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Proteomic analysis of mitochondria reveals a metabolic switch from fatty acid oxidation to glycolysis in the failing heart

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Science China(Life Sciences) 2009年第11期52卷 1003-1010页

作者： WANG Jun1,2, BAI Ling1,2, LI Jing3, SUN ChaoFeng1,2, ZHAO Jin1, CUI ChangCong1,2, HAN Ke1,2, LIU Yu1,2, ZHUO xiaoZhen1,2, WANG TingZhong1,2, LIU Ping1,2, FAN FenLing1,2, GUAN YouFei3 & MA AiQun1,2 1 Department of Cardiology, First affiliated hospital of medical college of xi’an Jiaotong University, xi’an 71.061. China 2.ion channel disease laboratory, key laboratory of environment and genes related to diseases of education ministry, xi’an 71.061. China 3 Department of Physiology and Pathophysiology key laboratory of Molecular Cardiovascular Sciences of the ministry of education, Peking University Health Science Center, Beijing 100083, China 1. Department of Cardiology First affiliated hospital of medical college of Xi’an Jiaotong University Xi’an 710061 China 2. ion channel disease laboratory Key Laboratory of Environment and Genes Related to Diseases of Education Ministry Xi’an 710061 China 3. Department of Physiology and Pathophysiology key laboratory of Molecular Cardiovascular Sciences of the ministry of education Peking University Health Science Center Beijing 100083 China

This work characterizes the mitochondrial proteomic profile in the failing heart and elucidates the molecular basis of mitochondria in heart failure. Heart failure was induced in rats by myocardial infarction, and mitochondria were isolated from hearts by differential centrifugation. Using two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization-time of flight mass spectrometry, a system biology approach was employed to investigate differences in mitochondrial proteins between normal and failing hearts. Mass spectrometry identified 27 proteins differentially expressed that involved in energy metabolism. Among those, the up-regulated proteins included tricarboxylic acid cycle enzymes and pyruvate dehydrogenase complex subunits while the down-regulated proteins were involved in fatty acid oxidation and the OXPHOS complex. These results suggest a substantial metabolic switch from free fatty acid oxidation to glycolysis in heart failure and provide molecular evidence for alterations in the structural and functional parameters of mitochondria that may contribute to cardiac dysfunction during ischemic injury.

关键词： mitochondria heart failure proteome two-dimensional electrophoresis energy metabolism

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Effects of lanthanum on calcium-activated K^+ currents and its kinetics in MC3T3 cells

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Science China Chemistry 2010年第6期53卷 1281-1286页

作者： ZHANG LiPing1,2 & YANG Pin1 1key laboratory of Chemical Biology and Molecular Engineering of ministry of education Institute of Molecular Science,Shanxi University,Taiyuan 030006,China 2College of environment and Safety,Taiyuan University of Science and Technology,Taiyuan 030024,China 1. key laboratory of Chemical Biology and Molecular Engineering of ministry of education Institute of Molecular Science Shanxi University Taiyuan 030006 China2. College of Environment and Safety Taiyuan University of Science and Technology Taiyuan 030024 China

Using the whole cell patch-clamp technique,we studied the effects of La3+ on calcium-activated K+ currents and its kinetics of activation and inactivation in non-excitable MC3T3 *** results showed that the calcium-activated outward K+ currents were promoted with increasing concentration of Ca2+ in the pipette solution and a voltage- and Ca2+-dependent ***3+ in the bath solution inhibited the currents in a concentration-dependent manner and the inhibition EC50 was 8.23 ± 1.45 μmol/*** the concentration of 50 μmol/L,La3+ significantly changed the Vh of the activation curve and shifted the activation curve to more positive potentials,but shifted the inactivation curve to more negative *** had no effect on the slope factor k of the activation and inactivation *** currents inhibition could induce a series of physiological and molecular biological functions,presumably because of its ability to depolarize the plasma membrane and enhance cell excitability,resulting in increasing Ca2+ influx and cytoplast Ca2+ *** process may be one of the molecular mechanisms by which La3+ affects the cell growth and function of MC3T3 cells.

关键词： MC3T3 cell potassium ion channel La3+ patch-clamp technique

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Chronic salt-loading downregulates large-conductance Ca^(2+)-activated potassium channel in mesenteric arterial smooth muscle cells from SD rats

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Journal of Pharmaceutical Analysis 2009年第4期21卷 215-221页

作者： Zhao-xia Zhou,Chao-feng Sun,Ai-qun Ma,Fang-yuan Chen,Na Wei,Fu-qiang Liu Department of Cardiovascular Medicine,the First Affiliated Hospital,Medical School of xi’an Jiaotong University Institute of Cardiovascular channelopathy,key laboratory of environment and genes related to diseases(xi’an Jiaotong University),ministry of education,xi’an 71.061.China DepartmentofCardiovascularMedicine theFirstAffiliatedHospitalMedicalSchoolofXi'anJiaotongUniversity InstituteofCardiovascularchannelopath KeyLaboratoryofEnvironmentandGenesRelatedtoDiseasesMinistryofEducationXi'an710061

Objective Large-conductance calcium-activated potassium(BKCa)channel modulates vascular smooth muscle *** the present study,we tested the hypothesis that salt,one of the factors which significantly influence blood pressure(BP),can regulate BKCa activity and then elevate blood *** Male Sprague-Dawley rats aged 6 weeks were randomized into high salt diet group(HS)and control group,fed with high salt diet(containing 5% NaCl)and standard rat chow(containing 0.4% NaCl)respectively for 16 *** systolic blood pressure(SBP),body weight(BW)and 24-hour urinary output were tested every 4 *** of urinary Na+ was detected using flame spectrophotometrical *** the end of 16 weeks,all the rats were killed,the mesenteric arteries were obtained,and single mesenteric smooth muscle cells were isolated at *** resting membrane potential(Em),the total potassium currents and the currents after perfusion with TEA solution of the cells were all recorded by whole cell patch *** transcriptions of BKCa channel α and β1 subunits in mesenteric arterial vascular smooth muscle cells(VSMC)of each group were calculated by real-time *** There was no difference in SBP and BW at each stage between control group and HS group;the urinary Na+ level in HS animals was elevated significantly after 4 *** negative values of Em in HS group VSMCs were reduced compared with those in the control *** of β1 subunit of BKCa channels were decreased in HS group,but α subunit transcriptions did not differ between the two *** cell potassium currents did not differ between HS and control groups,but BKCa currents of HS group VSMCs were lower than those of control group *** Even without elevating SBP,salt-loading can still modulate the expression and activity of BKCa channel in the mesenteric arterial VSMC and elevate vascular tone.

关键词： chronic salt-loading large-conductance calcium-activated potassium channel blood pressure

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μ-opioid presynaptic inhibition of GABA release in rat ventrolateral orbital cortex neurons

μ-opioid presynaptic inhibition of GABA release in rat vent...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Chao-Ling QU~1,Fu-Quan HUO~1,Fen-Sheng HUANG~1,Yun-Qing LI~2,Jing-Shi TANG~1 1 Department of Physiology and Pathophysiology,xi''an Jiaotong University School of Medicine,key laboratory of environment and genes related to diseases,ministry of education,xi''an 71.061.2 Department of Anatomy and K.K.Leung Brain Research Centre,The Fourth Military Medical University,xi''an 710032

＜正＞Previous studies have indicated that the ventrolateral orbital cortex（VLO） is involved in modulation of nociception as part of an endogenous analgesic system consisting of the spinal cord-nucleus submedius（Sm）-VLO-periaqueductal gray（PAG）-spinal cord *** of morphine into the VLO depresses the rat tail-flick reflex and suggests that the GABAergic modulation may be involved in the VLO morphine-induced *** provide electrophysiological evidence for the GABAergic modulation mechanism,the present study examined whether the presynapticμ-opioid activation inhibited release of the GAB A neurotransmitter in rat VLO *** TTX,a voltage-dependent Na+ channel blocker and kynurentic acid,a non-selective excitatory amino acid receptor antagonist,pharmacologically separated spontaneous GABAergic miniature inhibitory postsynaptic currents（mIPSCs） were recorded using the whole-cell patch clamp *** results showed that DAMGO,a specificμ-opioid receptor agonist,inhibited mlPSCs frequency in a dose-dependent manner without affecting mIPSC amplitude in the same VLO *** presynaptic opioid effect was blocked by CTOP,a specificμ-opioid receptor *** alone application did not affect the mIPSC amplitude or *** results provide support for the hypotheses that GABAergic modulation is involved in the opioidinduced antinociception,i.e.,theμ-opioid receptor activation presynaptically inhibits the inhibitory effect of GABAergic neurons on the projection neurons leading to activation of the VLO-PAG brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal cord level.

关键词： ventrolateral orbital cortex mIPSCs DAMGO CTOP whole-cell patch clamp

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多质粒共转染建立Cav1.3 L-型钙通道的研究模型

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陕西医学杂志 2009年第6期38卷 643-644,647页

作者：强华魏峰张爱峰史瑞明孙超峰马爱群西安交通大学医学院第一附属医院心内科教育部环境与疾病相关基因重点实验室离子通道病室西安710061

目的:提高多质粒转染效率,建立钙离子通道的研究模型。方法:在传统的脂质体转染过程中,通过不断调整细胞密度、转染质粒DNA的量,将含Cav1.3L-型钙通道相关亚基的质粒DNA转染至HEK293T细胞,采用全细胞膜片钳技术检测Cav1.3L-型钙通道的... 详细信息

目的:提高多质粒转染效率,建立钙离子通道的研究模型。方法:在传统的脂质体转染过程中,通过不断调整细胞密度、转染质粒DNA的量,将含Cav1.3L-型钙通道相关亚基的质粒DNA转染至HEK293T细胞,采用全细胞膜片钳技术检测Cav1.3L-型钙通道的电流表达。结果:转染后的HEK293T细胞在荧光显微镜下可见明显的绿色荧光;全细胞膜片钳技术检测出Cav1.3 L-型钙通道电流的表达。结论:通过调整细胞密度和转染质粒DNA的量,可以提高脂质体介导多质粒共转染HEK293T细胞的效率,建立钙离子通道的研究模型。

关键词：钙通道,L型基因脂质体 @人胚胎肾 293T细胞

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比索洛尔对心力衰竭兔心肌细胞L型钙通道的影响

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西安交通大学学报（医学版） 2021年第6期42卷 823-828页

作者：李溪王亭忠卢群韩克卓小桢马爱群宁夏医科大学总医院心脑血管病医院心内科宁夏银川750001 西安交通大学第一附属医院心内科教育部环境与疾病相关基因重点实验室陕西省分子心脏病学重点实验室陕西西安710061

目的探讨比索洛尔对心力衰竭兔心肌细胞ICa,L通道的影响。方法选择82只新西兰兔制备容量联合压力超负荷心力衰竭兔模型,随机分为假手术组(SO)、心力衰竭组(HF)、比索洛尔干预组(BF)。通过Real-time PCR和Western blotting法检测比索洛... 详细信息

目的探讨比索洛尔对心力衰竭兔心肌细胞ICa,L通道的影响。方法选择82只新西兰兔制备容量联合压力超负荷心力衰竭兔模型,随机分为假手术组(SO)、心力衰竭组(HF)、比索洛尔干预组(BF)。通过Real-time PCR和Western blotting法检测比索洛尔对心衰兔左室心肌细胞ICa,L表达的影响;通过膜片钳技术检测比索洛尔对心衰兔左室心肌细胞ICa,L功能的影响。结果 (1)心脏彩超及BNP等结果显示比索洛尔可以改善HF兔的心脏重构(P2)HF组兔心肌细胞ICa,L通道mRNA和蛋白的表达明显减低,BF组ICa,L通道表达没有上调(P>0.05);(3)HF兔心肌细胞电容增大,ICa,L激活速度加快,电流密度明显降低;BF组心肌细胞电容、ICa,L激活和电流密度没有明显改变;(4)HF组ICa,L通道激活曲线左移,使窗电流(window current)增大,BF组ICa,L通道的失活速度加快,使窗电流减小。结论比索洛尔可以改善心衰兔心功能,还可以影响心衰兔心肌细胞ICa,L的功能。

关键词：心力衰竭离子通道 L型钙通道比索洛尔

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