Characterization of emilin-2 in lung injury and regenerationusing single-cell transcriptomics
Başlık çevirisi mevcut değil.
- Tez No: 720972
- Danışmanlar: DR. HERBERT SCHİLLER
- Tez Türü: Yüksek Lisans
- Konular: Biyoloji, Biology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2020
- Dil: İngilizce
- Üniversite: Ludwıg-Maxımılıans Unıversıtat Munchen
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: Belirtilmemiş.
Özet
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Özet (Çeviri)
The lung functions as the body's gas exchange organ. The fibrotic diseases of the lung interstitium, such as idiopathic pulmonary fibrosis (IPF), can be characterized by alveolar epithelial injury and aberrant extracellular matrix deposition by fibroblasts and a faulty in repair mechanisms after chronic tissue injury, which results in loss of normal lung architecture and impairment in gas exchange. Previous study of the time-resolved proteome of the bleomycin lung injury mouse model by Schiller et al. in 2015 highlighted the kinetics of certain ECM proteins, including Emilin2, which was shown to be highly upregulated two weeks after injury and potentially driving a progressive scarring phenotype. In addition, previous studies in the Schiller lab suggest a delay in the resolution of fibrosis in the late stages of the bleomycin model. Here, we employed the bleomycin-induced lung fibrosis model to explore the impact of depletion of Emilin2 after injury by utilizing the single cell RNAseq platform Drop-seq. Investigation of diseased tissue milieu in lung fibrosis is complex due to great cellular heterogeneity. Single cell transcriptomics enables the unbiased single cell profiling and thereby allows to elucidate the contribution of individual cell types to cell population dynamics and transcriptional changes during fibrotic disease states. Analyses presented in this thesis revealed modules of differentially expressed genes in the lungs of Emilin2 knockout mice and the dynamic changes in immune cell populations in the late stages of the model.
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