title: Subcellular proteomic approach for identifying the signaling effectors of protein kinase C-β₂ under high glucose conditions in human umbilical vein endothelial cells.
abstract: The high glucose‑induced activation of protein kinase C‑β2 (PKC‑β2) has an essential role in the pathophysiology of diabetes‑associated vascular disease. In the present study, human umbilical vein endothelial cells (HUVECs) were cultured in high and normal glucose conditions prior to being infected with a recombinant adenovirus to induce the overexpression of PKC‑β2. The activity of PKC‑β2 was also decreased using a selective PKC‑β2 inhibitor. A series of two‑dimensional electrophoresis images detected ~800 spots in the nuclei, and ~600 spots in the cytosol. Following intra‑ and inter‑group cross‑matching, 38 significantly altered spots were identified as high glucose‑induced and PKC‑β2‑associated nuclear proteins. In addition to the observation that the regulation of key proteins involved in the nuclear factor (NF)‑κB signaling cascade occurred in the cytosol, various transcription factors, including peroxisome proliferator‑activated receptor δ (PPAR‑δ), were also altered in the nuclei. A human protein‑protein interaction network of potential connections of PKC‑β2‑associated proteins was constructed in the proteomics investigation using Biological General Repository for Interaction Datasets. The results indicated that PKC‑β2 may be involved in high glucose‑induced glucose and lipid crosstalk by regulating PPAR‑δ. In addition, NF‑κB inhibitor‑interacting Ras‑like protein 1 may be important in the PKC‑β2‑NF‑κB inhibitor‑NF‑κB signaling pathway in HUVECs under high‑glucose conditions.
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing 400042, P.R. China.
authors.forename: Fang
authors.initials: F
authors.lastname: Sun
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Fangfang
authors.initials: F
authors.lastname: Chen
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Bo
authors.initials: B
authors.lastname: Zhou
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Yaqian
authors.initials: Y
authors.lastname: Duan
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Hong
authors.initials: H
authors.lastname: Su
authors.affiliation: Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
authors.forename: Xuebo
authors.initials: X
authors.lastname: Lin
mesh_terms: D002352:Carrier Proteins / Q000378:metabolism; D002453:Cell Cycle; D002467:Cell Nucleus / Q000378:metabolism; D002478:Cells, Cultured; D005947:Glucose / Q000494:pharmacology; D061307:Human Umbilical Vein Endothelial Cells / Q000201:enzymology*; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism; D047494:PPAR delta / Q000378:metabolism; D047495:PPAR gamma / Q000378:metabolism; D060066:Protein Interaction Maps; D064546:Protein Kinase C beta / Q000378:metabolism*; D021381:Protein Transport; D020543:Proteome / Q000378:metabolism*; D040901:Proteomics; D015398:Signal Transduction
chemical_list: D002352:Carrier Proteins; D016328:NF-kappa B; C576702:NKIRAS1 protein, human; D047494:PPAR delta; D047495:PPAR gamma; D020543:Proteome; C579054:PRKCB protein, human; D064546:Protein Kinase C beta; D005947:Glucose