Ferroplasma sp. Type II
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ABSTRACT:
PROVIDER: PRJNA209807 | ENA |
REPOSITORIES: ENA
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Project description:Ferroplasma sp. Type II metagenomic assembly
| PRJNA29597 | ENA
Project description:Ferroplasma acidarmanus Type I metagenomic assembly
| PRJNA29595 | ENA
Project description:Pulmonary alveoli contain two distinct populations of epithelial cells. Type II cells produce pulmonary surfactant lipids and surfactant-associated proteins (SP) required for maintaining alveolar surface tension at the air-liquid interface and host defense against respiratory pathogens. Type II cells are also progenitors for epithelial type I cells, a terminally differentiated elongated cell that covers microvascular endothelial cells and participates in gas exchange. Despite some indirect evidence, it is unknown whether subpopulations of type II cells exist. We created a line of transgenic mice expressing enhanced green fluorescent protein (EGFP) under control of the human SP-C promoter. Expression of EGFP may define a subpopulation of type II cells because it is 1) expressed in approximately 10% of type II cells, 2) appears much later in embryonic development than SP-C, and 3) selectively proliferates in mice infected with influenza A virus. To determine whether EGFP defines a unique subpopulation of type II cells, RNA was isolated from EGFP-positive and negative type II cells and hybridized to affymetrix arrays. Of the genes detected in EGFP-positive cells, most were equally detected in EGFP-negative cells. However, approximately 350 genes were selectively elevated ≥5-fold in EGFP-positive cells and 1500 genes selectively expressed by EGFP-negative cells. These findings suggest EGFP defines a subpopulation of type II epithelial cells in this line of transgenic mice.
2010-12-03 | GSE25778 | GEO
Project description:Ferroplasma acidiphilum strain:Y Genome sequencing
| PRJNA316151 | ENA
Project description:Ferroplasma acidiphilum strain:DSM 28986 Genome sequencing and assembly
| PRJNA630245 | ENA
Project description:Leptospirillum sp. Group II '5-way CG' metagenomic assembly
| PRJNA29591 | ENA
Project description:Micromonospora sp. II strain:II Genome sequencing and assembly
| PRJNA322530 | ENA
Project description:Type II cell differentiation and expression of the major surfactant protein, SP-A, in midgestation human fetal lung (HFL) are markedly induced by cAMP and inhibited by TGF-β. cAMP induction of SP-A promoter activity is mediated by increased phosphorylation and in vivo binding of TTF-1/Nkx2.1, a critical transcription factor in lung development. To further define mechanisms for developmental induction of surfactant synthesis in HFL, herein, we investigated the potential role of microRNAs (miRNAs, miRs). To identify and characterize differentially regulated miRNAs in mid-gestation HFL explants during type II pneumocyte differentiation in culture, we performed miRNA microarray analysis of RNA isolated from epithelial cells from midgestation HFL explants before and after culture ± Bt2cAMP. Interestingly, the miR-200 family was significantly upregulated during type II cell differentiation; miR-200 family induction was inversely correlated with expression of its known targets, transcription factors ZEB1 and ZEB2, and TGF-b2. miR-200 antagonists inhibited TTF-1 and SP-A expression and upregulated TGF-β2 and ZEB1 expression in type II cells. Overexpression of ZEB1 in cultured type II cells decreased DNA binding of endogenous TTF-1, blocked cAMP stimulation of SP-A and inhibited miR-200 expression,whereas, cAMP markedly inhibited ZEB1/2 and TGF-β. Importantly, overexpression of ZEB1 or miR-200 antagonists in HFL type II cells markedly suppressed accumulation of lamellar bodies, organelles that store surfactant. Our findings suggest that the miR-200 family and ZEB1, which exist in a double-negative feedback loop regulated by TGF-β, serve important regulatory roles in the developmental regulation of type II cell differentiation and SP-A expression in HFL.
2015-10-01 | GSE61183 | GEO