Search bioRxiv⌕ Search

bioRxiv · 10.1101/381053

Urinary protein changes in the early phase of smoking-induced Chronic Obstructive Pulmonary Disease in a rat model

Abstract

Chronic obstructive pulmonary disease (COPD) is a group of severe respiratory diseases. Identifying COPD through early urinary biomarkers by proteomics technology may help to reduce the mortality rate of the disease, improve the quality of life of patients and reduce the burden on society. Urine samples from a COPD rat model induced by smoking were taken at week 2, week 4 and week 8. By LC-MS/MS, 15 differential proteins with human orthologs were identified. After smoking for 2 weeks when there were no significant pathological changes, 8 differential proteins were identified: 2 proteins had been reported to be markers of COPD, while 4 proteins were associated with COPD. After smoking for 4 weeks, which is when slight pathological changes were observed, 7 differential proteins were identified: 3 of them were reported to be associated with COPD, while 1 protein had been reported to be a marker of COPD. After smoking for 8 weeks, there were significant pathological changes: 5 differential proteins were identified, 3 of which were reported to be associated with COPD. The results of this study suggest that differential urinary proteins may provide important clues for the early diagnosis of COPD.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Huang, H., Wang, T., Gao, Y.. 2018-07-31. Urinary protein changes in the early phase of smoking-induced Chronic Obstructive Pulmonary Disease in a rat model. https://doi.org/10.1101/381053

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The intrinsically disordered N-terminal region of eIF5B nucleates RNA-driven phase separation

Recently, we found that eukaryotic Initiation Factor 5B (eIF5B) forms cytoplasmic puncta under conditions of cellular stress and that the puncta formation drives an increase in alternative translation initiation. The formation of these puncta depends on the intrinsically disordered N-terminal region of eIF5B (eIF5B-NTR). To address the driving force behind this observation, we reconstituted a purified, binary, in vitro system to study the phase separation potential of the eIF5B-NTR. Utilizing this system, we show that eIF5B-NTR forms RNA-driven condensates at physiological concentrations. Furthermore, we defined the properties of the eIF5B condensates and the amino acid sequence requirements of this polypeptide to form complex liquid-liquid condensates. Truncation mapping identified a central arginine-rich core (residues ~200-400) that drives condensation but forms nearly static droplets in the absence of the rest of the polypeptide. Finally, we tested this model in cells to determine if the in vitro observations apply to the complex cellular environment.

biochemistry↗

Structural basis of ribosomal RNA repair by RtcB2

Ribotoxins disable ribosomes by cleaving ribosomal RNA, but how repair enzymes recognize and restore these damaged machines remains unclear. Here, we report three cryo-electron microscopy structures of the RNA ligase RtcB2 bound to damaged Escherichia coli 30S subunits. An extended interface stabilizes the ribosomal head and decoding-center scaffold while positioning the cleaved 3'-phosphate end within the catalytic pocket. Two structures contain enzyme-linked guanosine monophosphate, whereas the third captures its transfer to the RNA. RNA activation accompanies RtcB2 reorientation and entry of the 5'-hydroxyl-containing segment into an adjacent cleft. Comparisons with assembled ribosomes reveal structural barriers to substrate access. These structures connect recognition of a damaged ribosome to chemical activation of its RNA for repair.

biochemistry↗

Enhancers Silence Coupled-coding RNAs in Animals

The exact working mechanism and biogenesis of regulatory non-coding RNAs (rncRNAs), including enhancer RNAs (eRNAs), microRNAs (miRNAs), piRNAs, small interfering RNAs (siRNAs), transposons, and other non-coding RNAs, remain enigmatic. Conversely, the unique transcriptional regulation mechanism that differentiates animals from simple unicellular organisms remains elusive in life sciences. We find that regulatory non-coding genes are independent transcription units marked with arginine methylation of nucleosomes within their gene bodies, which is regulated by JMJD5. Enhancer RNAs are similar to those of other regulatory RNAs in targeting the 3-prime UTRs of coupled coding RNAs. All regulatory RNA genes share transcription factors with their target coding genes, both of which are regulated by promoter-proximal RNA Polymerase II pausing and may control the development of animals. Temporal and spatial coding genes and regulatory non-coding genes are intrinsically coupled in animals.

biochemistry↗