JZUS - Journal of Zhejiang University SCIENCE

Journal of Zhejiang University SCIENCE B

Accepted manuscript available online (unedited version)

Partial least squares based identification of Duchenne muscular dystrophy specific genes

Author(s): Hui-bo An, Hua-cheng Zheng, Li Zhang, Lin Ma, Zheng-yan Liu
Affiliation(s): Department of Pathology, Children�s Hospital, Shijiazhuang 050031, China; more
Corresponding email(s): huiboan1@sina.com
Key Words: Partial least squares (PLS), Gene expression profile, supplementary materials Data S1 "&ck%5B%5D=keyword&opd=AND"> Duchenne muscular dystrophy (DMD)The online version of this article contains supplementary materials Data S1

Share this article to： More <<< Previous Paper \|Next Paper >>>

Hui-bo An, Hua-cheng Zheng, Li Zhang, Lin Ma, Zheng-yan Liu. Partial least squares based identification of Duchenne muscular dystrophy specific genes[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B1300060

@article{title="Partial least squares based identification of Duchenne muscular dystrophy specific genes",
author="Hui-bo An, Hua-cheng Zheng, Li Zhang, Lin Ma, Zheng-yan Liu",
journal="Journal of Zhejiang University Science B",
year="in press",
publisher="Zhejiang University Press & Springer",
doi="https://doi.org/10.1631/jzus.B1300060"
}

%0 Journal Article
%T Partial least squares based identification of Duchenne muscular dystrophy specific genes
%A Hui-bo An
%A Hua-cheng Zheng
%A Li Zhang
%A Lin Ma
%A Zheng-yan Liu
%J Journal of Zhejiang University SCIENCE B
%P 973-982
%@ 1673-1581
%D in press
%I Zhejiang University Press & Springer
doi="https://doi.org/10.1631/jzus.B1300060"

TY - JOUR
T1 - Partial least squares based identification of Duchenne muscular dystrophy specific genes
A1 - Hui-bo An
A1 - Hua-cheng Zheng
A1 - Li Zhang
A1 - Lin Ma
A1 - Zheng-yan Liu
J0 - Journal of Zhejiang University Science B
SP - 973
EP - 982
%@ 1673-1581
Y1 - in press
PB - Zhejiang University Press & Springer
ER -
doi="https://doi.org/10.1631/jzus.B1300060"

Abstract
Chinese Summary
Academic Network
Reviewer Comment

Abstract: Large-scale parallel gene expression analysis has provided a greater ease for investigating the underlying mechanisms of Duchenne muscular dystrophy (DMD). Previous studies typically implemented variance/regression analysis, which would be fundamentally flawed when unaccounted sources of variability in the arrays existed. Here we aim to identify genes that contribute to the pathology of DMD using partial least squares (PLS) based analysis. We carried out PLS-based analysis with two datasets downloaded from the Gene Expression Omnibus (GEO) database to identify genes contributing to the pathology of DMD. Except for the genes related to inflammation, muscle regeneration and extracellular matrix (ECM) modeling, we found some genes with high fold change, which have not been identified by previous studies, such as SRPX, GPNMB, SAT1, and LYZ. In addition, downregulation of the fatty acid metabolism pathway was found, which may be related to the progressive muscle wasting process. Our results provide a better understanding for the downstream mechanisms of DMD.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Altamirano, F., López, J.R., Henriquez, C., Molinski, T., Allen, P.D., Jaimovich, E., 2012. Increased resting intracellular calcium modulates NF-κB-dependent inducible nitric-oxide synthase gene expression in dystrophic mdx skeletal myotubes. J. Biol. Chem., 287(25):20876-20887.

[2]Burnicka-Turek, O., Kata, A., Buyandelger, B., Ebermann, L., Kramann, N., Burfeind, P., Hoyer-Fender, S., Engel, W., Adham, I.M., 2010. Pelota interacts with HAX1, EIF3G and SRPX and the resulting protein complexes are associated with the actin cytoskeleton. BMC Cell Biol., 11(1):28.

[3]Bushby, K., Finkel, R., Birnkrant, D.J., Case, L.E., Clemens, P.R., Cripe, L., Kaul, A., Kinnett, K., Mcdonald, C., Pandya, S., et al., 2010. Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and pharmacological and psychosocial management. Lancet Neurol., 9(1):77-93.

[4]Cai, B., Spencer, M.J., Nakamura, G., Tseng-Ong, L., Tidball, J.G., 2000. Eosinophilia of dystrophin-deficient muscle is promoted by perforin-mediated cytotoxicity by T cell effectors. Am. J. Pathol., 156(5):1789-1796.

[5]Chakraborty, S., Datta, S., 2012. Surrogate variable analysis using partial least squares (SVA-PLS) in gene expression studies. Bioinformatics, 28(6):799-806.

[6]Chen, Y.W., Zhao, P., Borup, R., Hoffman, E.P., 2000. Expression profiling in the muscular dystrophies: identification of novel aspects of molecular pathophysiology. J. Cell Biol., 151(6):1321-1336.

[7]Chen, Y.W., Nagaraju, K., Bakay, M., Mcintyre, O., Rawat, R., Shi, R., Hoffman, E.P., 2005. Early onset of inflammation and later involvement of TGFβ in Duchenne muscular dystrophy. Neurology, 65(6):826-834.

[8]Golub, T.R., Slonim, D.K., Tamayo, P., Huard, C., Gaasenbeek, M., Mesirov, J.P., Coller, H., Loh, M.L., Downing, J.R., Caligiuri, M.A., et al., 1999. Molecular classification of cancer: class discovery and class prediction by gene expression monitoring. Science, 286(5439):531-537.

[9]Gorospe, J.R., Tharp, M.D., Hinckley, J., Kornegay, J.N., Hoffman, E.P., 1994. A role for mast cells in the progression of Duchenne muscular dystrophy? Correlations in dystrophin-deficient humans, dogs, and mice. J. Neurol. Sci., 122(1):44-56.

[10]Gosselin, R., Rodrigue, D., Duchesne, C., 2010. A bootstrap-VIP approach for selecting wavelength intervals in spectral imaging applications. Chemometr. Intell. Lab. Syst., 100(1):12-21.

[11]Haslett, J.N., Sanoudou, D., Kho, A.T., Bennett, R.R., Greenberg, S.A., Kohane, I.S., Beggs, A.H., Kunkel, L.M., 2002. Gene expression comparison of biopsies from Duchenne muscular dystrophy (DMD) and normal skeletal muscle. PNAS, 99(23):15000-15005.

[12]Head, S.I., 2010. Branched fibres in old dystrophic mdx muscle are associated with mechanical weakening of the sarcolemma, abnormal Ca²⁺ transients and a breakdown of Ca²⁺ homeostasis during fatigue. Exp. Physiol., 95(5):641-656.

[13]Helland, I.S., 1988. On the structure of partial least squares regression. Commun. Stat. Simul. Comput., 17(2):581-607.

[14]Helland, I.S., 1990. Partial least squares regression and statistical model. Scand. J. Stat., 17:97-144.

[15]Irizarry, R.A., Hobbs, B., Collin, F., Beazer-Barclay, Y.D., Antonellis, K.J., Scherf, U., Speed, T.P., 2003. Exploration, normalization, and summaries of high density oligonucleotide array probe level data. Biostatistics, 4(2):249-264.

[16]Koenig, M., Hoffman, E.P., Bertelson, C.J., Monaco, A.P., Feener, C., Kunkel, L.M., 1987. Complete cloning of the Duchenne muscular dystrophy (DMD) cDNA and preliminary genomic organization of the DMD gene in normal and affected individuals. Cell, 50(3):509-517.

[17]Kunkel, L.M., Monaco, A.P., Hoffman, E., Koenig, M., Feener, C., Bertelson, C., 1987. Molecular studies of progressive muscular dystrophy (Duchenne). Enzyme, 38(1-4):72-75.

[18]Martins, J.P.A., Teofilo, R.F., Ferreira, M.M.C., 2010. Computational performance and cross-validation error precision of five PLS algorithms using designed and real data sets. J. Chemometr., 24(5-6):320-332.

[19]Mcdouall, R.M., Dunn, M.J., Dubowitz, V., 1990. Nature of the mononuclear infiltrate and the mechanism of muscle damage in juvenile dermatomyositis and Duchenne muscular dystrophy. J. Neurol. Sci., 99(2-3):199-217.

[20]Monici, M.C., Aguennouz, M., Mazzeo, A., Messina, C., Vita, G., 2003. Activation of nuclear factor-κB in inflammatory myopathies and Duchenne muscular dystrophy. Neurology, 60(6):993-997.

[21]Nishio, H., Wada, H., Matsuo, T., Horikawa, H., Takahashi, K., Nakajima, T., Matsuo, M., Nakamura, H., 1990. Glucose, free fatty acid and ketone body metabolism in Duchenne muscular dystrophy. Brain Dev., 12(4):390-402.

[22]Pescatori, M., Broccolini, A., Minetti, C., Bertini, E., Bruno, C., D′Amico, A., Bernardini, C., Mirabella, M., Silvestri, G., Giglio, V., et al., 2007. Gene expression profiling in the early phases of DMD: a constant molecular signature characterizes DMD muscle from early postnatal life throughout disease progression. FASEB J., 21(4):1210-1226.

[23]Spencer, M.J., Walsh, C.M., Dorshkind, K.A., Rodriguez, E.M., Tidball, J.G., 1997. Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity. J. Clin. Invest., 99(11):2745-2751.

[24]Straub, V., Campbell, K.P., 1997. Muscular dystrophies and the dystrophin-glycoprotein complex. Curr. Opin. Neurol., 10(2):168-175.

[25]Wong, B., Gilbert, D.L., Walker, W.L., Liao, I.H., Lit, L., Stamova, B., Jickling, G., Apperson, M., Sharp, F.R., 2009. Gene expression in blood of subjects with Duchenne muscular dystrophy. Neurogenetics, 10(2):117-125.

Open peer comments: Debate/Discuss/Question/Opinion

<1>

- Go to

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference