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本文引用的文献

1
The Mitochondrial Basis of Aging.衰老的线粒体基础
Mol Cell. 2016 Mar 3;61(5):654-666. doi: 10.1016/j.molcel.2016.01.028.
2
The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging.组蛋白去乙酰化酶抑制剂丁酸可改善衰老过程中的新陈代谢并减少肌肉萎缩。
Aging Cell. 2015 Dec;14(6):957-70. doi: 10.1111/acel.12387. Epub 2015 Aug 20.
3
Elevated oxygen consumption rate in response to acute low-glucose stress: Metformin restores rate to normal level.急性低血糖应激下氧消耗率升高:二甲双胍将该率恢复至正常水平。
Exp Gerontol. 2015 Oct;70:157-62. doi: 10.1016/j.exger.2015.08.002. Epub 2015 Aug 7.
4
Mitochondrial fission and fusion factors reciprocally orchestrate mitophagic culling in mouse hearts and cultured fibroblasts.线粒体分裂和融合因子相互协调小鼠心脏和培养的成纤维细胞中的线粒体自噬清除。
Cell Metab. 2015 Feb 3;21(2):273-286. doi: 10.1016/j.cmet.2014.12.011. Epub 2015 Jan 15.
5
Transient assembly of F-actin on the outer mitochondrial membrane contributes to mitochondrial fission.F-肌动蛋白在线粒体外膜上的瞬时组装有助于线粒体分裂。
J Cell Biol. 2015 Jan 5;208(1):109-23. doi: 10.1083/jcb.201404050. Epub 2014 Dec 29.
6
Overexpression of p49/STRAP alters cellular cytoskeletal structure and gross anatomy in mice.p49/STRAP的过表达改变了小鼠的细胞细胞骨架结构和大体解剖结构。
BMC Cell Biol. 2014 Sep 2;15:32. doi: 10.1186/1471-2121-15-32.
7
Mitochondrial fusion is frequent in skeletal muscle and supports excitation-contraction coupling.线粒体融合在骨骼肌中很频繁,支持兴奋-收缩耦联。
J Cell Biol. 2014 Apr 28;205(2):179-95. doi: 10.1083/jcb.201312066. Epub 2014 Apr 21.
8
Integrating mitochondrial organization and dynamics with cellular architecture.将线粒体组织和动态与细胞结构整合起来。
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A role for peroxisome proliferator-activated receptor γ coactivator-1 in the control of mitochondrial dynamics during postnatal cardiac growth.过氧化物酶体增殖物激活受体 γ 共激活因子 1 在出生后心脏生长过程中线粒体动力学控制中的作用。
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10
Mitochondrial dynamics controlled by mitofusins regulate Agrp neuronal activity and diet-induced obesity.由线粒体融合蛋白调控的线粒体动态控制 Agrp 神经元活性和饮食诱导的肥胖。
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p49/STRAP(一种血清反应因子结合蛋白(SRFBP1))是否会调节衰老过程中心脏线粒体的功能?

Does p49/STRAP, a SRF-binding protein (SRFBP1), modulate cardiac mitochondrial function in aging?

作者信息

Zhang Xiaomin, Williams Emmanuel D, Azhar Gohar, Rogers Steven C, Wei Jeanne Y

机构信息

Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, United States.

Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, United States.

出版信息

Exp Gerontol. 2016 Sep;82:150-9. doi: 10.1016/j.exger.2016.06.008. Epub 2016 Jun 20.

DOI:10.1016/j.exger.2016.06.008
PMID:27337995
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4969173/
Abstract

p49/STRAP (SRFBP1) is a transcriptional regulator that has been implicated in cardiac aging. p49/STRAP has a SRF binding domain and a BUD22 domain (which modulates cellular growth rate and cell size). We have observed that p49/STRAP alters the intracellular NAD/NADH ratio and induces protein deacetylation. Here we report that p49/STRAP overexpression caused the deacetylation of histone H4 on lysine 16 (H4K16) and suppressed the expression of PGC-1α as well as mitofusin-1 and mitofusin-2 at both the mRNA and protein levels. P49/STRAP also reduced mitochondrial size, mitochondrial membrane potential and the mitochondrial oxygen consumption rate. We noted that P49/STRAP expression was increased in the old versus young adult mouse hearts and also increased with advancing population doubling levels in cultured human umbilical vein endothelial cells (HUVECs). It is therefore very plausible that increased expression of p49/STRAP in late life may alter the status of histone acetylation and impact mitochondrial dynamics and thereby reduce mitochondrial function and cardiac performance during mammalian senescence.

摘要

p49/STRAP(SRFBP1)是一种转录调节因子,与心脏衰老有关。p49/STRAP具有一个SRF结合结构域和一个BUD22结构域(可调节细胞生长速率和细胞大小)。我们观察到p49/STRAP会改变细胞内NAD/NADH比值并诱导蛋白质去乙酰化。在此我们报告,p49/STRAP的过表达导致组蛋白H4赖氨酸16位点(H4K16)去乙酰化,并在mRNA和蛋白质水平上抑制PGC-1α以及线粒体融合蛋白1和线粒体融合蛋白2的表达。p49/STRAP还会减小线粒体大小、降低线粒体膜电位以及线粒体氧消耗率。我们注意到,与年轻成年小鼠心脏相比,老年小鼠心脏中p49/STRAP的表达增加,并且在培养的人脐静脉内皮细胞(HUVECs)中,随着群体倍增水平的提高其表达也增加。因此,很有可能在生命后期p49/STRAP表达的增加会改变组蛋白乙酰化状态,影响线粒体动力学,从而在哺乳动物衰老过程中降低线粒体功能和心脏性能。