ABSTRACT
Kimura's disease (KD) is an uncommon, chronic inflammatory disease characterized by tumor-like lesions in the soft tissue and lymph nodes and increased peripheral blood eosinophil counts and serum immunoglobulin E (IgE). Prednisone is widely used to treat the disease. Here, we reported a 59-year-old KD patient failed to response to prednisone. Leflunomide combined with methylprednisolone (Medrol) were carried out to treat KD and encouraging outcome was obtained during the medication and 1 year follow up period.
ABSTRACT
Human embryonic stem cells (hESCs) are pluripotent cells which can give rise to almost all adult cell lineages. Culture system of hESCs is complex, requiring exogenous b-FGF and feeder cell layer. Human mesenchymal stem cells (MSCs) not only synthesize soluble cytokines or factors such as b-FGF, but also provide other mechanism which might play positive role on sustaining hESCs propagation and pluripotency. Human amniotic fluid stem (AFS) cells, which share characteristics of both embryonic and adult stem cells, have been regarded as promising cells for regenerative medicine. Taking advantage by AFS cells, we studied the ability of AFS cells in supporting undifferentiated propagation and pluripotency of Chinese population derived X-01 hESCs. Human AF-type amniotic fluid stem cells (hAF-AFSCs) transcribed genes including Activin A, TGF-ß1, Noggin and b-FGF, which involved in maintaining pluripotency and self-renewal of hESCs. Compared to mouse embryonic fibroblasts (MEFs), hAF-AFSCs secreted higher concentration of b-FGF which was important in hESCs culture (P < 0.05). The hESCs were propagated more than 30 passages on hAF-AFSCs layer with exogenous b-FGF supplementation, keeping undifferentiated status. While exogenous b-FGF was obviated, propagation of hESCs with undifferentiated status was dependent on density of hAF-AFSC feeder layer. Lower density of hAF-AFSCs resulted in rapid decline in undifferentiated clone number, while higher ones hindered the growth of colonies. The most appropriate hAF-AFSCs feeder density to maintain the X-01 hESC line without exogenous b-FGF was 15-20×10(4)/well. To the best of our knowledge, this is the first study demonstrating that hAF-AFSCs could support undifferentiated propagation and pluripotency of Chinese population derived hESCs without exogenous b-FGF supplementation.
Subject(s)
Amniotic Fluid/cytology , Cell Culture Techniques/methods , Embryonic Stem Cells/cytology , Feeder Cells/cytology , Pluripotent Stem Cells/cytology , Animals , Cell Differentiation , Coculture Techniques/methods , Embryonic Stem Cells/metabolism , Enzyme-Linked Immunosorbent Assay , Feeder Cells/metabolism , Fibroblast Growth Factor 2/metabolism , Flow Cytometry , Humans , Immunohistochemistry , Mice , Pluripotent Stem Cells/metabolism , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Propranolol has been widely used in treating infantile hemangiomas (IHs). But recurrence of IHs was found in some cases on cessation of propranolol treatment. The other is that Chinese individuals reacted to propranolol differently from American Whites. Whether the difference of sensitivity is due to the ß adrenoceptor (ß-AR) expression pattern of hemangioma initiating cells remains unclear. In the present study, we isolated hemangioma-derived stem cells (hemSCs) from proliferative IHs and analyzed the biological characteristics and ß-AR expression pattern of hemSCs by immunostaining, Western blotting and multilineage differentiation assay as well. We also tested the effects of propranolol on hemSCs by evaluating VEGF expression, proliferation and apoptosis related parameters. Our results indicated that CD133(+) hemSCs located pre-vascular in proiferative IH tissues. Both ß1 and ß2-AR were expressed, while ß2-AR was dominant on hemSCs. Propranolol at 100-150 µM inhibited proliferation of hemSCs, not did 50 µM. Propranolol down-regulated VEGF expression of hemSCs, instead of inducing apoptosis. The adipogenic potential was enhanced by propranolol. Therefore, our current results suggested propranolol could not induce apoptosis of hemSCs, but played a curative role though suppressing VEGF synthesis and enhancement of adipogenesis of hemSCs. Our results might partially provide the insight of mechanism of relapse in some cases on cessation of propranolol treatment.