目的 分析国人动脉中心收缩压分数（FSP）和舒张压分数（FDP）与动脉粥样硬化性肾动脉狭窄的相关性。方法 应用Lead2000多导生理记录仪描记入选研究对象中心压力曲线，并计算中心FSP和FDP以肾动脉造影结果作为分组依据，分为肾动脉狭窄...目的 分析国人动脉中心收缩压分数（FSP）和舒张压分数（FDP）与动脉粥样硬化性肾动脉狭窄的相关性。方法 应用Lead2000多导生理记录仪描记入选研究对象中心压力曲线，并计算中心FSP和FDP以肾动脉造影结果作为分组依据，分为肾动脉狭窄组71例和非肾动脉狭窄组489例，分析中心动脉血压分数FSP、FDP与肾动脉狭窄的关系。结果 肾动脉狭窄组的中心FSP显著高于非肾动脉狭窄组[分别为1．50±0．14 vs 1.39±0．11]，而中心FDP显著低于非肾动脉狭窄组[分别为0．75±0．071 vs 0．80±0．058]，（均P〈0．01）。Logistic回归分析结果示：中心的而非外周的FSP和FDP为影响肾动脉狭窄的独立危险因素（OR=1.092，95％CI=1．03～1．28 for FSP；OR=0．87，95％CI=0．37～0．94 for FDP）。结论 中心动脉FSP。展开更多
Background The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway and the extracellular signal-regulated kinases 1/2 (ERK 1/2 ) pathway are the two major independent signal transduct...Background The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway and the extracellular signal-regulated kinases 1/2 (ERK 1/2 ) pathway are the two major independent signal transduction pathways However, it has recently been found that STAT 3 may be negatively regulated by ERK 1/2 in gp130-dependent signaling Cardiotrophin-1 (CT-1), a potent novel hypertrophic cytokine, depends on gp130 to induce signaling and depends on STAT 3 to exert hypertrophic effect In this study, we examined whether STAT 3 activity was negatively regulated by ERK 1/2 during CT-1-induced signaling in rat cardiomyocytes and, if so, whether such crosstalk interfered with the hypertrophic effect of CT-1 and, furthermore, whether the mechanism underlying the crosstalk involved phosphorylation of serine 727 (S727) in STAT 3 Methods The activities of ERK 1/2 and STAT 3 were assessed by in-gel kinase assay and Western blot analysis, respectively The role of S727 phosphorylation in the crosstalk between ERK 1/2 and STAT 3 was determined by a transient transfection study using a STAT 3S727A mutant Cardiomyocyte hypertrophy was evaluated by the cellular protein-to-DNA ratio and [ 3H]-leucine incorporation Results CT-1 simultaneously activated both ERK 1/2 and STAT 3 in rat cardiomyocytes Inhibition of ERK 1/2 by U0126 resulted in an increase of CT-1-induced tyrosine phosphorylation of STAT 3 and, consequently, the protein-to-DNA ratio and [ 3H]-leucine incorporation Transient transfection of the cells with STAT 3S727A had no significant effect on CT-1-induced tyrosine phosphorylation of STAT 3 Conclusions STAT 3 is activated by CT-1 in rat cardiomyocytes, but full activation is mitigated by the simultaneous activation of ERK 1/2 The inhibition of ERK 1/2 increases the activity of STAT 3, which, in turn, enhances the hypertrophic effect of CT-1 The crosstalk between ERK 1/2 and STAT 3 is independent of the phosphorylation of the S727 in STAT 3 Such crosstalk may contribute to the development of adequate cardiac hypertrophy展开更多
文摘目的 分析国人动脉中心收缩压分数（FSP）和舒张压分数（FDP）与动脉粥样硬化性肾动脉狭窄的相关性。方法 应用Lead2000多导生理记录仪描记入选研究对象中心压力曲线，并计算中心FSP和FDP以肾动脉造影结果作为分组依据，分为肾动脉狭窄组71例和非肾动脉狭窄组489例，分析中心动脉血压分数FSP、FDP与肾动脉狭窄的关系。结果 肾动脉狭窄组的中心FSP显著高于非肾动脉狭窄组[分别为1．50±0．14 vs 1.39±0．11]，而中心FDP显著低于非肾动脉狭窄组[分别为0．75±0．071 vs 0．80±0．058]，（均P〈0．01）。Logistic回归分析结果示：中心的而非外周的FSP和FDP为影响肾动脉狭窄的独立危险因素（OR=1.092，95％CI=1．03～1．28 for FSP；OR=0．87，95％CI=0．37～0．94 for FDP）。结论 中心动脉FSP。
文摘Background The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway and the extracellular signal-regulated kinases 1/2 (ERK 1/2 ) pathway are the two major independent signal transduction pathways However, it has recently been found that STAT 3 may be negatively regulated by ERK 1/2 in gp130-dependent signaling Cardiotrophin-1 (CT-1), a potent novel hypertrophic cytokine, depends on gp130 to induce signaling and depends on STAT 3 to exert hypertrophic effect In this study, we examined whether STAT 3 activity was negatively regulated by ERK 1/2 during CT-1-induced signaling in rat cardiomyocytes and, if so, whether such crosstalk interfered with the hypertrophic effect of CT-1 and, furthermore, whether the mechanism underlying the crosstalk involved phosphorylation of serine 727 (S727) in STAT 3 Methods The activities of ERK 1/2 and STAT 3 were assessed by in-gel kinase assay and Western blot analysis, respectively The role of S727 phosphorylation in the crosstalk between ERK 1/2 and STAT 3 was determined by a transient transfection study using a STAT 3S727A mutant Cardiomyocyte hypertrophy was evaluated by the cellular protein-to-DNA ratio and [ 3H]-leucine incorporation Results CT-1 simultaneously activated both ERK 1/2 and STAT 3 in rat cardiomyocytes Inhibition of ERK 1/2 by U0126 resulted in an increase of CT-1-induced tyrosine phosphorylation of STAT 3 and, consequently, the protein-to-DNA ratio and [ 3H]-leucine incorporation Transient transfection of the cells with STAT 3S727A had no significant effect on CT-1-induced tyrosine phosphorylation of STAT 3 Conclusions STAT 3 is activated by CT-1 in rat cardiomyocytes, but full activation is mitigated by the simultaneous activation of ERK 1/2 The inhibition of ERK 1/2 increases the activity of STAT 3, which, in turn, enhances the hypertrophic effect of CT-1 The crosstalk between ERK 1/2 and STAT 3 is independent of the phosphorylation of the S727 in STAT 3 Such crosstalk may contribute to the development of adequate cardiac hypertrophy
