Chronic alcohol ingestion exacerbates skeletal muscle myopathy in HIV-1 transgenic rats.
Chronic alcohol ingestion exacerbates skeletal muscle myopathy in HIV-1 transgenic rats.
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DOI：
10.1186/1742-6405-8-30
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发表时间：
2011-08-16
影响因子：
2.2
通讯作者：
Otis JS
中科院分区：
文献类型：
--
作者：
Clary CR;Guidot DM;Bratina MA;Otis JS
另外，慢性酒精摄入和HIV-1感染与严重的骨骼肌紊乱有关，包括萎缩和消瘦、虚弱和疲劳。一项前瞻性队列研究报告称，41%的HIV感染患者符合酒精中毒的标准，然而，很少有关于这两种疾病过程对骨骼肌稳态的共病影响的报道。因此，我们分析了HIV-1转基因大鼠慢性酒精摄入的萎缩效应，并确定了几个分解代谢和合成代谢因子的改变。与健康对照组大鼠相比，每个实验组的相对足底肌质量、总蛋白含量和纤维横截面积均降低。酒精滥用进一步减少了HIV-1转基因大鼠的足底纤维面积。与以前的报告一致，肌肉生长抑制素及其受体激活素IIB的基因水平在HIV-1转基因大鼠肌肉中没有增加。然而，肌肉生长抑制素和激活素IIB诱导健康和HIV-1转基因大鼠喂养酒精12周。与对照组相比，所有组的TGFβ1、TNFα和磷酸化p38/总p38等分解代谢信号传导因子均升高。在对照喂养的转基因大鼠中，对IL-6、白血病抑制因子（LIF）、心肌营养素-1（CT-1）或睫状神经营养因子（CNTF）没有影响。然而，慢性酒精滥用和HIV-1相关蛋白表达的共病降低了两种合成代谢因子CT-1和CNTF的表达。与以前的报告一致，在HIV/AIDS动物模型中，酒精滥用加重了骨骼肌萎缩。虽然已知驱动酒精或HIV-1相关肌病的一些分解代谢途径在这种共病模型中也升高（例如，TGFβ1），表达模式不一致。因此，特定的信号传导机制的改变，如肌生长抑制素/激活素IIB系统的诱导或通过CT-1和CNTF依赖性机制的生长因子信号传导的减少，可能在酒精，HIV-1模型的肌肉质量调节中发挥更大的作用。
Separately, chronic alcohol ingestion and HIV-1 infection are associated with severe skeletal muscle derangements, including atrophy and wasting, weakness, and fatigue. One prospective cohort study reported that 41% of HIV-infected patients met the criteria for alcoholism, however; few reports exist on the co-morbid effects of these two disease processes on skeletal muscle homeostasis. Thus, we analyzed the atrophic effects of chronic alcohol ingestion in HIV-1 transgenic rats and identified alterations to several catabolic and anabolic factors. Relative plantaris mass, total protein content, and fiber cross-sectional area were reduced in each experimental group compared to healthy, control-fed rats. Alcohol abuse further reduced plantaris fiber area in HIV-1 transgenic rats. Consistent with previous reports, gene levels of myostatin and its receptor activin IIB were not increased in HIV-1 transgenic rat muscle. However, myostatin and activin IIB were induced in healthy and HIV-1 transgenic rats fed alcohol for 12 weeks. Catabolic signaling factors such as TGFβ1, TNFα, and phospho-p38/total-p38 were increased in all groups compared to controls. There was no effect on IL-6, leukemia inhibitory factor (LIF), cardiotrophin-1 (CT-1), or ciliary neurotrophic factor (CNTF) in control-fed, transgenic rats. However, the co-morbidity of chronic alcohol abuse and HIV-1-related protein expression decreased expression of the two anabolic factors, CT-1 and CNTF. Consistent with previous reports, alcohol abuse accentuated skeletal muscle atrophy in an animal model of HIV/AIDS. While some catabolic pathways known to drive alcoholic or HIV-1-associated myopathies were also elevated in this co-morbid model (e.g., TGFβ1), consistent expression patterns were not apparent. Thus, specific alterations to signaling mechanisms such as the induction of the myostatin/activin IIB system or reductions in growth factor signaling via CT-1- and CNTF-dependent mechanisms may play larger roles in the regulation of muscle mass in alcoholic, HIV-1 models.
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DOI：
10.1073/pnas.95.25.14938
发表时间：
1998-12-08
影响因子：
11.1
作者：
Gonzalez-Cadavid, NF;Taylor, WE;Bhasin, S
通讯作者：
Bhasin, S
DOI：
10.1111/j.1530-0277.2008.00730.x
发表时间：
2008-09-01
影响因子：
3.2
作者：
Marcondes, Maria Cecilia G.;Watry, Debbie;Fox, Howard
通讯作者：
Fox, Howard
影响因子：
4.8
作者：
Amirouche, Adel;Durieux, Anne-Cecile;Freyssenet, Damien
通讯作者：
Freyssenet, Damien
影响因子：
2.2
作者：
Lassiter, Coy;Fan, Xian;Joshi, Pratibha C;Jacob, Barbara A;Sutliff, Roy L;Jones, Dean P;Koval, Michael;Guidot, David M
通讯作者：
Guidot, David M
DOI：
10.1111/j.1530-0277.2009.00975.x
发表时间：
2009-08
期刊：
Alcoholism, clinical and experimental research
影响因子：
--
作者：
Otis JS;Guidot DM
通讯作者：
Guidot DM