A differential peptidomics analysis of hippocampal tissue in a rat model of premature white matter injury

FENG Er-Cui; JIANG Li

doi:10.7499/j.issn.1008-8830.2019.11.012

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Chinese Journal of Contemporary Pediatrics ›› 2019, Vol. 21 ›› Issue (11) : 1116-1123. DOI: 10.7499/j.issn.1008-8830.2019.11.012

EXPERIMENTAL RESEARCH

A differential peptidomics analysis of hippocampal tissue in a rat model of premature white matter injury

FENG Er-Cui^1,2, JIANG Li²

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Abstract

Objective To observe differential peptidomics in the hippocampal tissue in a rat model of premature white matter injury, and to investigate the mechanism of premature white matter injury. Methods Twenty neonatal Sprague-Dawley rats were randomly and equally divided into a control group and a model group. Rats in the model group underwent permanent ligation of the right common carotid artery 2 days after birth, followed by 2 hours of hypoxia. For rats in the control group, the right common carotid artery was isolated, but without ligation and hypoxia. Brain tissue samples were collected from the two groups, and hippocampal tissue was isolated. Liquid chromatographytandem mass spectrometry combined with tandem mass spectrometry was used for peptidomic profiling of hippocampal tissue, and the differentially expressed peptides between the two groups were subjected to bioinformatics analysis to assess their possible roles in neural development and function. Results A total of 4164 peptides were identified and quantified, and 262 of them were differentially expressed (absolute fold change ≥ 2.5), including 164 upregulated peptides and 98 downregulated peptides. The numbers of differentially expressed peptides of the precursor proteins ELN, PCLO, MYO15a, MAP4, and MAP1b were the most, and may play significant roles in the pathogenesis of premature white matter injury. CDK5 signaling pathway in the hippocampus was activated in the rat model of premature white matter injury. Conclusions The differentially expressed peptides related to precursor proteins such as MAP1b may be key bioactive peptides involved in neural development and function in premature white matter injury, and activation of the CDK5 signaling pathway may be associated with premature white matter injury.

Key words

Premature white matter injury / Peptidomics analysis / Liquid chromatography-tandem mass spectrometry / Rats

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FENG Er-Cui, JIANG Li. A differential peptidomics analysis of hippocampal tissue in a rat model of premature white matter injury[J]. Chinese Journal of Contemporary Pediatrics. 2019, 21(11): 1116-1123 https://doi.org/10.7499/j.issn.1008-8830.2019.11.012

References

[1] du Plessis AJ. Neurology of the newborn infant. Preface[J]. Clin Perinatol, 2009, 36(4):xi-xiii.
[2] Volpe JJ. Brain injury in premature infants:a complex amalgam of destructive and developmental disturbances[J]. Lancet Neurol, 2009, 8(1):110-124.
[3] Rocha-Ferreira E, Hristova M. Plasticity in the neonatal brain following hypoxic-ischaemic injury[J]. Neural Plast, 2016, 2016:4901014.
[4] Dallas DC, Guerrero A, Parker EA, et al. Current peptidomics:applications, purification, identification, quantification, and functional analysis[J]. Proteomics, 2015, 15(5-6):1026-1038.
[5] Lone AM, Kim YG, Saghatelian A. Peptidomics methods for the identification of peptidase-substrate interactions[J]. Curr Opin Chem Biol, 2013, 17(1):83-89.
[6] 凤尔翠, 蒋犁. 瘦素对早产儿脑白质损伤模型大鼠远期空间记忆能力的影响[J]. 中国当代儿科杂志, 2017, 19(12):1267-1271.
[7] Feng EC, Jiang L. Effects of leptin on neurocognitive and motor functions in juvenile rats in a preterm brain damage model[J]. Mol Med Report, 2018, 18(4):4095-4102.
[8] Lin H, He L, Ma B. A combinatorial approach to the peptide feature matching problem for label-free quantification[J]. Bioinformatics, 2013, 29(14):1768-1775.
[9] Bortner JD Jr, Das A, Umstead TM, et al. Down-regulation of 14-3-3 isoforms and annexin A5 proteins in lung adenocarcinoma induced by the tobacco-specific nitrosamine NNK in the A/J mouse revealed by proteomic analysis[J]. J Proteome Res, 2009, 8(8):4050-4061.
[10] Hawasli AH, Benavides DR, Nguyen C, et al. Cyclin-dependent kinase 5 governs learning and synaptic plasticity via control of NMDAR degradation[J]. Nat Neurosci, 2007, 10(7):880-886.
[11] Mushtaq G, Greig NH, Anwar F, et al. Neuroprotective mechanisms mediated by CDK5 inhibition[J]. Curr Pharm Des, 2016, 22(5):527-534.
[12] Shahinian H, Tholen S, Schilling O. Proteomic identification of protease cleavage sites:cell-biological and biomedical applications[J]. Expert Rev Proteomics, 2013, 10(5):421-433.
[13] Ibi D, Nitta A, Ishige K, et al. Piccolo knockdown-induced impairments of spatial learning and long-term potentiation in the hippocampal CA1 region[J]. Neurochem Int, 2010, 56(1):77-83.
[14] Ho Kim J, Franck J, Kang T, et al. Proteome-wide characterization of signalling interactions in the hippocampal CA4/DG subfield of patients with Alzheimer's disease[J]. Sci Rep, 2015, 5:11138.
[15] Chapin SJ, Bulinski JC. Non-neuronal 210×10(3) Mr microtubule-associated protein (MAP4) contains a domain homologous to the microtubule-binding domains of neuronal MAP2 and tau[J]. J Cell Sci, 1991, 98(Pt 1):27-36.
[16] Villarroel-Campos D, Henríquez DR, Bodaleo FJ, et al. Rab35 functions in axon elongation are regulated by P53-related protein kinase in a mechanism that involves Rab35 protein degradation and the microtubule-associated protein 1b[J]. J Neurosci, 2016, 36(27):7298-7313.
[17] Jayachandran P, Olmo VN, Sanchez SP. Microtubule-associated protein 1b is required for shaping the neural tube[J]. Neural Dev, 2016, 11:1.
[18] Tortosa E, Galjart N, Avila J, et al. MAP1B regulates microtubule dynamics by sequestering EB1/3 in the cytosol of developing neuronal cells[J]. EMBO J, 2013, 32(9):1293-1306.
[19] Ketschek A, Jones S, Spillane M, et al. Nerve growth factor promotes reorganization of the axonal microtubule array at sites of axon collateral branching[J]. Dev Neurobiol, 2015, 75(12):1441-1461.
[20] Barnat M, Benassy MN, Vincensini L, et al. The GSK3-MAP1B pathway controls neurite branching and microtubule dynamics[J]. Mol Cell Neurosci, 2016, 72:9-21.
[21] Salatino-Oliveira A, Wagner F, Akutagava-Martins GC, et al. MAP1B and NOS1 genes are associated with working memory in youths with attention-deficit/hyperactivity disorder[J]. Eur Arch Psychiatry Clin Neurosci, 2016, 266(4):359-366.
[22] Liu YF, Sowell SM, Luo Y, et al. Autism and intellectual disability-associated KIRREL3 interacts with neuronal proteins MAP1B and MYO16 with potential roles in neurodevelopment[J]. PLoS One, 2015, 10(4):e0123106.
[23] Gomi F, Uchida Y. MAP1B 1-126 interacts with tubulin isoforms and induces neurite outgrowth and neuronal death of cultured cortical neurons[J]. Brain Res, 2012, 1433:1-8.
[24] Motavaf M, Soveizi M, Maleki M, et al. MYO15A splicing mutations in hearing loss:a review literature and report of a novel mutation[J]. Int J Pediatr Otorhinolaryngol, 2017, 96:35-38.
[25] World Health Organization. Preterm birth[DB/OL]. (2018-02-19). https://www.who.int/en/news-room/fact-sheets/detail/preterm-birth.