دورية أكاديمية
أعرض في EDS

Oxidative stress and premature senescence in corneal endothelium following penetrating keratoplasty in an animal model.

التفاصيل البيبلوغرافية
العنوان: Oxidative stress and premature senescence in corneal endothelium following penetrating keratoplasty in an animal model.
المؤلفون: Zhao X; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of medical Sciences, No. 5 Yanerdao Rd, Qingdao, 266071, China., Wang Y; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of medical Sciences, No. 5 Yanerdao Rd, Qingdao, 266071, China. wye112002@126.com.; Current affiliation: Central Laboratory of the Second Affiliated Hospital, Medical College of Qingdao University, Qingdao, 266042, China. wye112002@126.com., Wang Y; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of medical Sciences, No. 5 Yanerdao Rd, Qingdao, 266071, China., Li S; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of medical Sciences, No. 5 Yanerdao Rd, Qingdao, 266071, China., Chen P; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of medical Sciences, No. 5 Yanerdao Rd, Qingdao, 266071, China.
المصدر: BMC ophthalmology [BMC Ophthalmol] 2016 Feb 02; Vol. 16, pp. 16. Date of Electronic Publication: 2016 Feb 02.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 100967802 Publication Model: Electronic Cited Medium: Internet ISSN: 1471-2415 (Electronic) Linking ISSN: 14712415 NLM ISO Abbreviation: BMC Ophthalmol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : BioMed Central, [2001-
مواضيع طبية MeSH: Cellular Senescence* , Disease Models, Animal* , Oxidative Stress*, Endothelium, Corneal/*pathology , Graft Rejection/*etiology , Keratoplasty, Penetrating/*adverse effects, Adult ; Allografts ; Animals ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Endothelium, Corneal/drug effects ; Endothelium, Corneal/metabolism ; Gene Expression Regulation ; Graft Rejection/genetics ; Graft Rejection/pathology ; Humans ; Hydrogen Peroxide/toxicity ; MAP Kinase Kinase Kinase 5/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Middle Aged ; Reactive Oxygen Species/metabolism ; Real-Time Polymerase Chain Reaction ; Up-Regulation ; Young Adult ; beta-Galactosidase/genetics ; beta-Galactosidase/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
مستخلص: Background: The purpose of this study was to address the question of how the premature senescence process may affect corneal endothelium after penetrating keratoplasty, because the quality of donor corneal endothelial cells is important for corneal transplant success.
Methods: The cell senescence and induced oxidative stress in corneal endothelium were assessed using a normal-risk orthotopic mice corneal transplantation model. Senescence associated beta-galactosidase (SA-beta-Gal) staining was used to evaluate premature senescence in the endothelium of corneal allografts. Oxidative Stress and Antioxidant Defense RT(2)-PCR Arrays and in vitro experimental model using H2O2 treatment were used to investigate the possible mechanism.
Results: SA-beta-Gal positivity was observed obviously in mice corneal endothelium of allogenic group and the levels of p16(INK4a) message and protein increased in endothelium of allogenic group compared to syngenic group. By PCR array, an oxidant-antioxidant imbalance was found in the endothelium of corneal allograft after PKP. The results from mice model were validated using human endothelium samples of corneal allograft after PKP. We also developed an in vitro experimental model using H2O2 treatment to simulate a state of oxidative stress in cultured human corneal endothelial cells (HCECs) and found that elevated ROS levels, the up-regulation of CDK inhibitors and ROS-mediated p16(INK4A) up-regulation in HCECs occur via the ASK1-p38 MAPK pathway.
Conclusions: Our results demonstrate the presence of oxidative stress and premature senescence in the endothelium of corneal allografts following PKP.
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المشرفين على المادة: 0 (Cyclin-Dependent Kinase Inhibitor p16)
0 (Reactive Oxygen Species)
147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
BBX060AN9V (Hydrogen Peroxide)
EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
EC 2.7.11.25 (MAP Kinase Kinase Kinase 5)
EC 2.7.11.25 (Map3k5 protein, mouse)
EC 3.2.1.23 (beta-Galactosidase)
تواريخ الأحداث: Date Created: 20160204 Date Completed: 20160818 Latest Revision: 20181113
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4736695
DOI: 10.1186/s12886-016-0192-6
PMID: 26839109
قاعدة البيانات: MEDLINE
الوصف
تدمد:1471-2415
DOI:10.1186/s12886-016-0192-6