Open AccessNuclear Phosphoproteomics Features the Novel Smoking Markers in Mouse Lung Tissue Following Subacute Phase Exposure to Tobacco Smoke
Author(s) -
Kanako Niimori-Kita,
Fumiko Nakamura,
Daikai Koizumi,
Daisuke Niimori
Publication year - 2016
Publication title -
journal of bioanalysis and biomedicine
Language(s) - English
Resource type - Journals
ISSN - 1948-593X
DOI - 10.4172/1948-593x.1000146
Subject(s) - tobacco smoke , phosphoproteomics , medicine , lung , smoke , pathology , third hand smoke , cigarette smoke , biology , environmental health , chemistry , sidestream smoke , microbiology and biotechnology , protein kinase a , protein phosphorylation , phosphorylation , organic chemistry
Smoking is a risk factor of lung diseases including chronic obstructive pulmonary disease (COPD) and lungcancer. However, the molecular mechanisms inducing these diseases remain to be completely uncovered. Inorder to elucidate them, it is necessary to identify the signaling pathway activated by tobacco smoking exposure.Especially, it is important to identify nuclear phosphoproteins induced by tobacco smoking exposure because thesignaling pathways are modified by phosphoproteins. This time, to identify nuclear phosphoproteins as novel smokingmarkers, nuclear phosphoproteimics of mouse lung tissue following tobacco smoking exposure was examined.Tobacco smoking exposure against mice was examined using the nose-only, flow-past inhalation exposure chambersystem for one month. Phosphopeptides eluted from nuclear proteins of the tobacco exposured mice lungs wereidentified by mass spectrometry. The result showed that 77 phosphoproteins were totally identified. Among them, thesemiquantitative analysis using ProteoIQ proteomic software revealed that five phosphoproteins showed the differentexpression patterns between control and tobacco exposure groups. Furthermore, the classification by biologicalfunctions of the identified proteins revealed that these proteins were related to inflammation, regeneration, repair,proliferation, differentiation, morphological change and nicotine or stress response. Finally, we founded advancedglycosylation end product-specific receptor (RAGE) and serine/threonine-protein kinase SNF1-like kinase 2 (SIK2)as novel smoking markers