Project description:Klotho-deficient mice develop aortic valve annulus calcification by 6 weeks of age. Understanding the molecular basis by which aortic valve calcification is initiated will help define potential molecular targets which may be inhibited to reduce or prevent aortic valve calcification. Changes in gene expression related to aortic valve annulus calcification were analyzed by comparing gene expression in the aortic roots from wild type versus klotho-deficient mice.
Project description:The expression profiles of miRNAs in klotho-deficient and wild-type mice were examined by means of GenopalM-BM-.-MICM DNA chips. The data suggested that there was a difference in the expression of miRNAs between klotho-deficient and wild-type mice. Small RNA samples prevared from 5-week-old klotho-deficient and wild-type mice were examined.
Project description:The expression profiles of miRNAs in klotho-deficient and wild-type mice were examined by means of Genopal®-MICM DNA chips. The data suggested that there was a difference in the expression of miRNAs between klotho-deficient and wild-type mice.
Project description:Whole livers from HDAC6, HDAC9 deficient and wild type C57BL/6 mice, age 8-12 weeks, gender: female. Wild type mice with or without high fat diet
Project description:We used freshly isolated lacrimal glands isolated from wild type and Aire-/- mice on a Balbc background. Mice were 5 weeks of age, with an n=4 for wild type and n=3 for Aire-deficient.
Project description:The expression profiles of miRNAs in klotho-deficient and wild-type mouse brain subregions were examined. The data indicated that little or no marked difference in the miRNA expression was detected between them. Twelve samples prevared from 4- or 5-week-old klotho-deficient and wild-type mouse brain tissues (cerebrum, cerebellum and hippocampus) were examined.
Project description:Klotho knock-out mice are an important model for CKD-induced calcification. In CKD, serum magnesium (Mg2+) inversely correlates with vascular calcification. This study aims to determine the effects of Mg2+ on aortic calcification in Klotho knock-out mice. Klotho knock-out mice were treated with either a minimal or a high Mg2+ diet from birth. After eight weeks, serum biochemistry was studied and organs were harvested. Protective effects of Mg2+ were characterized by RNA-sequencing of aortic tissue. Micro-CT analysis was performed to study bone integrity. High Mg2+ diet prevented vascular calcification and reduced aortic gene expression of Runx2 and matrix Gla protein, demonstrating the protective effect on pro-osteogenic signaling. Differential expression of inflammation and extracellular matrix remodeling genes accompany the beneficial effects of Mg2+ on calcification. High dietary Mg2+ did not affect serum parathyroid hormone, vitamin D3 and calcium. High Mg2+ intake prevented calcification despite increasing fibroblast growth factor-23 and phosphate concentration in knock-out mice. In addition, mice on the high Mg2+ diet had a 20% reduced femoral bone mineral density and increased osteoid formation indicating osteomalacia, while osteoclast activity was decreased in Klotho knock-out mice. In Saos-2 osteoblasts, Mg2+ supplementation reduced mineralization independent of osteoblastic matrix production, alkaline phosphatase activity and maturation markers alpha-1 type-I collagen and sclerostin. In conclusion, high dietary Mg2+ prevents calcification in Klotho knock-out mice. These effects are potentially mediated by reduction of inflammatory and extracellular matrix remodeling pathways in the aorta. Mg2+ treatment is promising to prevent vascular calcification, but the risk for osteomalacia should be considered.
Project description:This SuperSeries is composed of the following subset Series: GSE34531: MicorRNA expression in various tissues of klotho-deficient and wild-type mice GSE34532: microRNA expression in young and elder mouse tissues Refer to individual Series
Project description:To explore the mechanisms underlying progression of atherosclerosis provoked by Nod1 ligand stimulation, we performed microarray gene expression profiling of aortic roots of 6- and 9-week-old Apoe KO mice with or without oral FK565 administration. A gene ontology analysis of the genes up-regulated in FK565-administrated group at both time points showed that a number of biological process terms were associated with immune response. Among chemokine/cytokine genes, we observed that only 3 genes such as Ccl5, Ccl8 and Cxcl16 elevated more than 2-fold in response to oral administration of FK565 at both time points. An eight chip study using total RNA recovered from aortic roots in Apoe KO mice with or without FK565 administration, at the age of 6 and 9 weeks. Two independent experiments were performed in each group. In FK565-administrated groups, mice were orally administrated FK565 (50 µg) twice a week for 1 or 4 weeks from 5 weeks of age.
