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Background: In order to shed light on the regenerative mechanism of mesenchymal stem cells (MSCs) in vivo, the bio-distribution profile of implanted cells using a stable and long-term tracking method is needed. We herein investigated the bio-distribution of human placental deciduas basalis derived MSCs (termed as PDB-MSCs) in nude mice after intravenous injection by carbon radioisotope labeling thymidine ((14)C-TdR), which is able to incorporate into new DNA strands during cell replication., Results: The proliferation rate and radioactive emission of human PDB-MSCs after labeled with different concentrations of (14)C-TdR were measured. PDB-MSCs labeled with 1 μCi possessed high radioactivity, and the biological characteristics (i.e. morphology, colony forming ability, differentiation capabilities, karyotype and cell cycle) showed no significant changes after labeling. Thus, 1 μCi was the optimal concentration in this experimental design. In nude mice, 1 × 10(6) (14)C-TdR-labeled PDB-MSCs were injected intravenously and the organs were collected at days 1, 2, 3, 5, 30 and 180 after injection, respectively. Radiolabeled PDB-MSCs were found mainly in the lung, liver, spleen, stomach and left femur of the recipient nude mice at the whole observation period., Conclusions: This work provided solid evidence that (14)C-TdR labeling did not alter the biological characteristics of human placental MSCs, and that this labeling method has potential to decrease the signal from non-infused or dead cells for cell tracking. Therefore, this labeling technique can be utilized to quantify the infused cells after long-term follow-up in pre-clinical studies.

Mesenchymal stem cells (MSCs) have been increasingly offered for tissue regeneration with the premise that they can survive and thrive amidst the microenvironment of injured or degenerate tissues. The role of high mobility group box 1 (HMGB1) and hypoxia in the proliferation and migration of rat bone marrow MSCs (rBM-MSCs) has been investigated. First, the effect of HMGB1 on the proliferation of rBM-MSCs was determined. Second, to evaluate the regulation of hypoxia and HMGB1 in the migration of rBM-MSCs, cells in the wound healing model were exposed to four conditions: normoxia (20% O2) and complete medium, normoxia and HMGB1, hypoxia (1% O2) and complete medium, hypoxia and HMGB1. RT-PCR and Western blotting were used to measure the expression of migration-related genes and proteins. HMGB1 inhibited the proliferation of rBM-MSCs; HMGB1 alone or together with hypoxia and promoted the migration of MSCs and upregulated the expression of HIF-1α and SDF-1. These results demonstrated that HMGB1 arrested the proliferation of rBM-MSCs, but enhanced the migration of rBM-MSCs which could be further improved by hypoxia. This study strengthens current understanding of the interaction between MSCs and the microenvironment of damaged tissues., (© 2014 International Federation for Cell Biology.)