surgical-models-of-gastroesophageal-reflux-with-mice

Surgical Models of Gastroesophageal Reflux with Mice

Multiple surgical procedures have been reported to induce gastroesophageal reflux in animals. Herein, we report three surgical models with mice aiming to ...

Ningxia Medical University General Hospital

North Carolina Central University

Lung is a complex organ lined with epithelial cells. In order to maintain its homeostasis and normal functions following injuries caused by varied extraneous and intraneous insults, such as inhaled environmental pollutants and overwhelming inflammatory responses, the respiratory epithelium normally undergoes regenerations by the proliferation and differentiation of region-specific epithelial stem/progenitor cells that resided in distinct niches along the airway tree. The importance of local epithelial stem cell niches in the specification of lung stem/progenitor cells has been recently identified. Studies using cell differentiating and lineage tracing assays, in vitro and/or ex vivo models, and genetically engineered mice have suggested that these local epithelial stem/progenitor cells within spatially distinct regions along the pulmonary tree contribute to the injury repair of epithelium adjacent to their respective niches. This paper reviews recent findings in the identification and isolation of region-specific epithelial stem/progenitor cells and local niches along the airway tree and the potential link of epithelial stem cells for the development of lung cancer.

Diversity of epithelial stem cell types in adult lung.

Objective To investigate the expression and biological significance of acetaldehyde dehydrogenase (ALDH) in cisplatin-resistant human A549/DDP lung adenocarcinoma cell line. Methods The expressions of biomarkers of cancer stem cells (CSCs) including CD44, CD73, CD90, CD105, epithelial cell adhesion molecule (EpCAM), ATP-binding cassette sub-family G member 2 (ABCG2) and ALDH in human lung adenocarcinoma A549 cells and cisplatin-resistant A549/DDP cells were ascertained by flow cytometry. The proliferation and sensitivity of A549/DDP cells to cisplatin were evaluated by MTT assay before and after ALDH inhibitor diethylaminobenzaldehyde (DEAB) treatment. The differential expression of ALDH subtypes in cells was determined by real-time quantitative PCR, and was further confirmed by a Western blotting. Results The frequencies of ABCG2 and ALDH positive cells were higher in cisplatin-resistant A549/DDP cells than those in A549 cells, in particular the expression of ALDH which was 97.7% in A549/DDP cells, and only 4.3% in A549 cells. There was no significantly differential expression of CD44, CD90, CD73, CD105 between A549/DDP cells and A549 cells, whereas less EpCAM was found in A549/DDP cells compared with A549 cells. Importantly, the ALDH inhibitor DEAB (100 μmol/L) was able to significantly reduce cisplatin resistance in A549/DDP cells. Compared with A549 cells, the expressions of ALDH subtypes ALDH1A3 and ALDH1B1 mRNA significantly went up in A549/DDP cells. Interestedly, Western blotting revealed that ALDH1B1 protein expression was elevated but ALDH1A3 protein was reduced in A549/DDP cells in comparison with A549 cells. Conclusion ALDH can serve as a useful surface marker for cisplatin-resistant human lung adenocarcinoma cells.ALDH1B1 may play a role in the chemoresistance of these cells. Therefore, ALDH1B1 may be an important target for developing novel therapeutic agents and strategies for patients with cisplatin-resistant lung adenocarcinoma.

[Increased expression of acetaldehyde dehydrogenase in cisplatin-resistant human lung adenocarcinoma A549/DDP cells].

Lung cancer is a leading cause of cancer mortality worldwide. Several molecular pathways underlying mechanisms of this disease have been partly elucidated, among which the epidermal growth factor receptor (EGFR) pathway is one of the well-known signaling cascades that plays a critical role in tumorigenesis. Dysregulation of the EGFR signaling is frequently found in lung cancer. The strategies to effectively inhibit EGFR signaling pathway have been mounted for developing anticancer therapeutic agents. However, most anti-EGFR-targeted agents fail to repress cancer progression because of developing drug-resistance. Therefore, studies of the mechanisms underpinning the resistance toward anti-EGFR agents may provide important findings for lung cancer treatment using anti-EGFR therapies. Recently, increasing numbers of miRNAs are correlated with the drug resistance of lung cancer cells to anti-EGFR agents, indicating that miRNAs may serve as novel targets and/or promising predictive biomarkers for anti-EGFR therapy. In this paper, we summarize the emerging role of miRNAs as regulators to modulate the EGFR signaling and the resistance of lung cancer cells to anti-EGFR therapy. We also highlight the evidence supporting the use of miRNAs as biomarkers for response to anti-EGFR agents and as novel therapeutic targets to circumvent the resistance of lung cancer cells to EGFR inhibitors.

Jinxi He

Department of Thoracic Surgery

Ningxia Medical University General Hospital

Surgical Models of Gastroesophageal Reflux with Mice

Jinxi He

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Thoracic Surgery

Ningxia Medical University General Hospital

Surgical Models of Gastroesophageal Reflux with Mice

Department of Thoracic Surgery