Fatty acid synthase (FAS; EC 2.3.1.85 ) supplies de novo fatty acids for pulmonary surfactant synthesis, and FAS gene expression is both developmentally and hormonally regulated in the fetal lung. To further examine hormonal regulation of FAS mRNA and to determine the cellular localization of FAS gene expression, we cultured human fetal lungs (18–22 wk gestation) as explants for 1–4 days in the absence (control) or presence of glucocorticoid [dexamethasone (Dex), 10 nM] and/or cAMP agents (8-bromo-cAMP, 0.1 mM and IBMX, 0.1 mM). FAS protein content and activity increased similarly in the presence of Dex (109 and 83%, respectively) or cAMP (87 and 111%, respectively), and responses were additive in the presence of both hormones (230 and 203%, respectively). With a rabbit anti-rat FAS antibody, FAS immunoreactivity was not detected in preculture lung specimens but appeared in epithelial cells lining the tubules with time in culture. Dex and/or cAMP markedly increased staining of epithelial cells, identified as type II cells, whereas staining of mesenchymal fibroblasts was very low under all conditions. With in situ hybridization, FAS mRNA was found to be enriched in epithelial cells lining the alveolar spaces, and the reaction product increased in these cells when the explants were cultured with the hormones. The increased FAS mRNA content in the presence of Dex and/or cAMP is primarily due to increased stabilization of mRNA, although Dex alone increased the transcription rate by ∼30%. We conclude that hormonal treatment of cultured human fetal lungs increases FAS gene expression primarily by increasing stability of the message. The induction of FAS during explant culture and by hormones occurs selectively in type II epithelial cells, consistent with the regulatory role of this enzyme in de novo synthesis of fatty acid substrate for surfactant synthesis in perinatal lungs.

Currently, Adipose-derived Stem Cells (hASCs) therapy is being promoted applied research in the treatment of many diseases, especially autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and type 1 diabetes. However, profound mechanisms of this potential therapy have not been understood entirely. It is questioned that which tissues transplanted cells home to, and how long they survive there?In this work, we evaluated the migration, and survival duration of GFP-expressed hASCs (hASCGFPs) in normal and STZ-induced diabetic mice. A number of 106 hASC-GFPs were intravenous transplanted into the mice. After 1, 3, 5, 7 days, the presence of hASC-GFPs in various organs such as heart, lungs, kidneys, spleen, liver and pancreas was detected by Imaging technique (iBox® ExplorerTM Imaging Microscope System_IMS) and the percentage of these cells in the tissues of diabetic mice was evaluated by Flow cytometry (FCM).The results showed that the transplanted cells could be identified by both IMS and FCM. By IMS, it was clear that hASC-GFPs homed to lung and heart most at day 1 and 3, respectively and the signals were decreased gradually in both tissues. These imaging results were similar in normal and diabetic mice. By FCM, we detected the signals of hASC-GFPs in all six diabetic organs at day 1, 3, 5, 7. The signals expressed highest at day 1 (liver, heart), day 3 (lungs, kidneys, spleen) or day 5 (pancreas) and all gradually decreased until day 7.Our results demonstrated that although difficult hASCs could home to the pancreas of normal as well as diabetic mice, but we need more experiments to make further conclusions regards the mechanism of their immigration and behaviour in the recipients

Background: CD47 is a transmembrane glycoprotein expressed on all cells in the body and particularly overexpressed on cancer cells and cancer stem cells of both hematologic and solid malignancies. In the immune system, CD47 acts as a "don't eat me" signal, inhibiting phagocytosis by macrophages by interaction with signal regulatory protein α (SIRPα). In cancer, CD47 promotes tumor invasion and metastasis. This study aimed to evaluate the stemness of breast cancer cells when CD47 is overexpressed. Methods: MCF-7 breast cancer cells were transfected with plasmid pcDNA3.4-CD47 containing the CD47 gene. The stemness of the transduced MCF7 cell population was evaluated by expression of CD44 and CD24 markers, anti-tumor drug resistance and mammosphere formation. Results: Transfection of plasmid pcDNA3.4-CD47 significantly increased the expression of CD47 in MCF-7 cells. The overexpression of CD47 in transfected MCF-7 cells led to a significant increase in the CD44+CD24-population, but did not increase doxorubicin resistance of the cells or their capacity to form mammospheres. Conclusion: CD47 overexpression enhances the CD44+CD24-phenotype of breast cancer cells as observed by an increase in the CD44+CD24-expressing population. However, these changes are insufficient to increase the stemness of breast cancer cells.

Background: Type 2 diabetes (T2D) is the most common form of diabetes and accounts for 90-95% of all existing diabetic cases. The main etiologies of T2D include insulin resistance in target tissues, insufficient secretion of insulin and subsequent decline of pancreatic β-cell function. Recently, many studies have suggested that adipose -derived stem cells (ASCs) were potential to alleviate insulin resistance and hyperglycemia and promote the islets repair. In this study, ASCs were hypothesized that they could have ameliorative effects on type 2 diabetic mice.