cell cycle assays 204 human dermal fibroblasts Search Results


93
ATCC ccd16lu normal human lung stromal cells
The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged <t>CCD16Lu</t> normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.
Ccd16lu Normal Human Lung Stromal Cells, 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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Miltenyi Biotec differentiation hipsc
The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged <t>CCD16Lu</t> normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.
Differentiation Hipsc, supplied by Miltenyi Biotec, 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 cell cycle assays 204 human dermal fibroblasts
The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged <t>CCD16Lu</t> normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.
Cell Cycle Assays 204 Human Dermal Fibroblasts, 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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94
ATCC ccd 1090sk
The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged <t>CCD16Lu</t> normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.
Ccd 1090sk, 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
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Lonza primary diseased human lung fibroblasts, idiopathic pulmonary fibrosis
The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged <t>CCD16Lu</t> normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.
Primary Diseased Human Lung Fibroblasts, Idiopathic Pulmonary Fibrosis, supplied by Lonza, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
R&D Systems cocktail recombinant murine il 4
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
Cocktail Recombinant Murine Il 4, supplied by R&D Systems, 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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Biotium calgranulin b / mrp-8/-14 / mac 387 / s100a8/a9 / macrophage ag(mac387)
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
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PeproTech human recombinant stem cell factor (scf)
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
Human Recombinant Stem Cell Factor (Scf), supplied by PeproTech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Mirus Bio transit lt1 transfection reagent
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
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MACHEREY NAGEL precipitation solution
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
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Mirus Bio transit x2 transfection reagent
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
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Miltenyi Biotec fgf
Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic <t>cytokines</t> <t>IL-4,</t> IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.
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Image Search Results


The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged CCD16Lu normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.

Journal: Cancer

Article Title: Targeting Burkitt lymphoma with a tumor cell–specific heptamethine carbocyanine‐cisplatin conjugate

doi: 10.1002/cncr.32033

Figure Lengend Snippet: The heptamethine carbocyanine fluorescent dye–cisplatin conjugate (DZ‐CIS) acts specifically on Burkitt lymphoma cells. (A) Near‐infrared (NIR) microscopy of Namalwa cells after treatment with 4 μM DZ‐CIS for 15 minutes. DZ‐CIS accumulated in all lymphoma cells. Blue fluorescence of the nuclei was from Hoechst 33342 co‐stain (200×). (B) Namalwa cells treated with 4 μM DZ‐CIS for 15 minutes were assayed for rapid uptake of the fluorescent dye–drug conjugate in live cells using flow cytometry. (C) Images of lymphoma and stromal cell coculture show that DZ‐CIS preferentially kills lymphoma but not stromal cells. In coculture with GFP‐tagged CCD16Lu normal human lung mesenchymal stromal cells, 24‐hour DZ‐CIS treatment preferentially killed Burkitt lymphoma cells (Namalwa), while stromal cells survived and displayed healthy morphology (magnification ×200). DZ‐CIS–induced death of lymphoma cells in coculture was confirmed with trypan blue stain. (D) Tumor‐specific uptake and retention of DZ‐CIS in vivo were evaluated with NCr nu/nu mice bearing Namalwa xenograft tumors. After treatment with DZ‐CIS for 2 weeks, mice were subjected to whole body NIR imaging (left). Necropsy tumor samples together with host organs were subjected to ex vivo NIR imaging (right). (E) Frozen sections of xenograft tumors were stained with 4’,6‐diamidino‐2‐phenyindole dihydrochloride (DAPI) and examined for retention of DZ‐CIS by NIR microscopy (magnification ×100). (F) Xenograft tumors diced in ex vivo culture were stained with DAPI (magnification ×100). Most tumor cells still carried DZ‐CIS signals after 3 days in the culture.

Article Snippet: CCD16Lu normal human lung stromal cells obtained from American Type Culture Collection were established by previously described protocols.

Techniques: Microscopy, Fluorescence, Staining, Flow Cytometry, In Vivo, Imaging, Ex Vivo

Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic cytokines IL-4, IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.

Journal: Mucosal immunology

Article Title: Group 2 innate lymphoid cells (ILC2) are regulated by stem cell factor during chronic asthmatic disease

doi: 10.1038/s41385-018-0117-1

Figure Lengend Snippet: Fibrotic phenotype in the lung of the α-SCF248 treated mice was reduced as observed by A) qPCR in lung tissue to measure expression of remodeling genes fibronectin and collagen 3a1. B) Fibroblasts grown from lungs of allergic antibody treated mice cultured at baseline C) or stimulated by profibrotic cytokines IL-4, IL-13, TNFa, and TGFb1 The cytokine stimulated fibroblasts are calculated by the fold increased expression of Col3a1 over the baseline measurement. D) The expression of the differential mRNA expression of SCF220 and SCF248 isoforms in the lungs of naїve and chronic allergen (CRA) challenge animals. E) Activation of lung fibroblasts by profibrotic cytokines promote SCF248 expression but not SCF220. Data represent mean ± SE from 5 mice/group. All data are representative of two to three independent experiments. *P<0.05, **P<0.01, ***P<0.001.

Article Snippet: Lung fibroblasts were restimulated with a cocktail recombinant murine IL-4 (10 ng/ ml;R&D Systems, Minneapolis, USA), recombinant murine IL-13 (10 ng/ml;R&D Systems, Minneapolis, USA), recombinant murine TNFa (5 ng/ml;R&D Systems, Minneapolis, USA) and recombinant human TGFb (10 ng/ml;R&D Systems, Minneapolis, USA) for 24 h for gene expression analysis.

Techniques: Expressing, Cell Culture, Activation Assay

SCF receptor mutant W/W v mice demonstrated the important role of the SCF-c-Kit activation during chronic allergic diseases. The lack of c-Kit signaling reduces the allergen-induced A) airway inflammation and mucus deposition in airway by histopathology, PAS staining B) qPCR of mucus-related genes Muc5 and Gob5, C) qPCR of lung cytokines IL-4 and IL-13 expression, D) decreased numbers of Mast cells, Eosinophils and ILC2 in the lung. Data represent mean ± SE from each group with 4 to 5 mice/group. All data are representative of two independent experiments. *P<0.05, **P<0.01, ***P<0.001

Journal: Mucosal immunology

Article Title: Group 2 innate lymphoid cells (ILC2) are regulated by stem cell factor during chronic asthmatic disease

doi: 10.1038/s41385-018-0117-1

Figure Lengend Snippet: SCF receptor mutant W/W v mice demonstrated the important role of the SCF-c-Kit activation during chronic allergic diseases. The lack of c-Kit signaling reduces the allergen-induced A) airway inflammation and mucus deposition in airway by histopathology, PAS staining B) qPCR of mucus-related genes Muc5 and Gob5, C) qPCR of lung cytokines IL-4 and IL-13 expression, D) decreased numbers of Mast cells, Eosinophils and ILC2 in the lung. Data represent mean ± SE from each group with 4 to 5 mice/group. All data are representative of two independent experiments. *P<0.05, **P<0.01, ***P<0.001

Article Snippet: Lung fibroblasts were restimulated with a cocktail recombinant murine IL-4 (10 ng/ ml;R&D Systems, Minneapolis, USA), recombinant murine IL-13 (10 ng/ml;R&D Systems, Minneapolis, USA), recombinant murine TNFa (5 ng/ml;R&D Systems, Minneapolis, USA) and recombinant human TGFb (10 ng/ml;R&D Systems, Minneapolis, USA) for 24 h for gene expression analysis.

Techniques: Mutagenesis, Activation Assay, Histopathology, Staining, Expressing