Biology subjects

Zhang, J.-y.

Publications and source records attributed to Zhang, J.-y..

4 recordsLinked to original sources

bioRxiv2022

Chronic Intermittent Hypobaric Hypoxia Prevents Contrast-Induced Acute Kidney Injury By Modulating The HIF-1α Signaling Pathway

The aim of this study was to explore the role of CIHH in preventing contrast-induced acute kidney injury (CI-AKI) in rats and its mechanism. Rats mean arterial pressure, heart rate, serum creatinine and blood urea nitrogen levels were measured. The kidney tissue pathological changes, superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, hypoxia inducible factor-1, Bcl-2/adenovirus E1B-19kDa-interacting protein3 (BNIP3) , cysteiny aspartate specific protease3(caspase3) and poly(ADP-ribose) polymerase (PARP) expression levels were testing. The results showed that CIHH prevented CI-AKI group mean arterial pressure, heart rate, serum creatinine and blood urea nitrogen levels were reduced, kidney tissue SOD activity was increased, MDA levels was reduced, HIF-1,BNIP3,caspase3 and PARP levels were increased than the CI-AKI group. This study indicates that CIHH pretreatment may have a protective effect on contrast-induced early kidney injury by activating the HIF-1/BNIP3 signaling pathway to regulate mitochondrial autophagy and enhance cellular anti-apoptotic and renal antioxidant capacity, for the first time.

physiology↗

bioRxiv2020

Detect Genomic G-Quadruplexes in Living Animal Cells with a Tiny Artificial Protein Probe

G-quadruplex (G4) structures formed by guanine-rich nucleic acids are implicated in essential physiological processes and serve as important drug targets. The genome-wide detection of G4s in living cells is important for exploring the biological role of G4s but has not yet been achieved due to the lack of a suitable G4 probe. We engineered a 6.7 kDa G4 probe (G4P) protein that binds G4s with high affinity and specificity. We used it to capture G4s in living human, mouse, and chicken cells with the ChIP-Seq technology, yielding genome-wide landscape as well as details on the positions, frequencies, and sequence identities of G4 formation in these cells. Our results indicate that transcription is accompanied by a robust formation of G4s in genes. In human cells, we detected up to >123,000 G4 peaks, of which >1/3 had a fold increase of [≥]5 and were present in >60% promoters and ~70% genes. Being much smaller than a scFv antibody (27 kDa) or even a nanobody (12-15 kDa), we expect that the G4P may find diverse applications in biology, medicine, and molecular devices as a G4 affinity agent.

biochemistry↗

bioRxiv2018

Helicobacter pylori-induced adrenomedullin modulates IFN-γ-producing T-cell responses and contribute to gastritis

Adrenomedullin (ADM) is a multifunctional peptide that is expressed by many surface epithelial cells, but its relevance to H. pylori-induced gastritis is unknown. Here, we found that gastric ADM expression was elevated in gastric mucosa of H. pylori-infected patients and mice. In H. pylori-infected human gastric mucosa, ADM expression was positively correlated with the degree of gastritis, accordingly, blockade of ADM resulted in decreased inflammation within the gastric mucosa of H. pylori-infected mice. During H. pylori infection, ADM production was promoted via PI3K-AKT signaling pathway activation by gastric epithelial cells in a cagA-dependent manner, and resulted in increased inflammation within the gastric mucosa. This inflammation was characterized by the increased IFN-{gamma}-producing T cells, whose differentiation was induced via the phosphorylation of AKT and STAT3 by ADM derived from gastric epithelial cells. ADM also induced macrophages to produce IL-12, which promoted the IFN-{gamma}-producing T-cell responses, thereby contributing to the development of H. pylori-associated gastritis. Accordingly, blockade of IFN-{gamma} or knockout of IFN-{gamma} decreased inflammation within the gastric mucosa of H. pylori-infected mice. This study identifies a novel regulatory network involving H. pylori, gastric epithelial cells, ADM, macrophages, T cells, and IFN-{gamma}, which collectively exert a pro-inflammatory effect within the gastric microenvironment.\n\nAuthor summaryH. pylori infect almost half the worlds population. Once infected, most of people carry the bacteria lifelong if left untreated, so that persistent H. pylori infection can lead to chronic gastritis, peptic ulceration and ultimately gastric cancer. H. pylori infection is accompanied with increased inflammation in gastric mucosa, but the mechanisms of chronic gastritis induced by H. pylori infection remains poorly understood. We studied a multifunctional peptide known as adrenomedullin (ADM) in gastric epithelial cells, which was known as a key factor of regulating gastrointestinal physiology and pathology. Here, we found that gastric ADM expression was elevated in gastric mucosa of H. pylori-infected patients and mice, and was positively correlated with the degree of gastritis. ADM production was promoted via PI3K-AKT signaling pathway activation by gastric epithelial cells in a cagA-dependent manner. Blockade of ADM during H. pylori infection resulted in decreased gastric inflammation that was characterized by the increased IFN-{gamma}-producing T cells which was induced via the phosphorylation of AKT and STAT3 by ADM derived from gastric epithelial cells. ADM also induced macrophages to produce IL-12, which promoted the IFN-{gamma}-producing T-cell responses. These data demonstrate that H. pylori-induced ADM modulates FN-{gamma}-producing T-cell responses and contribute to gastritis.

immunology↗

bioRxiv2018

On the regulatory evolution of new genes throughout their life history

Every gene has a birthplace and an age, i.e., a cis-regulatory environment and an evolution lifespan since its origination, yet how genes evolution trajectory is shaped by the two remains unclear. Here we address this basic question by comparing phylogenetically dated new genes of different ages among Drosophila and vertebrate species. For both, we find a clear out of testis transition from the testis-specific young genes to the broadly expressed old housekeeping genes. Particularly, many new genes have evolved specific activation at maternal-zygotic transition, or distinctive spatiotemporal embryonic expression patterns from the parental genes. We uncover an age-dependent gain/loss of active/repressive histone modifications and cis-regulatory elements, with variations between species and between somatic/germline tissues, which together underpin the stepwise acquisition of novel and important function by new genes. These results illuminate the general evolution trajectory and the underlying regulatory mechanisms of genes throughout their life history.

evolutionary biology↗