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HBE1Human Bronchial Epithelial Cells
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Schamberger et al .[22] studied CSE-induced primary human bronchial epithelial cell (PHBEC) transformation and discovered that smoke exposure led to a decrease in the number of ciliated cells, while the number of Clara and goblet cells increased.
Human bronchial epithelial cells (HBECs; ATCC) were cultured in 2 ml of DMEM containing 10% FBS and penicillin (100U/ml) at a density of 5-6 x [10.sup.5] cells per 6-well plate.
Transcriptome sequencing reveals e-cigarette vapor and mainstream-smoke from tobacco cigarettes activate different gene expression profiles in human bronchial epithelial cells. Sci Rep.
Culturing primary human bronchial epithelial cells at the air-liquid interface using current methods often results in unsatisfactory and inconsistent differentiation, according to the company.
Studies of human bronchial epithelial cells suggest that insulin-receptor activation is in itself insufficient for malignant transformation.
Human bronchial epithelial cells transformed by v-K-ras form poorly differentiated adenocarcinomas in athymic nude mice (24).
Other research reports indicate that cigarette smoking can induce STAT3 activation and inflammation in human bronchial epithelial cells (Liu, 2007).
Our previous study demonstrated that the CSE could induce cellular senescence in human bronchial epithelial cells, and the ROS/PI3K/AKT/mTOR signaling pathway may play an important role in this process [5].
Human bronchial epithelial cells are able to recognize Gram-positive and Gram-negative bacteria through different pattern recognition receptors (PRRs) [22], so we first evaluated the expression of Mtb recognizing PRRs such as TLR-2, MR, CD11b, and CD54 in 18 h-cultured uninfected and Mtb-infected Calu-6.
Either primary normal human bronchial epithelial cells (NHBEC, Lonza, Walkersville, MD) or an immortalized line of human bronchial epithelial cells, 16HBE (kindly provided by Dr.
Consistent with this supposition, our previous studies support a paracrine-dominant mechanism for IL-6 signaling mediated by lung fibroblasts that increases the risk of malignant transformation in human bronchial epithelial cells (Chen et al.
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