Project description:The goals of this study is to identify the differential expressed genes in cardiac tissue of C57BL/6 mice with or without Angiotensin II (AngII) treatment, and compare the differential expressed genes in the cardiac tissue of Ang II infused C57BL/6 mice after Ethoxysanguinarine (ETH), Baicalin (BAI), Gastrodin (GAS) or valsartan (VAL) treatment. Briefly, the mice (n=30) were randomly divided into 6 groups: control, AngII, AngII + ETH, AngII + BAI, AngII + GAS and AngII + VAL groups (n=5 for each group). Mice in Control and AngII groups were infused with saline and 500 ng/kg/min of AngII respectively, and orally administrated with saline; the mice in AngII + ETH, AngII + BAI and AngII + GAS groups were infused with AngII (500 ng/kg/min) and orally administrated with 5 mg/kg /day of ETH, BAI or GAS daily for total 4 weeks. The mice in AngII + VAL group were infused with AngII (500 ng/kg/min) and orally administrated with 10.4mg/kg /day of VAL. Then the cardiac tissues were used to identify differentially expressed genes among different groups.
Project description:The goals of this study is to identify the differential expressed genes in abdominal aorta of C57BL/6 mice with or without Angiotensin II (AngII) treatment, and compare the differential expressed genes in the abdominal aorta of Ang II infused C57BL/6 mice after Ethoxysanguinarine (ETH), Baicalin (BAI), Gastrodin (GAS) or valsartan (VAL) treatment. Briefly, the mice (n=30) were randomly divided into 6 groups: control, AngII, AngII + ETH, AngII + BAI, AngII + GAS and AngII + VAL groups (n=5 for each group). Mice in Control and AngII groups were infused with saline and 500 ng/kg/min of AngII respectively, and orally administrated with saline; the mice in AngII + ETH, AngII + BAI and AngII + GAS groups were infused with AngII (500 ng/kg/min) and orally administrated with 5 mg/kg /day of ETH, BAI or GAS daily for total 4 weeks. The mice in AngII + VAL group were infused with AngII (500 ng/kg/min) and orally administrated with 10.4mg/kg /day of VAL. Then the abdominal aortas were used to identify differentially expressed genes among different groups.
Project description:The goals of this study is to compare the differently expressed genes in renal tissue of C57BL/6 WT mice with or without Angiotensin II (AngII) treatment as well as differently expressed genes in the renal tissue of WT mice with AngII treatment with or without Qingda granule(QDG)treatment. The mice (n=15) were randomly divided into 3 groups: control, AngII,AngII+ QDG (n=5 for each group). Mice in Control and AngII groups were infused with saline or 500 ng/kg/min of AngII respectively, and intragastrically with double distilled water (dd H2O); while mice in AngII + QDG groups were infused with AngII (500 ng/kg/min) and intragastrically with 1.145 g/kg/D of QDG for 4 weeks. Then the renal tissue were used to identify differentially expressed genes among different groups.
Project description:The goals of this study is to compare the differently expressed genes in renal tissue of C57BL/6 WT mice with or without Angiotensin II (AngII) treatment as well as differently expressed genes in the renal tissue of WT mice with AngII treatment with or without Quercetin (Que) treatment. The mice (n=18) were randomly divided into 3 groups: control, AngII,AngII+ Que (n=6 for each group). Mice in Control and AngII groups were infused with saline or 500 ng/kg/min of AngII respectively, and intragastrically with double distilled water (dd H2O); while mice in AngII + Que groups were infused with AngII (500 ng/kg/min) and intragastrically with 5mg/kg/D of Que for 4 weeks. Then the renal tissue were used to identify differentially expressed genes among different groups.
Project description:The goals of this study is to compare the differently expressed genes in abdominal aorta of C57BL/6 WT mice with or without Angiotensin II (AngII) treatment as well as differently expressed genes in the abdominal aorta of WT mice with AngII treatment with or without Qingda granules (QDG) treatment. The mice (n=15) were randomly divided into 3 groups:control, AngII and QDG treated (n=5 for each group). Mice in Control and AngII groups were infused with saline or 500 ng/kg/min of AngII respectively, and orally administrated with saline; while mice in AngII + QDG group were infused with AngII (500 ng/kg/min) and orally administrated with 1.145 g/kg /day of QDG for 2 weeks. Then the abdominal aorta were used to identify differentially expressed genes among different groups.
Project description:RNA sequencing to detect the differentially expressed genes in AngII infused mice after Ethoxysanguinarine, Baicalin, Gastrodin or Valsartan treatment
Project description:The goals of this study is to compare the differently expressed genes in abdominal aorta of Rab22a KO mice and Rab22a WT mice with or without Angiotensin II treatment for 14 days at the concentration of 500ng/kg/min.The mice (n=20) were randomly divided into 4 groups:WT+AngII,WT+NS,KO+AngII,KO+NS (n = 5 for each group). Mice in WT+NS and KO+NS groups were infused with saline or 500 ng/kg/min of WT+AngII and KO+AngII respectively. Then the abdominal aorta were used to identify differentially expressed genes among different groups.
Project description:Objective-Aortic pathologies exhibit sexual dimorphism, with aneurysms in the ascending, thoracic and abdominal aorta (AAA) exhibiting higher prevalence in males. Despite lower incidence of aortic vascular disease in women, aneurysms progress rapidly. Mechanisms for these sex differences are unclear. We defined the role of sex chromosome complement and testosterone in regional development and progression of angiotensin II (AngII)-induced vascular pathologies. Approach and Results-We used transgenic male mice expressing Sry on an autosome to create low density lipoprotein receptor (Ldlr) deficient male mice with an XY or XX sex chromosome complement. Subjects were then sham operated or orcheictomized. Transcriptional profiling on abdominal aortas from XY or XX males demonstrated1746 genes influenced by sex chromosomes, sex hormones, or an interaction. A second cohort of animals was then infused with AngII for 28 days. Diffuse aortic aneurysm pathology developed in XY AngII-infused males, while XX males developed discrete AAAs. Castration reduced all AngII-induced aortic pathologies in XY and XX males. Thoracic aortas from AngII-infused XY males, but not XX males exhibited adventitial thickening. We infused male XY and XX mice with saline or AngII and quantified mRNA abundance of key genes in thoracic versus abdominal aortas. Regional differences in mRNA abundance existed before AngII infusions, which were differentially influenced by AngII between genotypes. Prolonged AngII infusions resulted in AAA aortic wall thickening in XY males with diffuse aortic pathology, while XX males had dilated focal AAAs. Conclusions-An XY sex chromosome complement mediates diffuse aortic pathology, while an XX sex chromosome complement contributes to discrete AngII-induced AAAs.