scholarly journals Expression of Transcription Factor GATA-6 in Alveolar Epithelial Cells Is Linked to Neonatal Lung Disease

Neonatology ◽  
2011 ◽  
Vol 99 (3) ◽  
pp. 231-240 ◽  
Author(s):  
Riika Vähätalo ◽  
Tiina M. Asikainen ◽  
Riitta Karikoski ◽  
Vuokko L. Kinnula ◽  
Carl W. White ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Epithelial Cells ◽  
Lung Disease ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Neonatal Lung

scholarly journals Forkhead Transcription Factor FOXO3a Protects Alveolar Epithelial Cells from Oxidative Stress

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Jamileh Ahmed ◽  
KiranKumar Battula ◽  
Ruan R Cox ◽  
Salman Aljubran ◽  
Narasaiah Kolliputi
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Forkhead Transcription Factor ◽  
Alveolar Epithelial

scholarly journals Modeling of fibrotic lung disease using 3D organoids derived from human pluripotent stem cells

2019 ◽  
Author(s):  
Hans-Willem Snoeck ◽  
Alexandros Strikoudis ◽  
Lucas Loffredo ◽  
Ya-Wen Chen
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Lung Disease ◽  
Lung Tissue ◽  
Embryonic Stem ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Recessive Mutations ◽  
Genome Expression ◽  
Fibrotic Lung Disease

Idiopathic pulmonary fibrosis (IPF) is an intractable interstitial lung disease for which no curative treatment is available except for lung transplantation. Its pathogenesis is unclear, but a role for injury to type 2 alveolar epithelial cells is hypothesized. Recessive mutations in some, but not all genes implicated in Hermansky-Pudlak Syndrome (HPS) cause HPS-associated interstitial pneumonia (HPSIP), a clinical entity similar to IPF. We previously reported that mutation in HPS1 in embryonic stem cells-derived 3D lung organoids caused fibrotic changes. Here we show that introduction of all HPS mutations associated with HPSIP (HPS1, 2 and 4) promote fibrosis in lung organoids, while mutation in HSP8, which is not associated with HPSIP, does not. Furthermore, genome-expression analysis of epithelial cells derived from these organoids revealed significant overlap with similar analyses of both affected and unaffected lung tissue of non-HPS IPF patients. Importantly, this analysis showed upregulation of interleukin-11 in HPS-mutant fibrotic organoids and in fibrotic and unaffected lung tissue from IPF patients. Furthermore, IL-11 induced fibrosis in WT organoids, while its deletion prevented fibrosis in fibrotic HPS4-mutant organoids, suggesting IL-11 as a therapeutic target in IPF and HPSIP. hPSC-derived 3D lung organoids are therefore a valuable resource to model fibrotic lung disease.

scholarly journals MTF1 Is Essential for the Expression of MT1B, MT1F, MT1G, and MT1H Induced by PHMG, but Not CMIT, in the Human Pulmonary Alveolar Epithelial Cells

Toxics ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 203
Author(s):  
Sang-Hoon Jeong ◽  
Cherry Kim ◽  
Jaeyoung Kim ◽  
Yoon-Jeong Nam ◽  
Hong Lee ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Rna Seq ◽  
Protein Expression Level ◽  
Early Growth Response ◽  
Alveolar Epithelial ◽  
Early Growth Response 1 ◽  
Transcription Factor 1 ◽  
Essential Transcription Factor

The inhalation of humidifier disinfectants (HDs) is linked to HD-associated lung injury (HDLI). Polyhexamethylene guanidine (PHMG) is significantly involved in HDLI, but the correlation between chloromethylisothiazolinone (CMIT) and HDLI remains ambiguous. Additionally, the differences in the molecular responses to PHMG and CMIT are poorly understood. In this study, RNA sequencing (RNA-seq) data showed that the expression levels of metallothionein-1 (MT1) isoforms, including MT1B, MT1E, MT1F, MT1G, MT1H, MT1M, and MT1X, were increased in human pulmonary alveolar epithelial cells (HPAEpiCs) that were treated with PHMG but not in those treated with CMIT. Moreover, upregulation of MT1B, MT1F, MT1G, and MT1H was observed only in PHMG-treated HPAEpiCs. The protein expression level of metal regulatory transcription factor 1 (MTF1), which binds to the promoters of MT1 isoforms, was increased in PHMG-treated HPAEpiCs but not in CMIT-treated HPAEpiCs. However, the expression of early growth response 1 (EGR1) and nuclear receptor superfamily 3, group C, member 1 (NR3C1), other transcriptional regulators involved in MT1 isomers, were increased regardless of treatment with PHMG or CMIT. These results suggest that MTF1 is an essential transcription factor for the induction of MT1B, MT1F, MT1G, and MT1H by PHMG but not by CMIT.

Alveolar epithelial cells type II show a high sensitivity to cigarette smoke extract

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Seehase ◽  
B Baron-Luehr ◽  
C Kugler ◽  
E Vollmer ◽  
T Goldmann
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
High Sensitivity ◽  
Cigarette Smoke Extract ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial
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