Fibronectin modified alginate coating enhances cell targeting and homing to bone marrow in BALB/c mice.

Stem cell homing to bone marrow (BM) suffers from premature differentiation of transfused cells within the blood stream, thereby reducing the efficiency of stem cell transplantation (SCT). This work is attempted to enhance the homing of cells in BM. Fibronectin modified alginate (A-F) was prepared and used to coat the cells. Biodistribution and survival advantage provided by A-F coating was evaluated in BALB/c mice. The A-F conjugate showed characteristic FT-IR peaks of alginate at 3308 cm-1 and 1634 cm-1, and Fibronectin peak at 675 cm-1. The A-F coating prevented antibodies from binding to their respective cell surface receptors. The A-F coat abolished haemagglutination. Significant distribution of coated cells was observed in BM after 24 h. This provided protection to 7 Gy irradiated mice. The A-F coating showed no histological toxicity in vivo. The coating formulation is likely to be useful for shielding clinically relevant cell types to improve targeting for organ regeneration.

Survival genes expression analysis following ionizing radiation to LiCl treated KG1a cells.

Purpose: Lithium chloride (LiCl) is clinically used for manic disorders. Its role has been shown in improving cell survival by decreasing Bax and p53 expression and increasing Bcl-2 concentration in the cell. This potential of LiCl is responsible for reducing irradiated cell death. In this study, we have explored the role of LiCl as a radioprotectant affecting survival genes.Materials and methods: To find out the cellular response upon LiCl pretreatment to radiation-exposed KG1a cells; viability, clonogenic assay and microarray studies were performed. This was followed by the detection of transcription factor binding motif in coregulated genes. These results were confirmed by reverse transcription-polymerase chain reaction (RT-PCR) and chromatin immunoprecipitation (CHIP).Results: LiCl improved irradiated KG1a cell survival and its clonogenicity at 2 mM concentration (clinically used). Microarray data analysis showed differential expression of cell-protecting genes playing an important role in apoptosis, cell cycle, adhesion and inflammation, etc. The coregulation analysis revealed genes involved in bile acid biosynthesis were also affected by LiCl treatment, these genes are likely to be responsible for radiation-induced gastrointestinal (GI) syndrome through bile production.Conclusions: This is the first study with respect to global genetic expression upon LiCl treatment to radiation-exposed cells. Our results suggest considering repurposing of LiCl as a protective agent for radiation injury.