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Hypoxic preconditioning promotes survival of human adipose derived mesenchymal stem cell via expression of prosurvival and proangiogenic biomarkers [version 3; peer review: 2 approved, 1 approved with reservations]

Background: Contributing factors for improved survival of human adipose derived mesenchymal stem cells (h-AMSCs) cultured through hypoxia preconditioning, in example apoptosis inhibition involving BCL2 and HSP27 expression, trigger signal expression (VEGF), SCF expression, OCT-4 expression, and CD44...

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Published in:F1000 research 2024-06, Vol.10, p.843
Main Authors: Suryawan, I Gde Rurus, Pikir, Budi Susetyo, Rantam, Fedik Abdul, Ratri, Anudya Kartika, Nugraha, Ricardo Adrian
Format: Article
Language:English
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Summary:Background: Contributing factors for improved survival of human adipose derived mesenchymal stem cells (h-AMSCs) cultured through hypoxia preconditioning, in example apoptosis inhibition involving BCL2 and HSP27 expression, trigger signal expression (VEGF), SCF expression, OCT-4 expression, and CD44+ expression. The objective if this study was to explain the mechanism and role of hypoxic preconditioning and the optimal duration of hypoxic preconditioning exposure to improve survival of h-AMSCs. Methods: An experimental laboratory explorative study ( in vitro ) with hypoxic preconditioning in h-AMSCs cultures. This research was conducted through four stages. First, isolation of h-AMSCs culture from adipose tissue of patients. Second, the characterization of h-AMSCs from adipose tissue by phenotype (flowcytometry) through CD44+, CD90+ and CD45-expression before being pre-conditioned for hypoxic treatment. Third, the hypoxic preconditioning in h-AMSCs culture ( in vitro ) was performed with an oxygen concentration of 1% for 24, 48 and 72 hours. Fourth, observation of survival from h-AMSCs culture was tested on the role of CD44+, VEGF, SCF, OCT-4, BCL2, HSP27 with Flowcytometry and apoptotic inhibition by Tunnel Assay method. Results: The result of regression test showed that time difference had an effect on VEGF expression ( p
ISSN:2046-1402
2046-1402
DOI:10.12688/f1000research.55351.3