ABSTRACT
MicroRNAs (miRNAs) are small endogenous non-coding RNA molecules.They regulate negatively the expression of target genes at post-transcriptional stages by means of affecting the stability of target mRNA or interfering with the transcriptional process.Recently,there is evidence demonstrating that miRNAs play important roles in the gene expressions of thyrotoxic heart diseases.Elevated levels of thyroid hormones profoundly influence the cardiovascular system through the renin-angiotensin system (RAS).As a principal active component of RAS,angiotensin Ⅱ receptor 1 (AT1 R) interacts with miRNAs in promoting or extenuating the progress of thyrotoxic heart disease.In this article,the roles of AT1R-associated miRNAs,miR-21,miR-155,miR-208a/b,and miR-499 in thyrotoxic heart disease were reviewed.
ABSTRACT
Type 2 diabetes mellitus (T2DM) is one of the most serious public health problems,while the detailed mechanisms underlying its pathology remain obscure.MicroRNAs (miRNAs),which are single-stranded noncoding RNAs,are considered to be involved in various pathological processes,especially in T2DM.MiRNA has become a noval player in insulin resistance,islet dysfunction,and even in the diabetes related complications.
ABSTRACT
It is evident that metabolic memory,whereby diabetic complications continue to develop and progress in individuals who returned to normal glycemic control after a period of transient hyperglycemia,has long lasting effects.Recent studies suggest that “metabolic memory” may be due to epigenetic changes in target oells.Understanding the molecular changes in chromatin structure and the functional relationship with altered signaling pathways is now considered to represent an important conceptual challenge to explain diabetes and the phenomenon of metabolic memory.Emerging evidences indicate that critical gene-activating epigenetic changes may confer future cell memories. Many experimental evidences show that histone acetyltransferases (HATs), histone deacetylases (HDACs),histone methyltransferases (HMTs),histone lysine demethylases (KDMs),and microRNAs play important roles in the epigenetic changes of several key genes related to diabetic complications. Transient hyperglycemia promotes gene-activating epigenetic changes and signaling events critical in the development and progression of diabetic vascular complications.Further characterisation of these glucose-induced epigenetic events and the identification of key enzymes involved will help us to develop new therapeutic strategies for diabetes and its complications.
ABSTRACT
Cultured primary human umbilical vein endothelial cells (HUVECs) were divided into 4 groups:normal control( NG ),persistent high glucose ( HG ),hyperglycemia group ( TG ),and mannitol control ( MA )groups.After 1,4,and 7 days of culture,cells were collected.Cell proliferation,cell apoptosis,ROS,SOD,MDA,and NO level,eNOS mRNA and protein level were measured.Endothelial cell proliferation was inhibited in HG,TG,and MA groups compared with NG group.Hyperglycemia memory induced apoptosis of endothelial cells,increased ROS and MDA generation,and down-regulated intracellular SOD level,findings similar to those in HG group.After 24 h of culturing,eNOS expression and NO generation in both HG and TG groups were higher than those in NG group.However,after 7 days of culturing,eNOS expression and NO generation in both HG and TG groups were lower than those in NG group.These results suggest that in hyperglycemia memory cell model,transient hyperglysemia may lead to persistent imbalance in oxidative stress and reduce endothelium-derived relaxing factor NO level,indicating that hyperglycemia memory may play an important role in persistent vascular endothelial cell injury.
ABSTRACT
Wistar rats(n=24) were divided into normal control group(NC), food restriction group(FR), and catch-up group(RN). Serum glucose,lipids, gastrin, the ratio of visceral fat to body fat, adipocyte CCK2R mRNA and protein levels were determined. Compared with NC group, FR rats had lower serum gastrin and visceral fat formation. The adipocyte CCK2R mRNA and protein levels of FR rats were lower than those of NC rats. Serum gastrin level of RN rats was higher than those of FR and NC rats(P＜0.05). The ratio of visceral fat to body fat in RN rats increased compared with FR rats and was close to that of NC rats. The adipocyte CCK2R mRNA and protein levels of RN rats were higher than those of FR and NC rats. Gastrin and its receptor pathway possibly play a role in the mechanism of visceral fat accumulation in catch-up rats.