Dataset Information

Next-generation sequencing facilitates quantitative analysis of the transcriptome in normal lung tissue and in lung tissue with LPS-induced acute lung injury

ABSTRACT: Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways and the function of all RNAs in a certain functional state of a specific cell was studied, mainly including non-coding RNAs.The aim of this study was to compare lung tissue transcriptome analysis (RNA-SEQ) with microarray and quantitative reverse transcription polymerase chain reaction (QRT-PCR) methods for LPS-induced acute lung injury and to evaluate the optimal high-throughput data analysis protocol. Methods: LncRNA profiles of normal lung tissue and LPS-induced acute lung injury after 24h in mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000 Results: A total of 8,610 lncRNAs were identified in the normal and LPS groups. Conclusions: Our study represents detailed analysis of lung tissue transcriptomes, withh biological replicates, generated by RNA-seq technology. Novel ideas are presented to expand our knowledge on the regulation mechanisms of lncRNA-related ceRNAs in the pathogenesis of ALI.

ORGANISM(S): Mus musculus

PROVIDER: GSE188492 | GEO | 2021/11/12

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an inflammatory process of the lungs characterized by increased permeability of the alveolar-capillary membrane with subsequent interstitial/alveolar edema and diffuse alveolar damage. ALI/ARDS can be the results of either direct or indirect lung injury, with pneumonia being the most common direct pulmonary insult and sepsis the most common extra-pulmonary cause. In this study, we employed the murine lipopolysaccharide (LPS)-induced direct and indirect lung injury model to explore the pathogenic mechanisms of pulmonary and extra-pulmonary ARDS, using an unbiased, discovery and quantitative proteomic approach. A total of 1,017 proteins were both identified and quantified in bronchoalveolar lavage fluid (BALF) from control, intratracheal LPS (I.T. LPS, 0.1 mg/kg) and intraperitoneal LPS (I.P. LPS, 5 mg/kg) treated mice. The two LPS groups shared 13 up-regulated and 22 down-regulated proteins compared to the control group. Among them, molecules related to bronchial and type II alveolar epithelial cell functions including cell adhesion molecule 1 and surfactant protein B were reduced, whereas lactotransferrin and resistin like alpha involved in lung innate immunity were upregulated in both LPS groups. Proteomic profiling also identified significant differences in BALF proteins between I.T. and I.P. LPS groups. Ingenuity pathway analysis revealed that acute-phase response signaling was activated by both I.T. and I.P. LPS, however, the magnitude of activation is much greater in I.T. LPS group compared to I.P. LPS group. Intriguingly, two canonical signaling pathways, liver X receptor/retinoid X receptor activation and the production of nitric oxide and reactive oxygen species in macrophages, were activated by I.T. LPS but suppressed by I.P. LPS. In addition, CXCL15 (also known as lungkine) was also up-regulated by I.T LPS but down-regulated by I.P. LPS. In conclusion, our quantitative discovery-based proteomic approach identified commonalities as well as significant differences in BALF protein expression profiles in LPS-induced direct and indirect lung injury, and importantly, LPS-induced indirect lung injury results in suppression of select components of lung innate immunity, which could contribute to the so-called “immunoparalysis” in sepsis patients.

Dataset Information

Next-generation sequencing facilitates quantitative analysis of the transcriptome in normal lung tissue and in lung tissue with LPS-induced acute lung injury

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets