RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia
| العنوان: | RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia |
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| المؤلفون: | Yohannes Tesfaigzi, Mauricio Rojas, Jonathan K. Alder, Chunbin Zou, Hannah Voic, Xiuying Li, Divay Chandra, Scott H. Randell, Rama K. Mallampalli, Prithu Sundd, Tyrone Ryba, Jun Ho Jang, Toru Nyunoya |
| المصدر: | BMC Genomics, Vol 20, Iss 1, Pp 1-12 (2019) BMC Genomics |
| بيانات النشر: | BMC, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | 0106 biological sciences, Senescence, lcsh:QH426-470, Cell Survival, lcsh:Biotechnology, Primary Cell Culture, RNA-Seq, Bronchi, Biology, 01 natural sciences, Cigarette Smoking, Transcriptome, 03 medical and health sciences, lcsh:TP248.13-248.65, Gene expression, Genetics, Humans, Gene, Cellular Senescence, 030304 developmental biology, chemistry.chemical_classification, 0303 health sciences, Reactive oxygen species, Sequence Analysis, RNA, NF-kappa B, RNA, Cigarette smoke, Epithelial Cells, NFKB1, 3. Good health, Cell biology, lcsh:Genetics, Primary human bronchial epithelial cells, chemistry, Gene Expression Regulation, Replicative senescence, RNA-seq, Reactive Oxygen Species, 010606 plant biology & botany, Biotechnology, Research Article, Signal Transduction |
| الوصف: | Background Aging is affected by genetic and environmental factors, and cigarette smoking is strongly associated with accumulation of senescent cells. In this study, we wanted to identify genes that may potentially be beneficial for cell survival in response to cigarette smoke and thereby may contribute to development of cellular senescence. Results Primary human bronchial epithelial cells from five healthy donors were cultured, treated with or without 1.5% cigarette smoke extract (CSE) for 24 h or were passaged into replicative senescence. Transcriptome changes were monitored using RNA-seq in CSE and non-CSE exposed cells and those passaged into replicative senescence. We found that, among 1534 genes differentially regulated during senescence and 599 after CSE exposure, 243 were altered in both conditions, representing strong enrichment. Pathways and gene sets overrepresented in both conditions belonged to cellular processes that regulate reactive oxygen species, proteasome degradation, and NF-κB signaling. Conclusions Our results offer insights into gene expression responses during cellular aging and cigarette smoke exposure, and identify potential molecular pathways that are altered by cigarette smoke and may also promote airway epithelial cell senescence. Electronic supplementary material The online version of this article (10.1186/s12864-018-5409-z) contains supplementary material, which is available to authorized users. |
| اللغة: | English |
| تدمد: | 1471-2164 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ee094585b2db1783369b9eb796cbdc31Test http://link.springer.com/article/10.1186/s12864-018-5409-zTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....ee094585b2db1783369b9eb796cbdc31 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14712164 |
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