EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #05008_C
无血清和无bpe培养基用于原代人气道上皮细胞的扩增
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总览
PneumaCult™- Ex是一款成份明确的，不含血清和BPE的细胞培养基，支持人呼吸道上皮细胞的快速扩增。使用PneumaCult™-Ex培养的原代呼吸道上皮细胞在至少3代内迅速扩增，同时保持鹅卵石状形态和基底细胞标记物p63和p75NTR的均匀表达。此外，这些细胞在 PneumaCult™-ALI 的气-液界面条件下可进一步分化，形成具黏液纤毛特征的假复层上皮结构。
PneumaCult™-ALI Medium和PneumaCult™-Ex Plus Medium（产品号：#05040）构成了一个完整、无BPE的人源呼吸道上皮体外建模系统，也与原代人鼻上皮细胞兼容。这一稳定、定义明确的培养系统是开展基础呼吸研究、毒理学研究和药物开发的宝贵工具。
欢迎观看我们的肺部研究课程，了解如何在 ALI 条件下培养人呼吸道上皮细胞，或浏览我们的常见问题解答（FAQs）关于使用PneumaCult™的ALI培养工作流程。
分类
专用培养基
细胞类型
气道细胞
种属
人
应用
细胞培养，扩增，培养
品牌
PneumaCult
研究领域
上皮细胞研究
制剂类别
无血清
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 (11)
文献 (14)
Impact of KLF4 on Cell Proliferation and Epithelial Differentiation in the Context of Cystic Fibrosis. International journal of molecular sciences 2020 sep
Abstract
Cystic fibrosis (CF) cells display a more cancer-like phenotype vs. non-CF cells. KLF4 overexpression has been described in CF and this transcriptional factor acts as a negative regulator of wt-CFTR. KLF4 is described as exerting its effects in a cell-context-dependent fashion, but it is generally considered a major regulator of proliferation, differentiation, and wound healing, all the processes that are also altered in CF. Therefore, it is relevant to characterize the differential role of KLF4 in these processes in CF vs. non-CF cells. To this end, we used wt- and F508del-CFTR CFBE cells and their respective KLF4 knockout (KO) counterparts to evaluate processes like cell proliferation, polarization, and wound healing, as well as to compare the expression of several epithelial differentiation markers. Our data indicate no major impact of KLF4 KO in proliferation and a differential impact of KLF4 KO in transepithelial electrical resistance (TEER) acquisition and wound healing in wt- vs. F508del-CFTR cells. In parallel, we also observed a differential impact on the levels of some differentiation markers and epithelial-mesencymal transition (EMT)-associated transcription factors. In conclusion, KLF4 impacts TEER acquisition, wound healing, and the expression of differentiation markers in a way that is partially dependent on the CFTR-status of the cell.
Aprotinin Inhibits SARS-CoV-2 Replication. Cells 2020 oct
Abstract
Severe acute respiratory syndrome virus 2 (SARS-CoV-2) is the cause of the current coronavirus disease 19 (COVID-19) pandemic. Protease inhibitors are under consideration as virus entry inhibitors that prevent the cleavage of the coronavirus spike (S) protein by cellular proteases. Herein, we showed that the protease inhibitor aprotinin (but not the protease inhibitor SERPINA1/alpha-1 antitrypsin) inhibited SARS-CoV-2 replication in therapeutically achievable concentrations. An analysis of proteomics and translatome data indicated that SARS-CoV-2 replication is associated with a downregulation of host cell protease inhibitors. Hence, aprotinin may compensate for downregulated host cell proteases during later virus replication cycles. Aprotinin displayed anti-SARS-CoV-2 activity in different cell types (Caco2, Calu-3, and primary bronchial epithelial cell air-liquid interface cultures) and against four virus isolates. In conclusion, therapeutic aprotinin concentrations exert anti-SARS-CoV-2 activity. An approved aprotinin aerosol may have potential for the early local control of SARS-CoV-2 replication and the prevention of COVID-19 progression to a severe, systemic disease.
Loss of versican and production of hyaluronan in lung epithelial cells are associated with airway inflammation during RSV infection. The Journal of biological chemistry 2020 nov
Abstract
Airway inflammation is a critical feature of lower respiratory tract infections caused by viruses such as respiratory syncytial virus (RSV). A growing body of literature has demonstrated the importance of extracellular matrix (ECM) changes such as the accumulation of hyaluronan (HA) and versican in the subepithelial space in promoting airway inflammation; however, whether these factors contribute to airway inflammation during RSV infection remains unknown. To test the hypothesis that RSV infection promotes inflammation via altered HA and versican production, we studied an ex vivo human bronchial epithelial cell (BEC)/human lung fibroblast (HLF) co-culture model. RSV infection of BEC/HLF co-cultures led to decreased hyaluronidase expression by HLFs, increased accumulation of HA, and enhanced adhesion of U937 cells as would be expected with increased HA. HLF production of versican was not altered following RSV infection; however, BEC production of versican was significantly downregulated following RSV infection. In vivo studies with epithelial-specific versican-deficient mice [SPC-Cre(+) Vcan-/-] demonstrated that RSV infection led to increased HA accumulation compared to control mice which also coincided with decreased hyaluronidase expression in the lung. SPC-Cre(+) Vcan-/- mice demonstrated enhanced recruitment of monocytes and neutrophils in bronchoalveolar lavage fluid and increased neutrophils in the lung compared to SPC-Cre(-) RSV-infected littermates. Taken together, these data demonstrate that altered ECM accumulation of HA occurs following RSV infection and may contribute to airway inflammation. Additionally, loss of epithelial expression of versican promotes airway inflammation during RSV infection further demonstrating that versican's role in inflammatory regulation is complex and dependent on the microenvironment.
更多信息
| 种属 | Human |
|---|---|
| 配方类别 | Serum-Free |
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