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    The Effects of Lung Ischaemia/Reperfusion on TRPM Gene Expression
    (Univ West Indies Faculty Medical Sciences, 2021) Atabay, H. D.; Demir, T.; Dokuyucu, Recep; Yumrutas, O.; Oztuzcu, S.; Ceribasi, A. O.; Bayraktar, R.
    Objective: Transient receptor potential melastatin (TRPM) are integral membrane proteins that have broad range of cellular functions. Roles of TRPM2, TRPM3, TRPM4 and TRPM7 among these channels are very important, and their roles in lung ischaemia/reperfusion injury have not been evaluated yet. The aim of this study is to investigate the contribution of these genes in lung ischaemia/reperfusion injury and evaluate histopathology of tissues. Methods: A total of 40 Wistar albino rats were enrolled for the study. Ischaemia was performed by the application of an atramvatic clamp to pulmonary artery. Gene expressions were determined by the semi-quantitative reverse transcription-polymerase chain reaction method. Histopatholical evaluations were held by a standard haematoxyline-eosin staining. Results: The major histopathological tissue damage was observed in ischaemia performed groups, and expression of TRPM channels was found to be obviously downregulated. Substantial changes were determined between TRPM2, TRPM3, TRPM4 and TRPM7 and lung ischaemia/reperfusion injury. In particular; expression of TRPM2 and TRPM7 was reversibly downregulated in ischaemia. Yet, the expression of TRPM3 and TRPM4 was irreversibly downregulated after ischaemia. Conclusion: Consequently, these results indicate that TRPM family of cation channels may have significant roles in the lung ischaemia/reperfusion injury.
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    The role of bronchial epithelial cell apoptosis in the pathogenesis of COPD
    (Springer, 2014) Gogebakan, B.; Bayraktar, R.; Ulasli, M.; Oztuzcu, S.; Tasdemir, D.; Bayram, H.
    There is an increased airway inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD), and it has been suggested that there may also be problem in the apoptosis and renewal of cells. However, there are limited human airway cell studies, in particular those from larger airways such as bronchi. We cultured primary human bronchial epithelial cells (HBECs) from bronchial explants of smokers (n = 6) without COPD and smokers with COPD (n = 8). Apoptosis was studied by fluorescence activated cell sorting. qRT-PCR was used to assess mRNA expression for proteins involving apoptosis including p21(CIP1/WAF1), p53, caspase-8 and caspase-9. Although there was no difference in the rate of viable cells between cells from smokers and COPDs, the level of early apoptotic cells was significantly increased in COPD cells [mean +/- A standard error of mean (SEM) = 4.86 +/- A 3.2 %, p = 0.015] as compared to smokers (mean +/- A SEM = 2.71 +/- A 1.62 %). In contrast, the rate of late apoptotic cells was significantly decreased in COPD cells (mean +/- A SEM = 9.82 +/- A 5.71 %) comparing to smokers (mean +/- A SEM = 15.21 +/- A 5.08 %, p = 0.003). Although expression of mRNA for p21(CIP1/WAF1) and caspase-9 was similar in both groups, p53 and caspase-8 mRNA expression was significantly greater in COPD cells. These findings suggest that HBEC apoptosis is increased in COPD, and that this involves p53 and caspase-8 pathways.