In-depth proteomic profiling of left ventricular tissues in human end-stage dilated cardiomyopathy.
In-depth proteomic profiling of left ventricular tissues in human end-stage dilated cardiomyopathy.
复制标题
人类末期扩张心肌病中左心室组织的深入蛋白质组学分析。
DOI：
10.18632/oncotarget.15689
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发表时间：
2017-07-18
期刊：
影响因子：
--
通讯作者：
Yang P
中科院分区：
文献类型：
--
作者：
Liu S;Xia Y;Liu X;Wang Y;Chen Z;Xie J;Qian J;Shen H;Yang P
扩张型心肌病（DCM）是由左心室（LV）心肌功能降低引起的，是心力衰竭（HF）的最常见原因之一。我们进行iTRAQ耦合2D-LC-MS/MS分析了健康对照和终末期DCM患者的LV组织的心脏蛋白质组。我们鉴定了4263种蛋白质，其中125种在DCM组织中与LV对照相比差异表达。其中大部分是与细胞连接和神经元代谢相关的膜蛋白。此外，这些蛋白质还参与了膜组织、线粒体组织、翻译、蛋白质转运和细胞死亡过程。蛋白质印迹法检测到4个参与细胞死亡过程的关键蛋白，表明DCM组织中细胞死亡被激活。此外，S100 A1和eEF 2分别在“细胞组装和组织”和“细胞周期”网络中富集。我们通过多反应监测（MRM）验证了终末期DCM LV样品中这两种蛋白质的减少。这些观察结果表明，我们可以加深对DCM的机制，通过比较正常LV组织的蛋白质组与终末期DCM在人类。
Dilated cardiomyopathy (DCM) is caused by reduced left ventricular (LV) myocardial function, which is one of the most common causes of heart failure (HF). We performed iTRAQ-coupled 2D-LC-MS/MS to profile the cardiac proteome of LV tissues from healthy controls and patients with end-stage DCM. We identified 4263 proteins, of which 125 were differentially expressed in DCM tissues compared to LV controls. The majority of these were membrane proteins related to cellular junctions and neuronal metabolism. In addition, these proteins were involved in membrane organization, mitochondrial organization, translation, protein transport, and cell death process. Four key proteins involved in the cell death process were also detected by western blotting, indicated that cell death was activated in DCM tissues. Furthermore, S100A1 and eEF2 were enriched in the “cellular assembly and organization” and “cell cycle” networks, respectively. We verified decreases in these two proteins in end-stage DCM LV samples through multiple reaction monitoring (MRM). These observations demonstrate that our understanding of the mechanisms underlying DCM can be deepened through comparison of the proteomes of normal LV tissues with that from end-stage DCM in humans.
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影响因子：
64.8
作者：
Kim, Min-Sik;Pinto, Sneha M.;Getnet, Derese;Nirujogi, Raja Sekhar;Manda, Srikanth S.;Chaerkady, Raghothama;Madugundu, Anil K.;Kelkar, Dhanashree S.;Isserlin, Ruth;Jain, Shobhit;Thomas, Joji K.;Muthusamy, Babylakshmi;Leal-Rojas, Pamela;Kumar, Praveen;Sahasrabuddhe, Nandini A.;Balakrishnan, Lavanya;Advani, Jayshree;George, Bijesh;Renuse, Santosh;Selvan, Lakshmi Dhevi N.;Patil, Arun H.;Nanjappa, Vishalakshi;Radhakrishnan, Aneesha;Prasad, Samarjeet;Subbannayya, Tejaswini;Raju, Rajesh;Kumar, Manish;Sreenivasamurthy, Sreelakshmi K.;Marimuthu, Arivusudar;Sathe, Gajanan J.;Chavan, Sandip;Datta, Keshava K.;Subbannayya, Yashwanth;Sahu, Apeksha;Yelamanchi, Soujanya D.;Jayaram, Savita;Rajagopalan, Pavithra;Sharma, Jyoti;Murthy, Krishna R.;Syed, Nazia;Goel, Renu;Khan, Aafaque A.;Ahmad, Sartaj;Dey, Gourav;Mudgal, Keshav;Chatterjee, Aditi;Huang, Tai-Chung;Zhong, Jun;Wu, Xinyan;Shaw, Patrick G.;Freed, Donald;Zahari, Muhammad S.;Mukherjee, Kanchan K.;Shankar, Subramanian;Mahadevan, Anita;Lam, Henry;Mitchell, Christopher J.;Shankar, Susarla Krishna;Satishchandra, Parthasarathy;Schroeder, John T.;Sirdeshmukh, Ravi;Maitra, Anirban;Leach, Steven D.;Drake, Charles G.;Halushka, Marc K.;Prasad, T. S. Keshava;Hruban, Ralph H.;Kerr, Candace L.;Bader, Gary D.;Iacobuzio-Donahue, Christine A.;Gowda, Harsha;Pandey, Akhilesh
通讯作者：
Pandey, Akhilesh
影响因子：
3.7
作者：
Cardona M;López JA;Serafín A;Rongvaux A;Inserte J;García-Dorado D;Flavell R;Llovera M;Cañas X;Vázquez J;Sanchis D
通讯作者：
Sanchis D
影响因子：
--
作者：
Kelly, Matthew;Semsarian, Christopher
通讯作者：
Semsarian, Christopher
影响因子：
24
作者：
Barth, Andreas S.;Kuner, Ruprecht;Sueltmann, Holger
通讯作者：
Sueltmann, Holger
影响因子：
3.9
作者：
Forman, K.;Vara, E.;Tresguerres, J. A. F.
通讯作者：
Tresguerres, J. A. F.