Langerhans cells (LCs), a subset of dendritic cells (DCs), reside in body surface presenting antigens from various pathogens and activate immune system after migrating to vicinal lymph nodes. We recently demonstrated that the E-cadherin interaction allowed peripheral blood (PB) CD14+ cells to differentiate into LC-like cells that closely resemble primary LCs. Here, with a combination of GM-CSF, TGF-β, and TNF-α, we induced LC-like cells from umbilical cord blood (UCB)derived CD34+ cells and compared them with those induced from PB CD14+ cells. In contrast to PB CD14+ cell-derived LC-like cells with an undetectable surface level of toll-like receptor (TLR)4 and an unresponsiveness feature to bacterial lipopolysaccharide (LPS), CB CD34+ cellsderived LC like cells expressed a low, but apparent, surface level of TLR4 and a reduced level of intracellular TLR3. Consistent with this result, they responded to bacterial LPS, but poorly to poly(I:C) reflecting viral RNA. These findings suggest that LC-precursors from circulating PB CD14+ cells seem to be arranged in the outer barrier of skin, while LC-precursors from local undifferentiated UCB-derived CD34+ cells may be arranged in the inner barrier of mucosal tissues and work together to combat against external pathogens as well as internal malignancies throughout body surface.
Although osteoarthritis (OA) is the most prevalent aging-related joint disease, the understanding of mechanisms of OA pathogenesis remains limited. Key features include the progressive degradation of articular cartilage, synovial hyperplasia, and angiogenesis in joint tissues. CD9, a member of the tetraspanin family, is localized in the cell membranes and partly in the endosomes of all mammalian cell types. CD9 is associated with inflammation and angiogenesis through cell adhesion, migration, and signal transduction. This study examined the role of CD9 in OA development in three different mouse models: an aging model, a surgical model and antigen-induced arthritis (AIA) model, using CD9 deficient mice. Our study showed that CD9 deficiency reduced the severity of hallmarks of OA including cartilage degradation and soft tissue inflammation in aged mice. In the AIA model, cartilage damage and inflammation were also reduced in CD9−/− mice. This was in contrast to the surgical OA model where disease severity was similar in wild-type and CD9−/− mice. Col2a1 and Aggrecan expression was increased in chondrocytes of CD9−/− mice compared with those of wild-type mice. Our results indicate that the suppression of cartilage degradation in CD9−/− could be in part related to an increase in the expression of the two main cartilage extracellular matrix proteins aggrecan and type II collagen.
The objective of this study is to investigate the responses of human cementoblasts to light compressive force in vitro. A human cementoblast cell line (HCEM) was loaded for 12 h by mounting coverslips (0.25 gf/cm2). The coverslips were removed and the cells were cultured for up to 21 days. Cells without glass loading were used as controls. Cell growth, morphological changes, and the mRNA expression of RUNX2, ALP, WNT5A and SPON1 were investigated. No significant differences were observed in cell numbers between the compressed group and control group. Morphology of the compressed cells was slightly flattened on day 0; however, no indications of cell death were detected. Expression of differentiation markers including RUNX2, ALP and WNT5A was significantly lower in the compressed group (0.7, 0.75 and 0.75-fold respectively, P < 0.05) than in the control group on day 7. The expression levels of SPON1, a differentiation marker of cementoblasts, were higher on days 7 and 14 than on day 0, but were lower in the compressed group than in the control group (P < 0.01). These results suggest that light compressive force does not affect cell growth and morphology, but restrains higher expression of cementogenic differentiation markers in human cementoblasts in vitro.
Overactive bladder is one of the major health problem especially in elderly people. Adenosine triphosphate (ATP) is released from urinary bladder cells and acts as a smooth muscle contraction and sensory signal in micturition but little is known about the role of ATP release in the pathophysiology of overactive bladder. To assess the relationship between ATP and overactive bladder, we used a partial bladder outlet obstruction (pBOO) model in rats. The bladder caused several changes by pBOO: An increase in bladder weight, hypertrophy of sub-urothelium and sub-serosal area, and frequent non-voiding bladder contraction during urine storage. Basal ATP release from urothelium and serosa of pBOO rats was significantly higher than that of normal rats. Distentioninduced ATP release from urothelium of normal and pBOO rats had no significant change. However, distention-induced ATP release from serosa of pBOO rats was higher than that of normal. These findings may identify ATP especially released from serosa as one of causes of non-voiding contractions and overactive bladder symptoms.
The aim of this study was to investigate the effect of consuming small amounts of beer or a nonalcoholic beer taste beverage (non-beer) on gastric emptying and the polymorphisms in alcohol metabolism-related enzyme-encoding genes. Twenty male healthy volunteers were questioned regarding their alcohol consumption status, and body measurement was performed. The genetic polymorphisms in ADH1B (rs1229984, Arg47His) and ALDH2 (rs671 Glu487Lys) were analyzed. The subjects consumed 150 mL of beer or non-beer once per week, followed by the ingestion of 200 kcal of the test nutrient containing 13C-acetate 15 min later, after which the subjects’ exhalations were collected up to 120 min. The concentration peak of 13C was measured as Tmax. Diamine oxidase (DAO) activity for the marker of small intestinal function activity was also measured the day after the test. Gastric emptying was significantly slower in the group that consumed a small amount of beer, and in daily beer consumption group, and also in the ADH1B *2/*2, ALDH2 *1/*2 genotypes compared to non-beer drinking group. DAO values were not significantly changed between beer and non-beer group. The consumption of even a small amount of beer and the polymorphisms in ADH1B / ALDH2 affects gastric motility.
Human mesenchymal stem cell (MSC) heterogeneity and problems associated with the ex vivo expansion of MSC are linked with the failure of MSC clinical trials. In this study, we compared the effect of MSCs cultured in different oxygen concentrations on GVHD in mice to elucidate whether hypoxia improves the immunosuppressive capacity of MSCs. Hypoxia increased the proliferative activity and the expression of several stemness and chemokine genes, such as KLF4, OCT4, C-MYC, CCL2, and CXCL10. Mice that received MSCs cultured in normoxia or hypoxia showed alleviated symptoms of GVHD and increased survival times. However, there was no significant difference in survival rates between mice that received MSCs cultured in normoxia and hypoxia. These data suggest that hypoxic culture is a useful method for maintaining and obtaining MSCs used for cell therapy and that the therapeutic potential of MSCs cultured in hypoxia warrants further investigation.
Non-neuronal and atropine-sensitive ileal contractile responses to short chain fatty acids (SCFAs) are detected in the neonatal stage, and change with age or inflammatory conditions. However, the roles of luminal SCFAs in developmental changes have not yet been elucidated. We examined ileal contractile responses to SCFAs in mice colonized with different SCFA-producing intestinal microbiota under normal and inflammatory conditions. Using conventional (Conv), germ-free (GF), and gnotobiotic mice infected with Bifidobacterium (GB-bif), Propionibacterium (GB-prop), or Lactobacillus (GB-lact), ileal contractions were measured in 1-day-old neonates and 7-week-old mice using an isotonic transducer. Contractions occurred in all 1-day-old neonates, and were significantly desensitized in the adult stage in the Conv, GB-bif, and GB-prop groups, but not in the GF and GB-lact groups. An injection of lipopolysaccharide frequently restored desensitized contractions; however, the contraction rate did not change in the GF and GB-lact groups. The relative mRNA expression of a SCFA receptor (GPR43) or nicotinic acetylcholine receptor α7 was weaker in the GF group (0.3-fold or 0.4-fold expression level, respectively) than in the Conv group. In conclusion, the luminal inhabitation of SCFA-producing bacteria may potentiate the regulation of non-neuronal and atropine-sensitive ileal contractile responses to SCFAs under healthy and inflammatory conditions.
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