Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA390739 | ENA |
REPOSITORIES: ENA
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Project description:The molecular mechanisms of lung injury and fibrosis are incompletely understood. microRNAs (miRNAs) are crucial biological regulators by suppression of their target genes and are involved in a variety of pathophysiologic processes. To gain insight into miRNAs in the regulation of lung fibrosis, total RNA was isolated from lung samples harvested at different days after bleomycin treatment, and miRNA array was performed thereafter. miRNAs expressed in lungs with bleomycin treatment at different time points were compared to miRNAs expressed in lungs without bleomycin treatment, resulting in 161 miRNAs differentially expressed. Furthermore, miRNA expression patterns regulated in initial and late periods after bleomycin were identified. Target genes were predicted in silico for differentially expressed miRNAs, including miR-7f, miR-7g, miR-196b, miR-16, miR-195, miR-25, miR-144, miR-351, miR-34a, miR-499, miR-704, miR-717, miR-10a, miR-211, miR-34a, miR-367 and miR-21, and then cross-referenced to molecular pathways including apoptosis, Wnt, Toll-like receptor, and TGF-? signaling, which are involved in different pathological phenotypes such as apoptosis, inflammation, and fibrosis. Our study demonstrated relative abundance of miRNA levels in bleomycin-induced lung fibrosis. The miRNAs and their potential target genes identified herein contribute to the understanding of the complex transcriptional program of lung fibrosis. Under anesthesia, 2.5 U/kg bleomycin dissolved in sterile PBS was administered via trachea as previously described. Lung tissues were harvested at the time point of day 0, 3, 7, 14, and 21 post bleomycin challenges. 3 sample in specific time point, except for day 14 where nday14 = 2.
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Project description:MicroRNAs are endogenously expressed small non-coding RNAs that regulate gene expression on the posttranscriptional level. The miR-17-92 cluster (encoding miR-17, -18a, -19a/b, -20a and miR-92a) is highly expressed in tumor cells and is up-regulated by ischemia. Whereas miR-92a was recently identified as negative regulator of angiogenesis, the specific functions of the other members of the cluster are less clear. Here we demonstrate that overexpression of miR-17, -18a, -19a and -20a significantly inhibited 3D spheroid sprouting in vitro, whereas inhibition of miR-17, -18a and -20a augmented endothelial cell (EC) sprout formation. Inhibition of miR-17 and miR-20a in vivo using antagomirs significantly increased the number of perfused vessels in matrigel plugs, whereas antagomirs, that specifically target miR-18a and miR-19a were less effective. However, systemic inhibition of miR-17/20 did not affect tumor angiogenesis. Further mechanistic studies showed that miR-17/20 targets several pro-angiogenic genes. Specifically, Janus kinase 1 (Jak1) was shown to be a direct target of miR-17. In summary, we show that miR-17/20 exhibit a cell intrinsic anti-angiogenic activity in ECs. Inhibition of miR-17/20 specifically augmented neovascularization of matrigel plugs, but did not affect tumor angiogenesis indicating a context-dependent regulation of angiogenesis by miR-17/20 in vivo. 6 samples of 3 independent experiments (n=3): per experiment Pre-miR-Co (10 nM, Ambion) and Pre-miR-17 (10 nM, Ambion) transfected HUVEC 24h after transfection
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Project description:The molecular mechanisms of lung injury and fibrosis are incompletely understood. microRNAs (miRNAs) are crucial biological regulators by suppression of their target genes and are involved in a variety of pathophysiologic processes. To gain insight into miRNAs in the regulation of lung fibrosis, total RNA was isolated from lung samples harvested at different days after bleomycin treatment, and miRNA array was performed thereafter. miRNAs expressed in lungs with bleomycin treatment at different time points were compared to miRNAs expressed in lungs without bleomycin treatment, resulting in 161 miRNAs differentially expressed. Furthermore, miRNA expression patterns regulated in initial and late periods after bleomycin were identified. Target genes were predicted in silico for differentially expressed miRNAs, including miR-7f, miR-7g, miR-196b, miR-16, miR-195, miR-25, miR-144, miR-351, miR-34a, miR-499, miR-704, miR-717, miR-10a, miR-211, miR-34a, miR-367 and miR-21, and then cross-referenced to molecular pathways including apoptosis, Wnt, Toll-like receptor, and TGF-β signaling, which are involved in different pathological phenotypes such as apoptosis, inflammation, and fibrosis. Our study demonstrated relative abundance of miRNA levels in bleomycin-induced lung fibrosis. The miRNAs and their potential target genes identified herein contribute to the understanding of the complex transcriptional program of lung fibrosis.
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Project description:MicroRNAs are endogenously expressed small non-coding RNAs that regulate gene expression on the posttranscriptional level. The miR-17-92 cluster (encoding miR-17, -18a, -19a/b, -20a and miR-92a) is highly expressed in tumor cells and is up-regulated by ischemia. Whereas miR-92a was recently identified as negative regulator of angiogenesis, the specific functions of the other members of the cluster are less clear. Here we demonstrate that overexpression of miR-17, -18a, -19a and -20a significantly inhibited 3D spheroid sprouting in vitro, whereas inhibition of miR-17, -18a and -20a augmented endothelial cell (EC) sprout formation. Inhibition of miR-17 and miR-20a in vivo using antagomirs significantly increased the number of perfused vessels in matrigel plugs, whereas antagomirs, that specifically target miR-18a and miR-19a were less effective. However, systemic inhibition of miR-17/20 did not affect tumor angiogenesis. Further mechanistic studies showed that miR-17/20 targets several pro-angiogenic genes. Specifically, Janus kinase 1 (Jak1) was shown to be a direct target of miR-17. In summary, we show that miR-17/20 exhibit a cell intrinsic anti-angiogenic activity in ECs. Inhibition of miR-17/20 specifically augmented neovascularization of matrigel plugs, but did not affect tumor angiogenesis indicating a context-dependent regulation of angiogenesis by miR-17/20 in vivo.
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