Abnormal sarcoplasmic reticulum Ca2+-sequestering properties in skeletal muscle in chronic obstructive pulmonary disease.
Abnormal sarcoplasmic reticulum Ca2+-sequestering properties in skeletal muscle in chronic obstructive pulmonary disease.
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慢性阻塞性肺疾病骨骼肌中异常肌浆网 Ca2 隔离特性。
DOI：
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Ouyang Jing
中科院分区：
文献类型：
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作者：
H. Green;M. Burnett;Todd A. Duhamel;C. D’Arsigny;D. E. O'Donnell;K. Webb;Ouyang Jing
本研究的目的是调查以下假设：中度至重度慢性阻塞性肺疾病 (COPD) 患者的骨骼肌中会发生肌浆网 (SR) Ca(2+) 循环特性的改变。为了研究这一假设，从 8 名 COPD 患者的股外侧肌中获取了组织样本 [年龄 65.6 +/- 3.2 岁； 1 秒用力呼气量 (FEV(1))/用力肺活量 (FVC) = 44 +/- 2%；对 10 名健康年龄匹配对照（CON，年龄 67.5 +/- 2.5 岁；FEV(1)/FVC = 77 +/- 2%）和匀浆进行了广泛的 SR 特性分析。与 CON 相比，COPD 显示（以 mumol.g 蛋白(-1).min(-1) 计）最大 Ca(2+)-ATP 酶活性[最大速度 (V(max))，158 +/- 10 与 133 +/- 7，P < 0.05] 降低 16%，Ca(2+) 摄取降低 17%（4.65 +/- 0.039 与 3.85 +/-） 0.26，P < 0.05），这是在 Ca(2+) 释放没有差异的情况下发生的。 COPD 中 V(max) 较低还伴随着 Ca(2+) 敏感性降低 11% (P < 0.05)，通过 Hill 系数测量（定义为 10-90% V(max) 时 Ca(2+)-ATPase 活性与游离胞质 Ca(2+) 浓度之间的关系）。对于肌（内）质网Ca(2+)-ATP酶（SERCA）亚型，COPD患者SERCA1a升高16%（P < 0.05），SERCA2a降低14%（P < 0.05）。结论是中度至重度 COPD 导致 SR Ca(2+)-ATPase 特性异常，而这不能用 SERCA 同工型表型的变化来解释。 SERCA 在 COPD 中催化性能的降低表明 Ca(2+) 循环受到干扰，可能导致 Ca(2+) 介导的机械功能和/或第二信使调节过程受损。
The objective of this study was to investigate the hypothesis that alterations in sarcoplasmic reticulum (SR) Ca(2+)-cycling properties would occur in skeletal muscle in patients with moderate to severe chronic obstructive pulmonary disease (COPD). To investigate this hypothesis, tissue samples were obtained from the vastus lateralis of 8 patients with COPD [age 65.6 +/- 3.2 yr; forced expiratory volume in 1 s (FEV(1))/forced vital capacity (FVC) = 44 +/- 2%; mean +/- SE] and 10 healthy age-matched controls (CON, age 67.5 +/- 2.5 yr; FEV(1)/FVC = 77 +/- 2%), and homogenates were analyzed for a wide range of SR properties. Compared with CON, COPD displayed (in mumol.g protein(-1).min(-1)) a 16% lower maximal Ca(2+)-ATPase activity [maximal velocity (V(max)), 158 +/- 10 vs. 133 +/- 7, P < 0.05] and a 17% lower Ca(2+) uptake (4.65 +/- 0.039 vs. 3.85 +/- 0.26, P < 0.05) that occurred in the absence of differences in Ca(2+) release. The lower V(max) in COPD was also accompanied by an 11% lower (P < 0.05) Ca(2+) sensitivity, as measured by the Hill coefficient (defined as the relationship between Ca(2+)-ATPase activity and free cytosolic Ca(2+) concentration for 10-90% V(max)). For the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) isoforms, SERCA1a was 16% higher (P < 0.05) and SERCA2a was 14% lower (P < 0.05) in COPD. It is concluded that moderate to severe COPD results in abnormalities in SR Ca(2+)-ATPase properties that cannot be explained by changes in the SERCA isoform phenotypes. The reduced catalytic properties of SERCA in COPD suggest a disturbance in Ca(2+) cycling, possibly resulting in impairment in Ca(2+)-mediated mechanical function and/or second messenger regulated processes.
影响因子：
2.9
作者：
R. Viner;T. Williams;C. Schöneich
通讯作者：
R. Viner;T. Williams;C. Schöneich
慢性阻塞性肺疾病对人膈肌钙泵 ATP 酶表达的影响。
DOI：
10.1152/japplphysiol.00767.2004
发表时间：
2005
期刊：
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子：
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作者：
Nguyen,Taitan;Rubinstein,NealA;Vijayasarathy,Camasamudram;Rome,LawrenceC;Kaiser,LarryR;Shrager,JosephB;Levine,Sanford
通讯作者：
Levine,Sanford
DOI：
10.1016/s0021-9258(19)49738-x
发表时间：
1992-07
期刊：
The Journal of biological chemistry
影响因子：
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作者：
J. Lytton;M. Westlin;S. E. Burk;G. Shull;D. Maclennan
通讯作者：
J. Lytton;M. Westlin;S. E. Burk;G. Shull;D. Maclennan