Simvastatin has been reported to attenuate the development of pulmonary hypertension through increased apoptosis as well as reduced proliferation of smooth muscle cells in obstructive vascular lesions. Microarray experiment can accomplish many genetic tests in parallel. The purpose of this study is to evaluate altered expressions of gene in rat hearts with monocrotaline (MCT)-induced pulmonary arterial hypertension after simvastatin treatment.
Six-week-old male rats were grouped as follows: control group (C group, saline injection), M group (MCT 60 mg/kg), and S group (MCT 60 mg/kg plus 10 mg/kg/day simvastatin by gavage during 28 days). Body weight, right ventricular pressure and right ventricular/left ventricle+septum ratio in each group were measured. The rats were sacrificed after 28 days. Total RNA was extracted from the rat heart tissue and microarray analysis was performed.
Administration of simvastatin significantly inhibited the progression of right ventricular hypertrophy at day 28 in the S group than in the M group. Compared with the C group, MCT was associated with a significant difference in expression of genes related to biosynthesis and with the regulation of heart contraction rate. Simvastatin treatment resulted in a significantly changed expression of genes about the regulation of progression through cell cycle and system development compared to the M group. The expressions of nitric oxide synthase and brain natriuretic peptide were significantly decreased after simvastatin treatment.
Administration of simvastatin exerted inhibitory effects on right ventricular hypertrophy during the development of MCT-induced pulmonary arterial hypertension in rats. Simvastatin changes the expression of genes associated with various functions.
The etiology for Kawasaki disease (KD) remains unknown, but several studies have suggested the involvement of immune dysregulation and genetic factors. The purpose of this study is to compare gene expressions before and after an infusion of intravenous immunoglobulin (IVIG) in KD patients.
Blood was obtained from both acute and sub-acute phases of 4 patients with KD and febrile control children. Blood was collected in PAXgene blood RNA tubes and RNA was extracted using a PAXgene blood RNA isolation kit. Labeled RNAs were analyzed using Roche NimbleGen human whole genome 12-plex array.
KD patients prior to IVIG injection showed more than a two-fold increase in the expression of 88 genes and more than a two-fold decrease in the expression of 98 genes compared to the control group. They also showed more than two-fold increase in the expression of 226 genes and more than a two-fold decrease in 117 genes in KD patients after IVIG treatment compared to the patients before IVIG injection. Through microarray evaluation, the expressions of genes involved in proliferation, translation, inflammatory response, immune response, cell adhesion, cell migration, cell differentiation, apoptosis, cell growth, transport, cell cycle, transcription, signal transduction and metastasis were observed.
Changes in gene expressions in pediatric patients with KD before and after IVIG were observed via microarray evaluation.
To develop the biomarkers for the immune dysfunction induced by dioxin, 2, 3, 7, 8-TCDD was administered C57BL/6N mice 0.1µg TCDD/??body weight. Colony forming assay showed that the proliferation potential of hemotopoieti progenitor cells in bone marrow was reduced 35-55% more by earlier exposure. The microarray experiments were duplicated, and the candidates were restricted for the genes expressed greater than 121-fold. Resulting candidates were 55 genes. The expression patterns of the whole genes were analyzed by self-organizing maps (SOM). From these results, we selected the stage-specific genes : one genes (SOM c21 : nadh dehydrogenase subunit 5 gene) for gestational 13.5day, 13 genes (c0 : sialophorin ; spn gene, etc) for postnatal 3 week. The above genes are proposed to be a potential use of biomarker for dioxin exposure in the case of immume dysfunctions.