ABSTRACT
Objective: To explore the expression and clinical significance of serum long chain non-encoded RNAANRIL (LncRNA ANRIL) in chronic heart failure (CHF) patients. Methods: Our research included in 2 groups: CHF group, n=120 patients treated in our hospital and Control group, n=28 healthy subjects at the same period of time. Based on NYHA classification, CHF patients were further divided into 4 subgroups: NYHAⅠ subgroup, n=28, NYHA Ⅱ subgroup, n=34, NYHA Ⅲ subgroup, n=35 and NYHA Ⅳ subgroup, n=23. Expressions of serum ANRIL and cystatin C were examined by real time fluorescence quantitative PCR (QRT-PCR) and compared between 2 groups; the relationship between ANRIL, cystatin C and cardiac function were studied. Results: Compared with Control group, CHF group had increased serum levels of ANRIL and cystatin C, P<0.05. ANRIL expression was gradually increasing by cardiac function decreasing in CHF I to CHF Ⅳ subgroups, P<0.05. Correlation analysis found that serum level of ANRIL was positively related to cystatin C (r=0.873, P<0.001). ANRIL was elevated by increased left ventricular end diastolic diameter and decreased ejection fraction, both P<0.05. Conclusion: Serum ANRIL level has been related to CHF at certain degree which may indirectly reflect the severity of HF in relevant patients.
ABSTRACT
To study the relationship between tau hyperphosphorylation and the function of glutamate transporter okadaic acid (OA), a protein phosphatase inhibitor, 20 ng in a 0.5 microl volume, was injected into the frontal cortex of rat brain and immunostaining was used to observe the phosphorylation of tau protein and the expression of excitatory amino acid transporter 1 (EAAT1) in the brain following the injection. The results showed that (1) the neurons in the center of the injection region displayed cytoplasmic shrinkage, swelling, nuclear pyknosis, and dislocation at the early stage, and necrosis appeared 3 d after the injection. However, most neurons in the peri-injected areas showed normal morphological characters with immuno positive reaction for AT8, a tau phosphorylated marker; (2) morphological analysis showed that tau hyperphosphorylation caused by OA treatment was mainly observed in the axons and dendrites of neuronal cells at 6 h in the cell body at 1 d, which brought about dystrophic neurites and neurofibrillary tangle (NFT)-like pathological changes; (3) the induction of glutamate transporter EAAT1 was observed in the involved areas corresponding to that with AT8 immunopositive staining, and the number of EAAT1-positive staining cells markedly increased at 12 h (P<0.01), peaked at 1 d (P<0.001), then decreased at 3 d following the injection. Combined with a confocal laser scanning microscopic analysis, double fluorescent immunostaining showed that EAAT1 positive staining appeared in neurons as well as astrocytes in the peri-injected areas of the frontal cortex. These results demonstrate that OA increases glutamate transporter EAAT1 expression in neurons while it induces tau hyperphosphorylation. However, the mechanism and significance of the induction of glutamate transporter EAAT1 expression remain to be further elucidated.