Association between plasma macrophage migration inhibitory factor concentration and coronary artery lesion severity / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between the plasma macrophage migration inhibitory factor (MIF), activator protein-1 (AP-1) and MMP-9 concentrations and the severity of coronary artery lesions in coronary heart disease (CHD) patients.</p><p><b>METHODS</b>Patients were divided into normal controls (n = 35), stable angina pectoris (SAP, n = 32) and acute coronary syndrome (ACS, n = 75) according to the coronary angiography (CAG), clinical and laboratory examinations. The CAG severity and extent of coronary lesions were analyzed by means of Gensini coronary score system. Enzyme linked immunosorent assay was used to measure the plasma MIF, AP-1 and MMP-9 concentrations.</p><p><b>RESULTS</b>Plasma MIF, AP-1 and MMP-9 concentrations were significant increased in CHD patients [MIF: (14.97 +/- 2.11) microg/L, AP-1: 1.43 +/- 0.33, MMP-9: (1.48 +/- 0.14) microg/L] compared to those in control group [MIF: (9.07 +/- 1.28) microg/L, AP-1: 0.71 +/- 0.13, MMP-9: (1.01 +/- 0.07) microg/L, all P < 0.05]. The MIF, AP-1 and MMP-9 concentrations in ACS group [MIF: (16.66 +/- 2.56) microg/L, AP-1: 1.56 +/- 0.22, MMP-9: (1.58 +/- 0.14) microg/L] were also significant higher than those in SAP group [MIF: (11.01 +/- 2.12) microg/L, AP-1: 1.04 +/- 0.25, MMP-9: (1.25 +/- 0.07) microg/L, all P < 0.05] and there was significant positive correlation between MIF, AP-1 and MMP-9 concentrations and the Gensini score of coronary artery lesions (all P < 0.05). AP-1 was positively correlated with MMP-9 in CHD patients (P < 0.05).</p><p><b>CONCLUSIONS</b>Plasma MIF, AP-1 and MMP-9 concentrations were positively correlated to the severity of coronary lesions in CHD patients. Higher MIF, AP-1 and MMP-9 concentrations in ACS patients than in SAP patients might suggest higher plaque instability in ACS patients.</p>

New insights into the activation mechanism of store-operated calcium channels: roles of STIM and Orai / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

The activation of Ca2+ entry through store-operated channels by agonists that deplete Ca2+ from the endoplasmic reticulum (ER) is a ubiquitous signaling mechanism, the molecular basis of which has remained elusive for the past two decades. Store-operated Ca2+-release-activated Ca2+ (CRAC) channels constitute the sole pathway for Ca2+ entry following antigen-receptor engagement. In a set of breakthrough studies over the past two years, stromal interaction molecule 1 (STIM1, the ER Ca2+ sensor) and Orai1 (a pore-forming subunit of the CRAC channel) have been identified. Here we review these recent studies and the insights they provide into the mechanism of store-operated Ca2+ channels (SOCCs).

Association between murine double minute 2 expression and AngII and ceramide induced endothelial cells apoptosis / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the relationship between murine double minute 2 (mdm2) expression and AngII and ceramide induced human umbilical endothelial cells apoptosis.</p><p><b>METHOD</b>Human umbilical endothelial cells (ECs) were cultured in vitro and treated with angiotensin II alone or in combination with losartan (an inhibitor of AT1), PD123319 (an inhibitor of AT2) and FB1 (an inhibitor of ceramidase) respectively. ECs were also treated with different doses of C2-ceramide. The apoptosis of ECs was detected with Tunel, the mdm2 mRNA and protein expressions were measured with reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.</p><p><b>RESULTS</b>PD123319 and FB1 but not losartan inhibited AngII induced ECs apoptosis and down-regulated the AngII induced increased mdm2 expressions. C2-ceramide also induces ECs apoptosis and down-regulated mdm2 expressions at protein and mRNA levels in a dose-dependent manner.</p><p><b>CONCLUSIONS</b>AngII binding with AT2 induces ECs apoptosis via ceramide. AngII and ceramide induce EC apoptosis by inhibiting mdm2.</p>

Stromal Interaction molecule 1 STIM1 Knockdown Inhibits Proliferation of Vascular Smooth Muscle Cells / 中华高血压杂志

Objective To explore the role of stromal interaction molecule 1(STIMI)on prohteration and intra- cellular Ca~(2+)change in vascular smooth muscle ceils(VSMC).Methods Rat VSMC were isolated from SD rats and primary cultured.Ad-si/rSTIM1 and Ad-hSTIM1 were transfected into VSMC.The protein of STIM1 was measured by Western blot,the proliferation of VSMC was analyzed by ~3H-thymidine(~3H-TdR)incorporation and cell count,the intracellular Ca~(2+)change was assessed By Aquaeosmos system.Ruselts Fourty-eight hours after transfection,as compared with Ad-hSTIMI group,the Ad-si/rSTIMI VSMC had lower expression of STIM1 protein (P

Angiotensin II up-regulates expression of inducible nitric oxide synthase in human umbilical endothelial cells: roles of AT1 and AT2 / 中华心血管病杂志

<p><b>OBJECTIVE</b>Angiotensin II is an important pro inflammation factor in the cardiovascular system. This experiment is aimed to study the effects of angiotensin II on inducible nitric oxide synthase expression in human umbilical endothelial cells.</p><p><b>METHODS</b>Human umbilical endothelial cells were cultured in vitro and treated with angiotensin II alone or in combination with AT1, AT2 and NF-kappaB inhibitors respectively. The inducible nitric oxide synthase expressions at protein and mRNA levels were measured with Western blot and reverse transcription-polymerase chain reaction (RT-PCR), and the activity of NF-kappaB was analyzed with EMSA.</p><p><b>RESULTS</b>Angiotensin II up-regulated inducible nitric oxide synthase expressions at the protein and mRNA levels at 5 h (P < 0.05), the activity of NF-kappaB was enhanced at 2 h (P < 0.05). These effects could be blocked by AT1 and NF-kappaB inhibitors but not by AT2 inhibitor.</p><p><b>CONCLUSION</b>Angiotensin II can upregulate the expression of inducible nitric oxide synthase through NF-kappaB pathway in human umbilical endothelial cells. AT1, other than AT2, play a key role in this process.</p>

Relationship of the expressions of PPAR-?mRNA and MMP-9 with coronary artery lesions in patients with coronary heart disease / 中华老年医学杂志

Objective To investigate the relationship of the levels of peroxisome proliferator- activated receptor-?(PPAR-?)mRNA,MMP-9 with the severity of coronary artery lesions in patients with coronary heart disease(CHD).Methods One hundred and fifty three patients with CHD who underwent coronary angiography were admitted.The expression of PPAR-?mRNA in lymphocytes of peripheral blood was detected by using RT-PCR,the level of MMP-9 enzyme was measured by enzyme-linked immunosorent assay,and the severity of coronary artery lesions were analyzed. Results As compared with control(0.624-0.13),PPAR-?mRNA expression was significantly lower in CHD patients(0.4+0.12).Negative correlation was found between PPAR-?mRNA and the classification(r=-0.56,P＜0.01)of coronary artery lesions,so was the number of coronary artery lesions(r=-0.42,P＜0.01).MMP-9 level was significantly higher in CHD patients(1.27?0.16)?g/L than that in controls(1.21?0.05)?g/L.Positive correlation was found between MMP-9 level and the classification(r=0.36,P＜0.01)of coronary artery lesions,so was the number of coronary artery lesions(r=0.30,P＜0.01).Negative correlation was also found between PPAR-?mRNA expression and MMP-9 level.Conclusions PPAR-?is a negative regulator of coronary artery lesions and PPAR-?inhibits the activation of MMP-9.It may be a valuable method for protecting patients from the incident of coronary artery disease to activate the expression of PPAR-?and decrease the level of MMP-9.