EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #05001_C
在气液界面培养的人气道上皮细胞的无血清和无bpe培养基
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专为您的实验方案打造的产品
要查看实验方案所需的所有配套产品，请参阅《实验方案与技术文档》。
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PneumaCult™-Ex Plus MediumSerum- and BPE-free medium for expansion of primary human airway epithelial cells
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Animal Component-Free Cell Dissociation KitDissociation kit for human stem and progenitor cells
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Hydrocortisone Stock SolutionCell culture supplement
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Heparin SolutionCell culture supplement
总览
PneumaCult™-ALI Medium（目录#05001）是一种不含血清和bpe的培养基，用于在气液界面（ALI）培养人气道上皮细胞。在PneumaCult™-ALI培养基中培养的气道上皮细胞经过广泛的粘膜纤毛分化形成假层状上皮，其形态和功能特征与体内的人类气道相似。PneumaCult™-ALI Medium也可在工具包中使用，包括12毫米Transwell®插入件（目录#05021）或6.5毫米Transwell®插入件（目录#05022）。
一起，PneumaCult™-ALI Medium和PneumaCult™-Ex Plus Medium（目录#05040）构成了一个完全集成的无bpe培养系统，用于体外人气道建模，也与原代人鼻上皮细胞兼容。这一强大而明确的系统是基础呼吸研究、毒性研究和药物开发的宝贵工具。
了解如何培养人类气道上皮细胞在我们的ALI按需肺课程或浏览我们的常见问题（FAQs）关于使用PneumaCult™的ALI培养工作流程。
Subtype
Specialized Media
Cell Type
Airway Cells
Species
Human
Application
Cell Culture, Differentiation, Maintenance, Organoid Culture
Brand
PneumaCult
Area of Interest
Disease Modeling, Drug Discovery and Toxicity Testing, Epithelial Cell Biology
Formulation Category
Serum-Free
实验数据
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (23)
文献 (98)
Choice of Differentiation Media Significantly Impacts Cell Lineage and Response to CFTR Modulators in Fully Differentiated Primary Cultures of Cystic Fibrosis Human Airway Epithelial Cells. Cells 2020 sep
Abstract
In vitro cultures of primary human airway epithelial cells (hAECs) grown at air-liquid interface have become a valuable tool to study airway biology under normal and pathologic conditions, and for drug discovery in lung diseases such as cystic fibrosis (CF). An increasing number of different differentiation media, are now available, making comparison of data between studies difficult. Here, we investigated the impact of two common differentiation media on phenotypic, transcriptomic, and physiological features of CF and non-CF epithelia. Cellular architecture and density were strongly impacted by the choice of medium. RNA-sequencing revealed a shift in airway cell lineage; one medium promoting differentiation into club and goblet cells whilst the other enriched the growth of ionocytes and multiciliated cells. Pathway analysis identified differential expression of genes involved in ion and fluid transport. Physiological assays (intracellular/extracellular pH, Ussing chamber) specifically showed that ATP12A and CFTR function were altered, impacting pH and transepithelial ion transport in CF hAECs. Importantly, the two media differentially affected functional responses to CFTR modulators. We argue that the effect of growth conditions should be appropriately determined depending on the scientific question and that our study can act as a guide for choosing the optimal growth medium for specific applications.
Glutaredoxin deficiency promotes activation of the transforming growth factor beta pathway in airway epithelial cells, in association with fibrotic airway remodeling. Redox biology 2020 sep
Abstract
S-glutathionylation of reactive protein cysteines is a post-translational event that plays a critical role in transducing signals from oxidants into biological responses. S-glutathionylation can be reversed by the deglutathionylating enzyme glutaredoxin (GLRX). We have previously demonstrated that ablation of Glrx sensitizes mice to the development of parenchymal lung fibrosis(1). It remains unclear whether GLRX also controls airway fibrosis, a clinical feature relevant to asthma and chronic obstructive pulmonary disease, and whether GLRX controls the biology of airway epithelial cells, which have been implicated in the pathophysiology of these diseases. In the present study we utilized a house dust mite (HDM) model of allergic airway disease in wild type (WT) and Glrx-/- mice on a C57BL/6 background prone to develop airway fibrosis, and tracheal basal stem cells derived from WT mice, global Glrx-/- mice, or bi-transgenic mice allowing conditional ablation of the Glrx gene. Herein we show that absence of Glrx led to enhanced HDM-induced collagen deposition, elevated levels of transforming growth factor beta 1 (TGFB1) in the bronchoalveolar lavage, and resulted in increases in airway hyperresponsiveness. Airway epithelial cells isolated from Glrx-/- mice or following conditional ablation of Glrx showed spontaneous increases in secretion of TGFB1. Glrx-/- basal cells also showed spontaneous TGFB pathway activation, in association with increased expression of mesenchymal genes, including collagen 1a1 and fibronectin. Overall, these findings suggest that GLRX regulates airway fibrosis via a mechanism(s) that involve the plasticity of basal cells, the stem cells of the airways.
Functional rescue of c.3846G\textgreaterA (W1282X) in patient-derived nasal cultures achieved by inhibition of nonsense mediated decay and protein modulators with complementary mechanisms of action. Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society 2020 sep
Abstract
BACKGROUND The nonsense mutation, c.3846G{\textgreater}A (aka: W1282X-CFTR) leads to a truncated transcript that is susceptible to nonsense-mediated decay (NMD) and produces a shorter protein that is unstable and lacks normal channel activity in patient-derived tissues. However, if overexpressed in a heterologous expression system, the truncated mutant protein has been shown to mediate CFTR channel function following the addition of potentiators. In this study, we asked if a quadruple combination of small molecules that together inhibit nonsense mediated decay, stabilize both halves of the mutant protein and potentiate CFTR channel activity could rescue the functional expression of W1282X-CFTR in patient derived nasal cultures. METHODS We identified the CFTR domains stabilized by corrector compounds supplied from AbbVie using a fragment based, biochemical approach. Rescue of the channel function of W1282X.-CFTR protein by NMD inhibition and small molecule protein modulators was studied using a bronchial cell line engineered to express W1282X and in primary nasal epithelial cultures derived from four patients homozygous for this mutation. RESULTS We confirmed previous studies showing that inhibition of NMD using the inhibitor: SMG1i, led to an increased abundance of the shorter transcript in a bronchial cell line. Interestingly, on top of SMG1i, treatment with a combination of two new correctors developed by Galapagos/AbbVie (AC1 and AC2-2, separately targeting either the first or second half of CFTR and promoting assembly, significantly increased the potentiated channel activity by the mutant in the bronchial epithelial cell line and in patient-derived nasal epithelial cultures. The average rescue effect in primary cultures was approximately 50{\%} of the regulated chloride conductance measured in non-CF cultures. CONCLUSIONS These studies provide the first in-vitro evidence in patient derived airway cultures that the functional defects incurred by W1282X, has the potential to be effectively repaired pharmacologically.
更多信息
| 种属 | Human |
|---|---|
| 配方类别 | Serum-Free |
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