ABSTRACT
The Ly-6 and uPAR (LU) domain-containing proteins represent a large family of cell-surface markers. In particular, mouse Ly-6A/Sca-1 is a widely used marker for various stem cells; however, its human ortholog is missing. In this study, based on a systematic survey and comparative genomic study of mouse and human LU domain-containing proteins, we identified a previously unannotated human gene encoding the candidate ortholog of mouse Ly-6A/Sca-1. This gene, hereby named LY6A, reversely overlaps with a lncRNA gene in the majority of exonic sequences. We found that LY6A is aberrantly expressed in pituitary tumors, but not in normal pituitary tissues, and may contribute to tumorigenesis. Similar to mouse Ly-6A/Sca-1, human LY6A is also upregulated by interferon, suggesting a conserved transcriptional regulatory mechanism between humans and mice. We cloned the full-length LY6A cDNA, whose encoded protein sequence, domain architecture, and exon-intron structures are all well conserved with mouse Ly-6A/Sca-1. Ectopic expression of the LY6A protein in cells demonstrates that it acts the same as mouse Ly-6A/Sca-1 in their processing and glycosylphosphatidylinositol anchoring to the cell membrane. Collectively, these studies unveil a novel human gene encoding a candidate biomarker and provide an interesting model gene for studying gene regulatory and evolutionary mechanisms.
Subject(s)
Humans , Membrane Proteins/genetics , Pituitary Neoplasms/genetics , BiomarkersABSTRACT
BACKGROUND:Proliferation, migration and phenotypic changes of vascular smooth muscle cells is the core of the occurrence of atherosclerosis, and a series of related genes via methylation are involved in the process. OBJECTIVE:To investigate the effects of oxidized low density lipoprotein (ox-LDL) on DNA methylation in the promoter region of the p21 gene and its potential mechanism in the pathogenesis of atherosclerosis. METHODCultured human vascular smooth muscle cells were treated with different concentrations of ox-LDL (0, 10, 20, 40 mg/L) for 24 hours. The degree of DNA methylation was assayed by methylation-specific polymerase chain reaction, the expression of p21 mRNA was measured by reverse transcriptional polymerase chain reaction and the proliferative activity of vascular smooth muscle cells was determined by the MTT assay. RESULTS AND CONCLUSION:The ox-LDL treatment resulted in a promotion in the methylation in the promoter region of the p21 gene and a decrease in mRNA expression with a concentration-dependent manner;it also induced a dose-dependent promoting effect on vascular smooth muscle cellproliferation. The atherogenic mechanism of ox-LDL might promote vascular smooth muscle cellproliferation by the hypermethylation of the p21 gene that may lead to the occurrence and development of atherosclerosis.
ABSTRACT
Objective To investigate the role of total bile acid (TBA) in pathogenesis of essential hypertension.Methods The concentration of serum TBA was measured by enzymatic method in 127 cases including 30 healthy controls,21 secondary hypertensive patients and 76 essential hypertensive patients.Results There was a significant increase of TBA in essential hypertensive group compared with that of control group and secondary hypertension (P 0.05) .In essential hypertensive group,the levels of TBA in grade 3 hypertension were higher than that of grade 1 hypertension (P0.05).Conclusion The abnormal increasing of TBA may play a role in pathogenesis of essential hypertension.
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Objectives To study the relationship between the severity of coronary lesions and serum uric acid.Methods Coronary heart disease(CHD) was diagnosed or excluded by coronary angiography; concentration of serum uric acid was measured with method of uric acid enzyme.Relationship between the severity of coronary lesions and serum uric acid was analysed by linear correlation and multiple stepwise regression.Results The level of serum uric acid in CHD group was significantly higher than that of control group(P
ABSTRACT
AIM: To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of G?q/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP 3 was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats ( P 0.05). At 10 days, the level of IP 3 significantly increased in left ventricle of CA rats compared with the control animals ( P
ABSTRACT
AIM: To investigate the changes of Gq-phosphoinositide pathway in left ventricular tissue of rats with chronic heart failure in order to assess the role of this signal pathway in the formation of heart failure. METHODS: Male Sprague-Dawle rats were divided into three groups: control, chronic heart failure and benazepril therapy group. Chronic heart failure was induced with adriamycin. Rats in benazepril group received benazepril 10 mg?kg-1?d-1 and adriamycin at the same time. Hemodynamic measurement was carried out after 4 weeks. The expression of G? q/11 protein in left ventricle was detected by Western blotting analysis and activity of phospholipase C was measured by the method of hydrolysis of nuclear substrate. RESULTS: Compared with control group, the ?dp/dtmax in chronic heart failure group significantly decreased, and protein G? q/11 expression, basic and stimulated phospholipase C activity significantly increased (P
