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human aortic endothelial cells haec  (ATCC)


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    Structured Review

    ATCC human aortic endothelial cells haec
    Human Aortic Endothelial Cells Haec, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 433 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human aortic endothelial cells haec/product/ATCC
    Average 99 stars, based on 433 article reviews
    human aortic endothelial cells haec - by Bioz Stars, 2026-05
    99/100 stars

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    ATCC primary human airway epithelial cells haecs
    Effect of targeting the GSH metabolism on TDI-HSA-treated <t>HAECs.</t> ( A – C ) Detection of cytotoxicity by CCK8 of different groups. ( D ) Measurement of the LDH release rate of different groups. ( E ) MitoSOX and MDC stained HAECs of different groups. Representative H&E-stained HAECs of different groups at 400× original magnification. ( F , G ) Analysis of oxygen consumption rate (OCR) by Seahorse assay. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. GSTO-IN-2 (20 μM), L-glutathione (1 mM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05, n = 5.
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    Effect of targeting the GSH metabolism on TDI-HSA-treated <t>HAECs.</t> ( A – C ) Detection of cytotoxicity by CCK8 of different groups. ( D ) Measurement of the LDH release rate of different groups. ( E ) MitoSOX and MDC stained HAECs of different groups. Representative H&E-stained HAECs of different groups at 400× original magnification. ( F , G ) Analysis of oxygen consumption rate (OCR) by Seahorse assay. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. GSTO-IN-2 (20 μM), L-glutathione (1 mM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05, n = 5.
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    Effect of targeting the GSH metabolism on TDI-HSA-treated <t>HAECs.</t> ( A – C ) Detection of cytotoxicity by CCK8 of different groups. ( D ) Measurement of the LDH release rate of different groups. ( E ) MitoSOX and MDC stained HAECs of different groups. Representative H&E-stained HAECs of different groups at 400× original magnification. ( F , G ) Analysis of oxygen consumption rate (OCR) by Seahorse assay. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. GSTO-IN-2 (20 μM), L-glutathione (1 mM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05, n = 5.
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    Epithelix origin haec
    Effect of targeting the GSH metabolism on TDI-HSA-treated <t>HAECs.</t> ( A – C ) Detection of cytotoxicity by CCK8 of different groups. ( D ) Measurement of the LDH release rate of different groups. ( E ) MitoSOX and MDC stained HAECs of different groups. Representative H&E-stained HAECs of different groups at 400× original magnification. ( F , G ) Analysis of oxygen consumption rate (OCR) by Seahorse assay. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. GSTO-IN-2 (20 μM), L-glutathione (1 mM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05, n = 5.
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    Effect of targeting the GSH metabolism on TDI-HSA-treated HAECs. ( A – C ) Detection of cytotoxicity by CCK8 of different groups. ( D ) Measurement of the LDH release rate of different groups. ( E ) MitoSOX and MDC stained HAECs of different groups. Representative H&E-stained HAECs of different groups at 400× original magnification. ( F , G ) Analysis of oxygen consumption rate (OCR) by Seahorse assay. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. GSTO-IN-2 (20 μM), L-glutathione (1 mM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05, n = 5.

    Journal: Antioxidants

    Article Title: Nrp1 Signaling Reprograms Glutathione Metabolism to Drive Mitochondrial Dysfunction in Severe Asthma

    doi: 10.3390/antiox15040463

    Figure Lengend Snippet: Effect of targeting the GSH metabolism on TDI-HSA-treated HAECs. ( A – C ) Detection of cytotoxicity by CCK8 of different groups. ( D ) Measurement of the LDH release rate of different groups. ( E ) MitoSOX and MDC stained HAECs of different groups. Representative H&E-stained HAECs of different groups at 400× original magnification. ( F , G ) Analysis of oxygen consumption rate (OCR) by Seahorse assay. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. GSTO-IN-2 (20 μM), L-glutathione (1 mM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05, n = 5.

    Article Snippet: Primary human airway epithelial cells (HAECs) were obtained from ATCC.

    Techniques: Staining, Expressing, Permeability, Control

    TDI inhibits SLC25A39 to induce GSH transport and mitochondrial dysfunction. ( A ) Volcano plot of untargeted metabolomics of the mitochondria extracted from healthy and TDI-exposed mice. ( B ) Heat map analysis of oxidized glutathione, glutathione, glutamate, and L-glutamic acid of untargeted metabolomics. ( C ) Construction diagram of the SLC25A39 overexpression plasmid. Asterisk (*) indicates a restriction enzyme site that can be recognized and cleaved by both BspDI and ClaI. ( D ) Measurement of mitochondrial GSH. ( E ) qPCR analysis of the mRNA expression of SLC25A39 in the HAECs. ( F ) Measurement of LDH release rate in the HAECs. ( G ) Detection of cytotoxicity by CCK8 of different groups. ( H ) MDC and MitoSox stained HAECs of different groups. PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05.

    Journal: Antioxidants

    Article Title: Nrp1 Signaling Reprograms Glutathione Metabolism to Drive Mitochondrial Dysfunction in Severe Asthma

    doi: 10.3390/antiox15040463

    Figure Lengend Snippet: TDI inhibits SLC25A39 to induce GSH transport and mitochondrial dysfunction. ( A ) Volcano plot of untargeted metabolomics of the mitochondria extracted from healthy and TDI-exposed mice. ( B ) Heat map analysis of oxidized glutathione, glutathione, glutamate, and L-glutamic acid of untargeted metabolomics. ( C ) Construction diagram of the SLC25A39 overexpression plasmid. Asterisk (*) indicates a restriction enzyme site that can be recognized and cleaved by both BspDI and ClaI. ( D ) Measurement of mitochondrial GSH. ( E ) qPCR analysis of the mRNA expression of SLC25A39 in the HAECs. ( F ) Measurement of LDH release rate in the HAECs. ( G ) Detection of cytotoxicity by CCK8 of different groups. ( H ) MDC and MitoSox stained HAECs of different groups. PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05.

    Article Snippet: Primary human airway epithelial cells (HAECs) were obtained from ATCC.

    Techniques: Over Expression, Plasmid Preparation, Expressing, Staining, Control

    Effects of targeting the b1 domain of Nrp1 on TDI-HSA-treated primary human airway epithelial cells. ( A , B ) Detection of cytotoxicity by CCK8 of different groups. ( C ) Measurement of the LDH release rate of different groups. ( D ) MitoSOX and MDC stained primary human airway epithelial cells (HAECs) of different groups. ( E , F ) Analysis of OCR by Seahorse assay. ( G ) Representative H&E-stained HAECs of different groups at 400× original magnification. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. EG00229 (5 μM), olopatadine (0.1 mM), dabrafenib (0.5 μM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05.

    Journal: Antioxidants

    Article Title: Nrp1 Signaling Reprograms Glutathione Metabolism to Drive Mitochondrial Dysfunction in Severe Asthma

    doi: 10.3390/antiox15040463

    Figure Lengend Snippet: Effects of targeting the b1 domain of Nrp1 on TDI-HSA-treated primary human airway epithelial cells. ( A , B ) Detection of cytotoxicity by CCK8 of different groups. ( C ) Measurement of the LDH release rate of different groups. ( D ) MitoSOX and MDC stained primary human airway epithelial cells (HAECs) of different groups. ( E , F ) Analysis of OCR by Seahorse assay. ( G ) Representative H&E-stained HAECs of different groups at 400× original magnification. ( H , I ) qPCR analysis of the mRNA expression of TSLP, IL-25, IL-33, E-cadherin, ZO-1 and occludin of the HAECs. ( J ) Relative permeability of HAECs detected by FITC-dextran. EG00229 (5 μM), olopatadine (0.1 mM), dabrafenib (0.5 μM). PBS was used as the vehicle (control). * p < 0.05, ** p < 0.005, *** p < 0.0005, ns > 0.05.

    Article Snippet: Primary human airway epithelial cells (HAECs) were obtained from ATCC.

    Techniques: Staining, Expressing, Permeability, Control