Y

Yan Zhou

Xuzhou Medical College

ORCID: 0000-0002-8822-5276

Publishes on Neuroinflammation and Neurodegeneration Mechanisms, Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis, Intracranial Aneurysms: Treatment and Complications. 165 papers and 4.9k citations.

165Publications
4.9kTotal Citations

Is this you? Claim your profile.

Add your photo, update your bio, and get notified when your ranking changes.

Top publicationsby citations

Transcriptome-wide investigation of circular RNAs in rice
Cited by 434Open Access

Various stable circular RNAs (circRNAs) are newly identified to be the abundance of noncoding RNAs in Archaea, Caenorhabditis elegans, mice, and humans through high-throughput deep sequencing coupled with analysis of massive transcriptional data. CircRNAs play important roles in miRNA function and transcriptional controlling by acting as competing endogenous RNAs or positive regulators on their parent coding genes. However, little is known regarding circRNAs in plants. Here, we report 2354 rice circRNAs that were identified through deep sequencing and computational analysis of ssRNA-seq data. Among them, 1356 are exonic circRNAs. Some circRNAs exhibit tissue-specific expression. Rice circRNAs have a considerable number of isoforms, including alternative backsplicing and alternative splicing circularization patterns. Parental genes with multiple exons are preferentially circularized. Only 484 circRNAs have backsplices derived from known splice sites. In addition, only 92 circRNAs were found to be enriched for miniature inverted-repeat transposable elements (MITEs) in flanking sequences or to be complementary to at least 18-bp flanking intronic sequences, indicating that there are some other production mechanisms in addition to direct backsplicing in rice. Rice circRNAs have no significant enrichment for miRNA target sites. A transgenic study showed that overexpression of a circRNA construct could reduce the expression level of its parental gene in transgenic plants compared with empty-vector control plants. This suggested that circRNA and its linear form might act as a negative regulator of its parental gene. Overall, these analyses reveal the prevalence of circRNAs in rice and provide new biological insights into rice circRNAs.

Genetic Control of Seed Shattering in Rice by the APETALA2 Transcription Factor <i>SHATTERING ABORTION1</i>
Yan Zhou, Danfeng Lu, Canyang Li et al.|The Plant Cell|2012
Cited by 230Open Access

Seed shattering is an important agricultural trait in crop domestication. SH4 (for grain shattering quantitative trait locus on chromosome 4) and qSH1 (for quantitative trait locus of seed shattering on chromosome 1) genes have been identified as required for reduced seed shattering during rice (Oryza sativa) domestication. However, the regulatory pathways of seed shattering in rice remain unknown. Here, we identified a seed shattering abortion1 (shat1) mutant in a wild rice introgression line. The SHAT1 gene, which encodes an APETALA2 transcription factor, is required for seed shattering through specifying abscission zone (AZ) development in rice. Genetic analyses revealed that the expression of SHAT1 in AZ was positively regulated by the trihelix transcription factor SH4. We also identified a frameshift mutant of SH4 that completely eliminated AZs and showed nonshattering. Our results suggest a genetic model in which the persistent and concentrated expression of active SHAT1 and SH4 in the AZ during early spikelet developmental stages is required for conferring AZ identification. qSH1 functioned downstream of SHAT1 and SH4, through maintaining SHAT1 and SH4 expression in AZ, thus promoting AZ differentiation.

Aucubin alleviates oxidative stress and inflammation via Nrf2-mediated signaling activity in experimental traumatic brain injury
Han Wang, Xiaoming Zhou, Lingyun Wu et al.|Journal of Neuroinflammation|2020
Cited by 211Open Access

Abstract Background Aucubin (Au), an iridoid glycoside from natural plants, has antioxidative and anti-inflammatory bioactivities; however, its effects on a traumatic brain injury (TBI) model remain unknown. We explored the potential role of Au in an H 2 O 2 -induced oxidant damage in primary cortical neurons and weight-drop induced-TBI in a mouse model. Methods In vitro experiments, the various concentrations of Au (50 μg/ml, 100 μg/ml, or 200 μg/ml) were added in culture medium at 0 h and 6 h after neurons stimulated by H 2 O 2 (100 μM). After exposed for 12 h, neurons were collected for western blot (WB), immunofluorescence, and M29,79-dichlorodihydrofluorescein diacetate (DCFH-DA) staining. In vivo experiments, Au (20 mg/kg or 40 mg/kg) was administrated intraperitoneally at 30 min, 12 h, 24 h, and 48 h after modeling. Brain water content, neurological deficits, and cognitive functions were measured at specific time, respectively. Cortical tissue around focal trauma was collected for WB, TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, Nissl staining, quantitative real time polymerase chain reaction (q-PCR), immunofluorescence/immunohistochemistry, and enzyme linked immunosorbent assay (ELISA) at 72 h after TBI. RNA interference experiments were performed to determine the effects of nuclear factor erythroid-2 related factor 2 (Nrf2) on TBI mice with Au (40 mg/kg) treatment. Mice were intracerebroventricularly administrated with lentivirus at 72 h before TBI establishment. The cortex was obtained at 72 h after TBI and used for WB and q-PCR. Results Au enhanced the translocation of Nrf2 into the nucleus, activated antioxidant enzymes, suppressed excessive generation of reactive oxygen species (ROS), and reduced cell apoptosis both in vitro and vivo experiments. In the mice model of TBI, Au markedly attenuated brain edema, histological damages, and improved neurological and cognitive deficits. Au significantly suppressed high mobility group box 1 (HMGB1)-mediated aseptic inflammation. Nrf2 knockdown in TBI mice blunted the antioxidant and anti-inflammatory neuroprotective effects of the Au. Conclusions Taken together, our data suggest that Au provides a neuroprotective effect in TBI mice model by inhibiting oxidative stress and inflammatory responses; the mechanisms involve triggering Nrf2-induced antioxidant system.

The analysis of large-scale gene expression correlated to the phase changes of the migratory locust
Le Kang, XiangYong Chen, Yan Zhou et al.|Proceedings of the National Academy of Sciences|2004
Cited by 199Open Access

The migratory locust is one of the most notorious agricultural pests that undergo a well known reversible, density-dependent phase transition from the solitary to the gregarious. To demonstrate the underlying molecular mechanisms of the phase change, we generated 76,012 ESTs from the whole body and dissected organs in the two phases. Comparing 12,161 unigene clusters, we identified 532 genes as phase-related (P < 0.01). Comprehensive assessment of the phase-related expression revealed that, whereas most of the genes in various categories from hind legs and the midgut are down-regulated in the gregarious phase, several gene classes in the head are impressively up-regulated, including those with peptidase, receptor, and oxygen-binding activities and those related to development, cell growth, and responses to external stimuli. Among them, a superfamily of proteins, the JHPH super-family, which includes juvenile hormone-binding protein, hexamerins, prophenoloxidase, and hemocyanins, were highly expressed in the heads of the gregarious hoppers and hind legs of the solitary hoppers. Quantitative PCR experiments confirmed in part the EST results. These differentially regulated genes have strong functional implications that numerous molecular activities are involved in phase plasticity. This study provides ample molecular markers and genomic information on hemimetabolous insects and insights into the genetic and molecular mechanisms of phase changes in locusts.

Effects of Arachidonic Acid Metabolites on Cardiovascular Health and Disease
Yan Zhou, Haroon Khan, Jianbo Xiao et al.|International Journal of Molecular Sciences|2021
Cited by 185Open Access

Arachidonic acid (AA) is an essential fatty acid that is released by phospholipids in cell membranes and metabolized by cyclooxygenase (COX), cytochrome P450 (CYP) enzymes, and lipid oxygenase (LOX) pathways to regulate complex cardiovascular function under physiological and pathological conditions. Various AA metabolites include prostaglandins, prostacyclin, thromboxanes, hydroxyeicosatetraenoic acids, leukotrienes, lipoxins, and epoxyeicosatrienoic acids. The AA metabolites play important and differential roles in the modulation of vascular tone, and cardiovascular complications including atherosclerosis, hypertension, and myocardial infarction upon actions to different receptors and vascular beds. This article reviews the roles of AA metabolism in cardiovascular health and disease as well as their potential therapeutic implication.