Effect of prostaglandin E1 on paracrine and migration of rat bone marrow mesenchymal stem cells / 中国组织工程研究

BACKGROUND: Currently, there are few studies about prostaglandin E1 in the paracrine and migration of bone marrow mesenchymal stem cells. OBJECTIVE: To explore the effects of prostaglandin E1 in the paracrine and migration of bone marrow mesenchymal stem cells. METHODS: Bone marrow mesenchymal stem cells isolated from Sprague Dawley rats were cultured in vitro. Passage 3 cells were co-cultured with prostaglandin E1 at concentrations of 10 μg/L, and then culture supernatant was collected at 3, 6, 9, 12, 24, 48, and 72 hours after co-culture. The level of vascular endothelial growth factor was detected by enzyme-linked immunosorbent assay. Effects of prostaglandin E1 on the migration of bone marrow mesenchymal stem cells were detected by Transwell assay and cell scratch assay. RESULTS AND CONCLUSION: After treatment with prostaglandin E1 for 3 hours, bone marrow mesenchymal stem cells began to secrete vascular endothelial growth factors, and the secretion level was peaked at 24 hours and then gradually decreased. Results from the Transwell assay and cell scratch assay showed that the migration ability of bone marrow mesenchymal stem cells was significantly promoted by prostaglandin E1 (P < 0.05). Overall findings reveal that prostaglandin E1 promotes the secretion of vascular endothelial growth factor from bone marrow mesenchymal stem cells and enhances cell migration.

Role of bone marrow-derived mesenchymal stem cells in reduction of graft-versus-host disease by effecting CD4+CD25+ regulatory T cells in rats / 中国实验血液学杂志

The study was purposed to investigate the effects and mechanism of bone marrow-derived mesenchymal stem cells (MSCs) on graft-versus-host desease (GVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). The model of GVHD in rat had been established by allo-HSCT with donor derived T cells. The occurence of GVHD in recipients was observed in condition with or without donor derived MSC co-transplantation. Effects of MSCs on GVHD were analyzed by model rat survival rate and pathology. Proportions of CD4+CD25+ regulatory T cells were determined by using label spleen lymphocytes and thymocytes with double fluorescent-labeled antibodies and flow cytometry. The results showed that MSCs inhibited the lethal GVHD after HSC co-transplantation and increased the survival rate. The ratio of CD4/CD8 deceased in GVHD group in different levels, as compared with that in the experimental group. The proportion of CD4+CD25+ regulatory T cells of spleen lymphocytes was 31.55 +/- 7.58% and 20.90 +/- 1.90% in experimental and GVHD groups, respectively. Similarly, the proportion of CD4+CD25+ regulatory T cells of thymocytes was 93.20 +/- 2.69% and 57.17 +/- 6.79% in experimental and the GVHD groups, respectively. Meanwhile the proportion of CD4+CD25+ regulatory T cells was higher in experimental group than that in GVHD group. It is concluded that MSCs may prevent the lethal GVHD after allo-HSC co-transplantation and raise the survival rate of model rats by acting on the CD4+CD25+ regulatory T cells in vivo.

Functional recovery after rhesus monkey spinal cord injury by transplantation of bone marrow mesenchymal-stem cell-derived neurons / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The treatment of spinal cord injury is still a challenge. This study aimed at evaluating the therapeutical effectiveness of neurons derived form mesenchymal stem cells (MSCs) for spinal cord injury.</p><p><b>METHODS</b>In this study, rhesus MSCs were isolated and induced by cryptotanshinone in vitro and then a process of RT-PCR was used to detect the expression of glutamic acid decarboxylase (GAD) gene. The induced MSCs were tagged with Hoechst 33342 and injected into the injury site of rhesus spinal cord made by the modified Allen method. Following that, behavior analysis was made after 1 week, 1 month, 2 months and 3 months. After 3 months, true blue chloride retrograde tracing study was also used to evaluate the re-establishment of axons pathway and the hematoxylin-eosin (HE) staining and immunohistochemistry were performed after the animals had been killed.</p><p><b>RESULTS</b>In this study, the expression of mRNA of GAD gene could be found in the induced MSCs but not in primitive MSCs and immunohistochemistry could also confirm that rhesus MSCs could be induced and differentiated into neurons. Behavior analysis showed that the experimental animals restored the function of spinal cord up to grade 2-3 of Tarlov classification. Retrograde tracing study showed that true blue chollide could be found in the rostral thoracic spinal cords, red nucleus and sensory-motor cortex.</p><p><b>CONCLUSIONS</b>These results suggest that the transplantation is safe and effective.</p>

Progress of research on protein composition and gene therapy of Fanconi anaemia - review / 中国实验血液学杂志

Fanconi anaemia (FA) is an autosomal recessive inherited disorder caused by defects in hematopoietic stem cells. The clinical manifestations of FA are diverse and complicated. FA cells display high hypersensitivity to agents which produce interstrand DNA cross-links such as mitomycin C (MMC) or diepoxybutane (DEB). At least eight complementation groups with defects in eight genes (FANCA, FANCB, FANCC, FANCD(1), FANCD(2), FANCE, FANCF and FANCG) have been identified by gene analysis. Six genes (corresponding to subtypes A, C, D(2), E, F and G) have been coloned, and the encoded FA proteins interact in a common cellular pathway - "FA Pathway", through which modulate DNA repair. The progress of research on FA molecular mechanism provides gene therapy of FA with theory basis. FA cells transduced with the use of retrovirus carring the normal FA gene cDNA manifestate phenotypic correction of hypersensitivity to DNA cross-linking agents, such as MMC. In this review the clinical manifestations and gene composition of FA, and the functions of encoded FA proteins were summarized. The hematopoietic stem cell transplantation and gene therapy for FA patients were discussed.