Similar Datasets
Project description:Effects of zinc deficiency on the regeneration of olfactory epithelium in mice
| PRJNA937279 | ENA
Project description:Progenitor cells were purified from methimazole-lesioned olfactory epithelium based on c-Kit expression, and miRNA expression was assayed in c-Kit (+) and c-Kit (-) cell populations.
2017-09-26 | GSE104185 | GEO
Project description:Zinc is an essential trace micronutrient and exerts important physiological and biochemical roles. Zinc deficiency is a global public-health problem. Standing untreated zinc deficiency can cause series adverse effects, including growth retardation, poor appetite, delayed sexual development, impaired neurologic and immune systems, diabetes and obesity, et al. However, the underlying mechanisms of these adverse effects remain elusive in most cases and a comprehensive understanding of the adverse effects (known and unknown) induced by zinc deficiency is lacking. As we know, zinc is a critical component of over 3000 enzymes and is required for numerous catalytic, structural, and regulatory functions of proteins. Thus, the impairments in enzyme actions are responsible for the gross symptoms of zinc deficiency. Altered enzymes may induce to the extensive changes in diverse molecular components of body, including DNA, mRNA and metabolites; and all above changes may work together to induce the adverse effects and affect the health of body. Therefore, protein changes associated with zinc deficiency are very necessary to be unraveled and described for revealing the known and unknown adverse effects and underlying mechanisms. In this project, we first performed a multi-omics study by integrating plasma metabolomics and proteomics, liver proteomics and metal ionomics on zinc deficient rats in order to identify biomarkers (proteins, metabolites and metal elements) of zinc deficiency and reveal the changed metabolic pathways. Eventually, we expected to completely present known adverse effects and their underlying molecular mechanisms, and uncover unknown adverse effects of zinc deficiency.
2019-06-05 | PXD014079 |
Project description:Zinc is an essential trace element that is closely related to learning and memory ability. The hippocampus plays an important role in learning and memory and has the highest zinc concentration in the brain. Severe zinc deficiency (zinc-deprived diet) significantly alter hippocampal protein expression and impair learning and memory abilities. However, no study has investigated the effects of marginal zinc deficiency (low zinc diet) on hippocampal proteins and learning and memory abilities. In this study, the rat model after 4 and 8 weeks of feeding with low zinc diet was first used to identify and quantify the hippocampal proteins of low zinc rats by high-thoughput proteomics technology. Explore the changes of hippocampus proteome patterns after 4 and 8 weeks of feeding with low zinc diet were compared with those in control rats.
2021-10-04 | PXD028998 |
Project description:This study aims to identify the molecular basis for age-related decline in olfactory function and regeneration. To extend our characterization of olfactory stem cell regeneration during aging, we performed single-cell RNA sequencing on whole olfactory epithelium (OE) of 2-month-old and 18-month-old mice in uninjured state and at 24 hours after injury.
2024-04-10 | GSE173999 | GEO
Project description:Zinc is an essential nutrient because of its role in catalysis and in stabilizing protein structure, but excess zinc can also be deleterious. Four nutritional zinc states have been identified in the alga Chlamydomonas reinhardtii: zinc toxic, zinc replete, zinc deficient and zinc limited. Growth is inhibited in zinc-limited and zinc toxic cells relative to zinc-replete cells, while zinc-deficiency is visually asymptomatic but distinguished by the accumulation of transcripts encoding ZIP family transporters. To identify targets of zinc deficiency and mechanisms of zinc acclimation, we used RNA-seq to probe zinc nutrition responsive changes in gene expression. We identified a subset of genes encoding zinc-handling components, including ZIP family transporters and candidate zinc chaperones. In addition, we noted an impact on two other regulatory pathways, the carbon concentrating mechanism (CCM) and the nutritional copper regulon. Targets of transcription factor Ccm1 and various CAH genes are up-regulated in zinc-deficiency, as a likely consequence of reduced carbonic anhydrase activity, which is validated by mass spectrometry and immunoblot analysis of Cah1, Cah3 and Cah4. Chlamydomonas is therefore not able to grow photoautotrophically in air in zinc limiting conditions, but supplementation with 1% CO2 restores growth to wild-type rates, suggesting that the inability to maintain CCM is a major consequence of zinc limitation. Surprisingly, we noted also that the Crr1 regulon, which responds to Cu limitation, is also turned on in zinc deficiency, and in fact, Crr1 is required for growth in zinc-limiting conditions. Zinc deficient cells are functionally copper deficient, as evidenced by reduced plastocyanin abundance, even though they hyperaccumulate copper up to 50-fold over normal levels. We suggest that zinc-deficient cells sequester Cu in a bio-unavailable form, perhaps to prevent mis-metallation of critical zinc sites. Zn-limited wild-type cells were generated by transfer of cells from the first round of growth in medium with no supplemental Zn into TAP medium supplemented or not with 2.5 µM Zn-EDTA The control samples for this study are represented in GSE25622
2013-05-03 | E-GEOD-41096 | biostudies-arrayexpress
Project description:Zinc is an essential micronutrient in pregnancy and zinc deficiency impairs fetal growth. We used a mouse model of moderate zinc deficiency to determine how zinc is important to placental morphogenesis. Global placental gene expression at gestational day 18.5 was analysed using microarray to determine the effects of zinc deficiency on placental function.
2018-02-13 | GSE97112 | GEO
Project description:Mouse Olfactory Epithelium, whole olfactory mucosa, mouse
| PRJNA660060 | ENA
Project description:The Coronavirus Disease 2019 (COVID-19) is mainly a respiratory syndrome that can affect multiple organ systems, causing a variety of symptoms. Among the most common and characteristic symptoms are deficits in smell and taste perception, which may last for weeks/months after COVID-19 diagnosis owing to mechanisms that are not fully elucidated. In order to identify the determinants of olfactory symptom persistence, we obtained olfactory mucosa (OM) from 21 subjects, grouped according to clinical criteria: i) with persistent olfactory symptoms; ii) with transient olfactory symptoms; iii) without olfactory symptoms; and iv) non-COVID-19 controls. Cells from the olfactory mucosa were harvested for transcriptome analyses. RNA-Seq assays showed that gene expression levels are altered for a long time after infection. The expression profile of micro RNAs appeared significantly altered after infection, but no relationship with olfactory symptoms was found. On the other hand, patients with persistent olfactory deficits displayed increased levels of expression of genes involved in the inflammatory response and zinc homeostasis, suggesting an association with persistent or transient olfactory deficits in individuals who experienced SARS-CoV-2 infection.
2023-07-11 | GSE209806 | GEO