Mesenchymal Stem Cells Improve Regeneration of Damaged Salivary Glands
This paper addresses the mechanisms by which mesenchymal stem cells (MSCs) can improve the regeneration of salivary glands damaged by ionizing radiation.
Eur J Dent. 2019 Sep 11. doi: 10.1055/s-0039-1694697. [Epub ahead of print]
Mulyani SWM1, Astuti ER1, Wahyuni OR1, Ernawati DS2, Ramadhani NF1.
- Department of Dentomaxillofacial Radiology, Faculty of Dental Medicine, Airlangga University, Surabaya, Indonesia.
- Department of Oral Medicine, Faculty of Dental Medicine, Airlangga University, Surabaya, Indonesia.
The aim of this study was to describe the process of regeneration of damaged salivary glands due to ionizing radiations by bone marrow mesenchymal stem cells (BM-MSCs) transplantation that have been given hypoxic preconditioning with 1% O2 concentration.
MATERIALS AND METHODS:
Stem cell culture was performed under normoxic (O2: 21%) and hypoxic conditions by incubating the cells for 48 hours in a low oxygen tension chamber consisting of 95% N2, 5% CO2, and 1% O2. Thirty male Wistar rats were divided into four groups: two groups of control and two groups of treatment. A single dose of 15 Gy radiation was provided to the ventral region of the neck in all treatment groups, damaging the salivary glands. BM-MSCs transplantation was performed in the treatment groups for normoxia and hypoxia 24-hour postradiation.
Statistical analysis was done using normality test, followed by MANOVA test (p < 0.05).
There was a significant difference in the expression of binding SDF1-CXCR4, Bcl-2 (p < 0.05) and also the activity of the enzyme α-amylase in all groups of hypoxia. BM-MSCs transplantation with hypoxic precondition increases the expression of binding SDF1-CXCR4, Bcl-2 that contributes to cell migration, cell survival, and cell differentiation.
Dental Investigation Society.
BM-MSCs transplantation with hypoxic precondition increases the expression of binding SDF1-CXCR4, Bcl-2 that contributes to cell migration, cell survival, and cell differentiation.