wallis for HSAECs; Friedman test for eosinophils, neutrophils). B – C Bone marrow-derived MCs (BMMCs) and peritoneal cell-derived MCs (PCMCs) treated under the same conditions as in ( A ) for 24 h. BMMCs, n = 5 from two independent experiments; PCMCs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA). Untreated (control) cells were used for statistical comparisons to all other groups in all figures. The bar charts show mean values + SEM or median + interquartile range. * P < 0.05; ** P < 0 .01; **** P < 0.0001. D Effect of TFP on DNA degradation. MCs were preincubated with bafilomycin A1 (Baf A1) (20 nM) for 2 h followed by treatment with TFP (10 μΜ) for 2 h. DNA was extracted from MCs and fragmentation was assessed by agarose gel electrophoresis. St standard marker.

Journal: Cell Death Discovery

Article Title: Trifluoperazine causes mast cell apoptosis through a secretory granule-mediated pathway

doi: 10.1038/s41420-026-03122-x

Figure Lengend Snippet: A Human lung smooth muscle cells (HLSMCs), lung fibroblasts (HLFs), and small airway epithelial cells (HSAECs) were treated with TFP at the indicated concentrations for 24 h. Human peripheral blood eosinophils and neutrophils were treated with TFP for 2 h. Cell viability was assessed by staining the cells with Annexin V (AnnV) and DRAQ7. Viable cells, AnnV − DRAQ7 − ; apoptotic cells, AnnV + DRAQ7 − ; necrotic/late apoptotic cells, AnnV + DRAQ7 + . HSAECs, n = 6 from three independent experiments; HLSMCs, eosinophils, neutrophils, n = 4 from four independent experiments; HLFs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA for HLSMCs, HLFs; Kruskal-Wallis for HSAECs; Friedman test for eosinophils, neutrophils). B – C Bone marrow-derived MCs (BMMCs) and peritoneal cell-derived MCs (PCMCs) treated under the same conditions as in ( A ) for 24 h. BMMCs, n = 5 from two independent experiments; PCMCs, n = 3 from one individual experiment representative of three independent experiments (One-way ANOVA). Untreated (control) cells were used for statistical comparisons to all other groups in all figures. The bar charts show mean values + SEM or median + interquartile range. * P < 0.05; ** P < 0 .01; **** P < 0.0001. D Effect of TFP on DNA degradation. MCs were preincubated with bafilomycin A1 (Baf A1) (20 nM) for 2 h followed by treatment with TFP (10 μΜ) for 2 h. DNA was extracted from MCs and fragmentation was assessed by agarose gel electrophoresis. St standard marker.

Article Snippet: Primary human lung fibroblasts (HLFs) (PCS-201-013) and primary human lung smooth muscle cells (HLSMCs)(PCS-130-010) were obtained from American Type Culture Collection (ATCC, Manassas, VA) and cultured following the manufacturer’s instructions.

Techniques: Staining, Derivative Assay, Control, Agarose Gel Electrophoresis, Marker