The Effects of Hypoxia-Reoxygenation in Mouse Digital Flexor Tendon-Derived Cells
المؤلفون المشاركون
Chen, Chen
Mao, Wei Feng
Wu, Ya Fang
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-12-15
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Objective.
Ischemia-reperfusion injury refers to the exacerbated and irreversible tissue damage caused by blood flow restoration after a period of ischemia.
The hypoxia-reoxygenation (H/R) model in vitro is ideal for studying ischemia-reperfusion injury at the cellular level.
We employed this model and investigated the effects of cobalt chloride- (CoCl2-) induced H/R in cells derived from mouse digital flexor tendons.
Materials and Methods.
Various H/R conditions were simulated via treatment of tendon-derived cells with different concentrations of CoCl2 for 24 h, followed by removal of CoCl2 to restore a normal oxygen state for up to 96 h.
Cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay.
Cell growth was determined via observation of cell morphology and proliferation.
Oxidative stress markers and mitochondrial activity were detected.
The expression levels of hypoxia-inducible factor- (HIF-) 1α, vascular endothelial growth factor-A (VEGF-A), collagen I, and collagen III were determined using Western blot (WB), real-time PCR, and immunofluorescence staining.
Cellular apoptosis was analyzed via flow cytometry, and the expression of apoptosis-related proteins Bax and bcl-2 was examined using WB.
Results.
The cells treated with low concentrations of CoCl2 showed significantly increased cell viability after reoxygenation.
The increase in cell viability was even more pronounced in cells that had been treated with high concentrations of CoCl2.
Under H/R conditions, cell morphology and growth were unchanged, while oxidative stress reaction was induced and mitochondrial activity was increased.
H/R exerted opposite effects on the expression of HIF-1α mRNA and protein.
Meanwhile, the expression of VEGF-A was upregulated, whereas collagen type I and type III were significantly downregulated.
The level of cellular apoptosis did not show significant changes during H/R, despite the significantly increased Bax protein and reduced bcl-2 protein levels that led to an increase in the Bax/bcl-2 ratio during reoxygenation.
Conclusions.
Tendon-derived cells were highly tolerant to the hypoxic environments induced by CoCl2.
Reoxygenation after hypoxia preconditioning promoted cell viability, especially in cells treated with high concentrations of CoCl2.
H/R conditions caused oxidative stress responses but did not affect cell growth.
The H/R process had a notable impact on collagen production and expression of apoptosis-related proteins by tendon-derived cells, while the level of cellular apoptosis remained unchanged.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Chen, Chen& Mao, Wei Feng& Wu, Ya Fang. 2020. The Effects of Hypoxia-Reoxygenation in Mouse Digital Flexor Tendon-Derived Cells. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1205338
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Chen, Chen…[et al.]. The Effects of Hypoxia-Reoxygenation in Mouse Digital Flexor Tendon-Derived Cells. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-13.
https://search.emarefa.net/detail/BIM-1205338
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Chen, Chen& Mao, Wei Feng& Wu, Ya Fang. The Effects of Hypoxia-Reoxygenation in Mouse Digital Flexor Tendon-Derived Cells. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-13.
https://search.emarefa.net/detail/BIM-1205338
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1205338
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر