ABSTRACT
Objective: To explore the mechanism of Profilin-1 in regulating eNOS/NO pathway and its role in the development of myocardial hypertrophy. Methods: Spontaneously hypertensive rats (SHR) aged 5 weeks were injected with different adenovirus vectors to induce Profilin-1 expression knockdown (SHR-I) or over express (SHR-H) or to use as control (SHR-C). All these treatment were compared with Wistar-Kyoto rats (SKY) treated with control adenovirus vectors (WKY-C). The same injection was executed at the sixth week during the experiment of 12 weeks. After experiment, the left ventricular weight-to-heart weight ratio (LVW/HW) and left ventricular long axis (LVLA) were measured. Meanwhile, NO contents in blood and myocardium, Profilin-1, eNOS and Caveolin-3 mRNA and protein levels and phosphorylated eNOS (P-eNOS) protein level in myocardium were determined. Results: Compared with WKY-C group, the SHR-C group was statistically higher in LVW/HW (0.79±0.03), LVLA (11.82±0.58 mm) and Profilin-1 mRNA and protein level (P<0.05), but lower in NO content [(18.63±6.23) μmol/L] in blood and [(2.71±0.17) μmol/L] in myocardium), eNOS activity and Caveolin-3 expression (P<0.05). The over expressing Profilin-1 led SHR-H group to a higher value of LVW/HW [(0.93±0.03) mm and LVLA (14.17±0.69) mm] in comparison with SHR-C group (P<0.05), and to a lower value of NO content (in myocardium), eNOS activity and Caveolin-3 expression (P<0.05); however, this phenomenon was reversed by the knockdown Profilin-1 expression (SHR-I group). Conclusions: Profilin-1 expression, being negative in regulating Caveolin-3 expression and eNOS/NO pathway activity, promotes the development of myocardial hypertrophy which can be reversed by Profilin-1 silencing.
ABSTRACT
Objective: To investigate the relationship between the expression level of miR-155 and the severity of coronary lesion, and explore the action mechanism. Methods: Peripheral blood mononuclear cells (PBMC) were isolated form blood simple from patients with acute myocardial infarction (AMI), unstable angina (UAP), stable angina (SAP) and chest pain syndrome (CPS). RT-PCR was performed to analysis the expression level of miR-155 in peripheral blood mononuclear cells, plasma and RAW264.7 macrophagocyte. MTT was used to analyze the cell viability of OxLDL treated RAW264.7 macrophagocyte. Results: The expression level of miR-155 in blood sample from coronary heart disease patients was much lower than in the blood sample of non-coronary heart disease (. P<0.05). The level of miR-155 in PBMCs was much higher in the blood sample from CPS group than the other three group, and the level of miR-155 in plasma was higher in the CPS group than in the UAP and the AMI group, the difference was statistically significant (. P<0.05). The expression level of miR-155 in PBMCs is positively associated with the level in the plasma (. r=0.861, P=0.000). OxLDL can induce the expression of miR-155 in RAW264.7 macrophagocyte, decrease the cell viability of RAW264.7 macrophagocyte, and with the concentration and the treatment time of OxLDL increased, the effort become more obvious. The inhibition effort of OxLDL to RAW264.7 macrophagocyte with high miR-155 expression is much lower than the control group, and it is statistically significant after treated for 12, 24 and 48 h. Conclusions: miR-155 plays a protective role in the progression of atherosclerosis, and it may be achieved by reducing the apoptosis effort of OxLDL to RAW264.7 macrophagocyte.
ABSTRACT
OBJECTIVE@#To investigate the relationship between the expression level of miR-155 and the severity of coronary lesion, and explore the action mechanism.@*METHODS@#Peripheral blood mononuclear cells (PBMC) were isolated form blood simple from patients with acute myocardial infarction (AMI), unstable angina (UAP), stable angina (SAP) and chest pain syndrome (CPS). RT-PCR was performed to analysis the expression level of miR-155 in peripheral blood mononuclear cells, plasma and RAW264.7 macrophagocyte. MTT was used to analyze the cell viability of OxLDL treated RAW264.7 macrophagocyte.@*RESULTS@#The expression level of miR-155 in blood sample from coronary heart disease patients was much lower than in the blood sample of non-coronary heart disease (P<0.05). The level of miR-155 in PBMCs was much higher in the blood sample from CPS group than the other three group, and the level of miR-155 in plasma was higher in the CPS group than in the UAP and the AMI group, the difference was statistically significant (P<0.05). The expression level of miR-155 in PBMCs is positively associated with the level in the plasma (r=0.861, P=0.000). OxLDL can induce the expression of miR-155 in RAW264.7 macrophagocyte, decrease the cell viability of RAW264.7 macrophagocyte, and with the concentration and the treatment time of OxLDL increased, the effort become more obvious. The inhibition effort of OxLDL to RAW264.7 macrophagocyte with high miR-155 expression is much lower than the control group, and it is statistically significant after treated for 12, 24 and 48 h.@*CONCLUSIONS@#miR-155 plays a protective role in the progression of atherosclerosis, and it may be achieved by reducing the apoptosis effort of OxLDL to RAW264.7 macrophagocyte.
ABSTRACT
OBJECTIVE@#To explore the mechanism of Profilin-1 in regulating eNOS/NO pathway and its role in the development of myocardial hypertrophy.@*METHODS@#Spontaneously hypertensive rats (SHR) aged 5 weeks were injected with different adenovirus vectors to induce Profilin-1 expression knockdown (SHR-I) or over express (SHR-H) or to use as control (SHR-C). All these treatment were compared with Wistar-Kyoto rats (SKY) treated with control adenovirus vectors (WKY-C). The same injection was executed at the sixth week during the experiment of 12 weeks. After experiment, the left ventricular weight-to-heart weight ratio (LVW/HW) and left ventricular long axis (LVLA) were measured. Meanwhile, NO contents in blood and myocardium, Profilin-1, eNOS and Caveolin-3 mRNA and protein levels and phosphorylated eNOS (P-eNOS) protein level in myocardium were determined.@*RESULTS@#Compared with WKY-C group, the SHR-C group was statistically higher in LVW/HW (0.79±0.03), LVLA (11.82±0.58 mm) and Profilin-1 mRNA and protein level (P<0.05), but lower in NO content [(18.63±6.23) μmol/L] in blood and [(2.71±0.17) μmol/L] in myocardium), eNOS activity and Caveolin-3 expression (P<0.05). The over expressing Profilin-1 led SHR-H group to a higher value of LVW/HW [(0.93±0.03) mm and LVLA (14.17±0.69) mm] in comparison with SHR-C group (P<0.05), and to a lower value of NO content (in myocardium), eNOS activity and Caveolin-3 expression (P<0.05); however, this phenomenon was reversed by the knockdown Profilin-1 expression (SHR-I group).@*CONCLUSIONS@#Profilin-1 expression, being negative in regulating Caveolin-3 expression and eNOS/NO pathway activity, promotes the development of myocardial hypertrophy which can be reversed by Profilin-1 silencing.
ABSTRACT
<p><b>OBJECTIVE</b>To exacted analysis each time interval in isovolumic relaxation time (IVRT) of normal subjects through observin the changes of cardiac structure and hemodynamics during the IVRT. Then to provide the evidence of cardiac resynchronization therapy.</p><p><b>METHODS</b>Quantitative analysis was performed for 60 subjects. The dual-channel echocardiography(DCE), pulse wave doppler (PW) and tissue wave dapper (TDI) examination of all the subjects were recorded, and IVRT was divided into two intervals, isovolumic relaxation time of early intervals (IVRTe) and isovolumic relaxation time of late interval (IVRT1). Then measured the time of each interval. Indicators were used including: (1) IVRT; (2) IVRTe; (3) IVRTI; (4) IVRTI/IVRT; calculating the data after heart rate corrected; (5) cIVRT; (6) clVRTe; (7) clVRTI; (8) clVRTI/clVRT; (9) measuring the time difference in mitral blood and tissue (TE-é) of DCE group.</p><p><b>RESULTS</b>The i-wave within IVRT in PW images was found in 45 subjects, and the i-wave was about 1/2 of IVRT (49.17 +/- 5.37) ms. IVRT was divided into IVRTe and IVRTI by a turning point at descending branch of i-wave as t-point. The j-wave was observed in 84% TDI images, and the j-wave was about 1/2 of IVRT (43.13 +/- 4.83) ms. IVRT was divided into IVRTe and IVRTI by a turning point of the onset of j-wave as t-point. A significant difference was found between PW and TDI with measurement of IVRT, IVRTe, IVRTI (P < 0.05). There were no significant differences between the common group and DCE group (P > 0.05). After heart rate corrected, the data showed no significant difference using pairwise comparisons among the three groups (P > 0.05). The mean and standard deviation of IVRTI/IVRT, cIVRTI/clVRT were (0.50 +/- 0.12) ms. There were little difference of time intervals and good consistenc using DCE measured IVRT with multiple tests confinmed.</p><p><b>CONCLUSION</b>The study found that IVRT might be divided into IVRTe and IVRT1 phases. There were i-wave in IVRTe and j-wave in IVRT1. The t-point was nearly midpoint inisovolumic relaxation time.</p>