|
|
Comparisons Between Molecular Features of Dilated and Restrictive Cardiomyopathy Based on Gene Co-Expression Network Analysis |
Li Sang1,2,Wang Guangbin1,2,Li Zhengwen1,2,Zeng Wei1,2,Rao Nini1,2,3* |
1(Center for Information Biology, University of Electronic Science and Technology of China, Chengdu 611731, China) 2(School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu 610054, China) 3(Guangdong Electronic Information Engineering Research Institute, University of Electronic Science and Technology of China, Dongguan 523808, Guangdong,China) |
|
|
Abstract With the development of molecular biology, the study on dilated cardiomyopathy (DCM) and restrictive cardiomyopathy (RCM) has been made much progress. However, the pathogenesis and molecular mechanism of progression of DCM and RCM are not yet clear. In clinic, RCM is easy to be misdiagnosed as DCM. This paper firstly made the difference significant analysis of RNA-Seq data for the two kinds of myocardial diseases, from which 451 and 1326 differentially expressed genes related to DCM and RCM were selected respectively. Then, the DCM and RCM co-expression networks were respectively constructed using their differentially expressed genes and the key nodes genes of the two classes of myocardial diseases were found based on the network features. Next, we performed biological function analysis for 21 and 65 genetic markers related to DCM and RCM respectively, and illustrated some important development mechanisms of the two kinds of myocardial diseases. Finally, DCM and RCM were compared from the angles of genetic markers, biological functions and signal pathways, which provided some new ideas about distinguishing DCM from RCM at molecular level.
|
|
|
|
|
|
[1] PDF (K). Report of the WHO/ISFC task force on the definition and classification of cardiomyopathies[J]. British Heart Journal, 1980, 44(6): 672. [2] Menon S C, Olson T M, Michels V V. Genetics of familial dilated cardiomyopathy[J]. Progress in Pediatric Cardiology, 2008, 25(1): 57-67. [3] 梁华生, 张黔桓, 陈泗林. 扩张型心肌病致病基因的研究进展[J]. 国际心血管病杂志, 2016, 43(1): 22-24. [4] Chinnaiyan KM, Leff CB, Marsalese DL. Constrictive pericarditis versus restrictive cardiomyopathy: challenges in diagnosis and management[J]. Cardiology in Review, 2004, 12(6): 314-320. [5] Mogensen J, Kubo T, Duque M, et al. et al. Idiopathic restrictive cardiomyopathy is part of the clinical expression of cardiac troponin I mutations[J]. Journal of Clinical Investigation, 2003, 111(2): 209-216. [6] Kaski JP, Syrris P, Burch M, et al. Idiopathic restrictive cardiomyopathy in children is caused by mutations in cardiac sarcomere protein genes[J]. Heart, 2008, 94(11): 1478-1484. [7] Ware SM, Quinn ME, Ballard ET, et al. Pediatric restrictive cardiomyopathy associated with a mutation in beta-myosin heavy chain[J]. Clinical Genetics, 2008, 73(2): 165-170. [8] Arbustini E, Pasotti M, Pilotto A, et al. Desmin accumulation restrictive cardiomyopathy and atrioventricular block associated with desmin gene defects[J]. European Journal of Heart Failure, 2006, 8(5): 477-483. [9] Caleshu C, Sakhuja R, Nussbaum RL, et al. Furthering the link between the sarcomere and primary cardiomyopathies: Restrictive cardiomyopathy associated with multiple mutations in genes previously associated with hypertrophic or dilated cardiomyopathy[J]. American Journal of Medical Genetics Part A, 2011, 155(9): 2229-2235. [10] Li H, Handsaker B, Wysoker A, et al. The sequence alignment/map format and SAMtools[J]. Bioinformatics, 2009, 25(16): 2078-2079. [11] Anders S, Pyl PT, Huber W. HTSeq-a Python framework to work with high-throughput sequencing data[J]. Bioinformatics, 2015, 31(2):166. [12] Risso D, Schwartz K, GC-content normalization for RNA-seq data[J]. BMC Bioinformatics, 2011, 12(1): 480. [13] Soneson C, Delorenzi M. A comparison of methods for differential expression analysis of RNA-seq data [J]. BMC Bioinformatics, 2013, 14(1): 91. [14] Zhang B, Horvath S. A general Framework for weighted gene co-expression network analysis[J]. Statistical Applications in Genetics & Molecular Biology, 2005, 4(1): Article17. [15] 谢彬, 刘深泉, 李炎烽, 等. 生物神经系统的编码特性和小世界特性[J]. 生物数学学报, 2009(3): 507-512. [16] Kathrin P, Jan S, Michaela N, et al. How MicroRNA and transcription factor co-regulatory networks affect osteosarcoma cell proliferation[J]. PLoS Computational Biology, 2013, 9(8): e1003210. [17] Baliga RR, Pimental DR, Zhao YY, et al. NRG-1-induced cardiomyocyte hypertrophy. Role of PI-3-kinase, p70(S6K), and MEK-MAPK-RSK[J]. American Journal of Physiology, 1999, 277(2): 2026-2037. [18] Fukazawa R, Miller T A, Kuramochi Y, et al. Neuregulin-1 protects ventricular myocytes from anthracycline-induced apoptosis via erbB4-dependent activation of PI3-kinase/Akt[J]. Journal of Molecular & Cellular Cardiology, 2003, 35(12):1473-1479. [19] Bingong LI, Xiao J, Yong LI, et al. Gene transfer of human neuregulin-1 attenuates ventricular remodeling in diabetic cardiomyopathy rats[J]. Experimental & Therapeutic Medicine, 2013, 6(5):1105-1112. [20] 张斌. MAB21L2基因的克隆及初步功能研究[D]. 北京:中国协和医科大学, 2002. [21] Palaniyandi SS, Watanabe K, Ma M, et al. Involvement of mast cells in the development of fibrosis in rats with postmyocarditis dilated cardiomyopathy[J]. Biological & Pharmaceutical Bulletin, 2005, 28(11): 2128-2132. [22] Oka T, Xu J, Kaiser R A, et al. Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling[J]. Journal of Cardiac Failure, 2007, 13(6):313-321. [23] Suleiman MS, Singh RJR, Stewart CEH. Apoptosis and the cardiac action of insulin-like growth factor I [J]. Pharmacology & Therapeutics, 2007, 114(3): 278-294. [24] Lin D, Chai Y, Reza I, et al. NPR3 protects cardiomyocytes from apoptosis through inhibition of cytosolic BRCA1 and TNF-α [J]. Cell Cycle, 2016, 15(18):2414-2419. [25] Xiong S, Van Pelt CS, Elizondofraire AC, et al. Loss of Mdm4 results in p53-dependent dilated cardiomyopathy[J]. Circulation, 2007, 115(23): 2925-2930. [26] Zhang D, Contu R, Latronico, MV,, et al. Mtorc1 regulates cardiac function and myocyte survival through 4e-bp1 inhibition in mic [J]. Journal of Clinical Investigation, 2010,120(10): 3735-3735. [27] Cohen ED, Miller MF, Wang Z, et al. Wnt5a and Wnt11 are essential for second heart field progenitor development [J]. Development, 2012, 139(11):1931. [28] Stylianidis V, Hermans KCM, Blankesteijn WM. Wnt signaling in cardiac remodeling and heart failure [M]// Handbook of Experimental Pharmacology. Oxford: Oxford Univ Press, 2016: 371-393. [29] Liao P, Georgakopoulos D, Kovacs A, et al. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy [J]. Proceedings of the National Academy of Sciences, 2001, 98(21):12283-12288. [30] 冯华松, 南柏松. 扩张型心肌病与红细胞钠钾钙镁离子及ATP[J]. 中华医学杂志, 1992(9): 547-549. |
|
|
|