Project description:The rabbit hemorrhagic disease virus (RHDV) represents the causative agent of a highly contagious disease in rabbits that is often associated with high mortality. Because of the lack of a suitable cell culture system for RHDV, the pathogenic mechanism and replication of RHDV remains unclear. In order to analyze the pathogenic mechanism of RHDV to rabbits, we used New Zealand white rabbits infected with RHDV, collected liver tissues 32 hours after infection, and used TMT labeling for LC-MS analysis. Subsequently, it was compared and analyzed with the protein data of the liver tissue of the uninfected rabbits. Perform bioinformatics analysis on significantly different proteins. Finally, comprehensively analyze the influence of RHDV on host protein and pathway expression levels. This study provides clues to clarify the pathogenic mechanism of RHDV in rabbits.
Project description:Peritoneal macrophages from healthy New Zealand White rabbits were treated with exosomes from Cysticercus pisiforms and treated with PBS were used as control.
Project description:In this study, human particulated dentin (HPD) was developed. The characteristic of HPD was examinated by XRD, EDX and cytotoxicity test. HPD was used to implant in the calvarial defects of New Zealand White rabbits. bone tissue and blood samples were taken at 3, 5 and 7 days post-implantation for microarray experiment. The gene expression profiles and signaling pathways were monitored using GeneSpring software and Ingenuity Pathways Analysis (IPA), respectively. We used microarray and IPA to elucidate the global programme of gene expression and identified distinct classes of up- and down- regulated genes during HPD treated healing process.
Project description:Microarray analysis of white adipose tissue (WAT) and bone marrow adipose tissue (BMAT) from 22-week-old or 13-week-old male New Zealand White rabbits. From both cohorts, BMAT was sampled from the distal tibia (dBMAT) and the radius and ulna (ruBMAT), while WAT was sampled from the inguinal (iWAT) and gonadal (gWAT) depots. From the 13-week-old cohort, BMAT was also sampled from the proximal tibia (pBMAT). Sufficient RNA could not be isolated from all tissues for all rabbits, so for some rabbits only a subset of tissues is included.
Project description:Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), is an exquisitely adapted human pathogen capable of surviving for decades in the lungs of immune competent individuals in absence of disease. The World Health Organization estimates that 2 billion people have latent TB infection (LTBI), defined by positive immunologic response to Mtb antigens with no clinical signs of disease. A better understanding of host and pathogen determinants of LTBI and subsequent reactivation would benefit TB control efforts. Animal models of LTBI have been hampered mainly by an inability to achieve complete bacillary clearance. We have characterized a rabbit model of LTBI in which, similar to most humans, complete clearance of pulmonary Mtb infection and pathology occurs spontaneously. The evidence that Mtb-CDC1551-infected rabbits achieve LTBI, rather than sterilization, is based on the ability of the bacilli to be reactivated following immune suppression. The microarray experiments involves comparison of: 1) Changes in rabbit gene expression between Mtb-CDC1551 infected and uninfected animals at 2,4,8 and 12 weeks post infection. New Zealand White rabbits were infected with Mtb CDC1551 at 3.5log10 (on day 0). Lung tissue from Mtb-infected rabbits were isolated from uninfected (control) and at 2, 4, 8 and 16 weeks post infection and used for total RNA extraction. Total rabbit lung RNA was used for microarray analysis to determine infection induced changes in host gene expression.
Project description:Background: Right ventricular (RV) and left ventricular (LV) myocardium differ in their response to pressure-overload hypertrophy (POH). In this report we use microarray and proteomic analyses to identify pathways modulated by LV-, and RV-POH in the immature heart. Methods: Newborn New Zealand White rabbits underwent banding of the descending thoracic aorta (LV-POH; n=6). RV-POH was achieved by banding the pulmonary artery (n=6). Sham–control animals (SC; n=6 each) were sham-manipulated. Following 4 (LV-POH) and 6 weeks (RV-POH) recovery, the hearts were removed and matched sample RNA and proteins were isolated for microarray and proteomic analysis. Results: There was no difference in body weight in RV-, LV-POH vs. SC but there was a significant increase vs. SC in RV (3.2±0.8g vs. 1.2±0.3g; P<0.01) and LV weight (7.08±0.6g vs. 4.02±0.2g; P<0.01). Fractional area change (RV-POH) and shortening fraction (LV-POH) decreased significantly (23±6 vs. 47±6 and 21±4 vs.44±2, respectively, P<0.01). Microarray analysis demonstrated that LV-POH enriched pathways for oxidative phosphorylation, mitochondria energy pathways, actin, ILK, hypoxia, calcium and protein kinase-A signalling. RV-POH enriched pathways for cardiac oxidative phosphorylation. Proteomic analysis revealed 19 proteins were uniquely expressed in LV-POH vs. SC. Functional annotation clustering analysis indicated significant enrichment for the mitochondrion, cellular macromolecular complex assembly and oxidative phosphorylation. RV-POH had 15 uniquely expressed proteins vs. SC. Functional annotation clustering analysis indicated significant enrichment in structural constituents of muscle, cardiac muscle tissue development and calcium handling. Conclusion: Our results identify unique transcript and protein expression profiles in LV, RV-POH and provide new insight into the biological basis of ventricular specific hypertrophy. 3 different conditions: PAB-RV vs. Sham-control RV, PAB-RV [test] vs. PAB-LV [control], AOB-LV vs. Sham-control LV.
Project description:High-flow causes the remodeling of arteries, in which smooth muscle cells play an important role. To know the profile of smooth muscle gene expression under high-flow conditions in vivo, flow of rabbit basilar artery was increased by ligation of both common carotid arteries. Microarrays were performed to profile the gene expression of smooth muscle cells isolated from rabbit basilar artery. Expression profiles indicate 43603 differentially expressed genes in smooth muscle cells exposed to high-flow insult compared with the sham control, of which 1470 genes were upregulated and 780 genes downregulated using 2 fold-changes and P<0.05 as a cut-off. Bilateral common carotid arteries of female New Zealand White rabbits were ligated to increase vascular flow.The control group was performed the same procedure to expose the CCAs without ligation. Rabbits were euthanized at day 5 after ligation or exposure of bilateral CCAs in both groups (n=3 for each group). The rabbits used and all procedures in this study were approved by the local Institutional Animal Care and Use Committee. Smooth muscle cells were isolated. After euthanization of rabbits, the whole basilar arteries were removed. The arteries were cleaned in PBS buffer,cannulated and perfused at a constant flow with a cocktail which contains PBS and 0.4 mg/ml elastase (Sigma) and 1 mg/ml collagenase (type 1A, Sigma). After an incubation time of 45 min, the tissue left was removed and stored in PBS. SMCs were released from the artery by trituration. Then Total RNA was extracted and gene chip tests were performed.
Project description:Analysis of embronic day 30.5 (E30.5) fetal rabbit left lung after creation of diapragmatic hernia (DH) at E25 and tracheal occlusion (TO) at E27. The fetuses of timed pregnant New Zealand rabbits were subjected to creation of a left diaphragmatic hernia at E25 with or without tracheal occlusion at E27. At E30.5, the fetuses were sacrificed with collection of the lateral aspect of the left upper lobe for NextGen mRNA sequencing.