Project description:Sarcopenic muscles exhibit reduced EV secretion and altered EV cargoes, promoting cancer progression. Her we performed miRNA-seq of exosomes secreted by young muscle (12-week-old NOD/SCID mouse) and old muscle (>12 month old NOD/SCID old mouse) to identify miRNAs that are potentially involved in this process.
Project description:Background: Activation of stress pathways intrinsic to the β cell are thought to both accelerate β cell death and increase β cell immunogenicity in type 1 diabetes (T1D). However, information on the timing and scope of these responses is lacking. Methods: To identify temporal and disease-related changes in islet β cell protein expression, SWATH-MS/MS proteomics analysis was performed on islets collected longitudinally from NOD mice and NOD-SCID mice rendered diabetic through T cell adoptive transfer. Findings: In islets collected from female NOD mice at 10, 12, and 14 weeks of age, we found a time-restricted upregulation of proteins involved in the maintenance of β cell function and stress mitigation, followed by loss of expression of protective proteins that heralded diabetes onset. Pathway analysis identified EIF2 signaling and the unfolded protein response, mTOR signaling, mitochondrial function, and oxidative phosphorylation as commonly modulated pathways in both diabetic NOD mice and NOD-SCID mice rendered acutely diabetic by adoptive transfer, highlighting this core set of pathways in T1D pathogenesis. In immunofluorescence validation studies, β cell expression of protein disulfide isomerase A1 (PDIA1) and 14-3-3b were found to be increased during disease progression in NOD islets, while PDIA1 plasma levels were increased in pre-diabetic NOD mice and in the serum of children with recent-onset T1D compared to age and sex-matched non-diabetic controls. Interpretation: We identified a common and core set of modulated pathways across distinct mouse models of T1D and identified PDIA1 as a potential human biomarker of β cell stress in T1D.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
Project description:Glioblastoma cell lines were xenografted onto mice and resulting tumors were profiled by microarray. Xenograft recipient mice were NOD/SCID/gamma (NSG) male mice 3 months old.
Project description:Prostate Cancer Stem Cells (CSCs) are considered one of the main reasons the tumor recurrence after chemotherapy. Here we employed a chemoresistant xenograft prostate cancer model in NOD/SCID mice and found CD54 is a reliable new marker for prostate CSCs. Gene expression profile were utilized to analyze stemness-related genes in cancer stem cells. 12 Male NOD/SCID mice were obtained from the Animal Center of the Chinese Academy of Medical Science (Beijing, China). For xenograft generation, 1Ã106 LNCaP cells were subcutaneously injected into the backs of NOD/SCID mice (n=24). When tumors reached a diameter of 5 mm after 3 d, mice were randomly divided into two groups without castration (12 per group). Mice in the treatment group were administered with cisplatin at a dose of 5 mg/kg every 3 d for 30 d. Mice in the control group were treated with vehicle PBS. Tumors were taken out for microarray assay after 30 d.