PhoenixBio

Higashihiroshima, Japan

PhoenixBio

Higashihiroshima, Japan
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Kojima H.,Dokkyo Medical University | Kobayashi A.,Dokkyo Medical University | Sakurai D.,Dokkyo Medical University | Kanno Y.,Dokkyo Medical University | And 6 more authors.
Journal of Immunology | Year: 2010

Hypoxia-inducible factor (HIF)-1α plays a central role in oxygen homeostasis and energy supply by glycolysis in many cell types. We previously reported that an HIF-1α gene deficiency caused abnormal B cell development and autoimmunity. In this study we show that HIF-1α-enabled glycolysis during B cell development is required in a developmental stage-specific manner. Supporting this conclusion are observations that the glycolytic pathway in HIF-1α-deficient B220+ bone marrow cells is much less functionally effective than in wild-type control cells. The expression of genes encoding the glucose transporters and the key glycolytic enzyme, 6-phosphofructo-2-kinase/fructose-2,6-bishosphatase 3, was greatly reduced in HIF-1α-deficient cells. The compensatory adaptation to the defect of glycolysis was reflected in higher levels of expression of respiratory chain-related genes and TCA cycle-related genes in HIF-1α-deficient cells than in wild-type cells. In agreement with these findings, HIF-1α- deficient cells used pyruvate more efficiently than wild-type cells. The key role of HIF-1α-enabled glycolysis in bone marrow B cells was also demonstrated by glucose deprivation during in vitro bone marrow cell culture and by using a glycolysis inhibitor in the bone marrow cell culture. Taken together, these findings indicate that glucose dependency differs at different B cell developmental stages and that HIF-1α plays an important role in B cell development. Copyright © 2009 by The American Association of Immunologists, Inc.


Yamao M.,PhoenixBio | Inamatsu M.,PhoenixBio | Ogawa Y.,PhoenixBio | Toki H.,PhoenixBio | And 4 more authors.
Journal of Investigative Dermatology | Year: 2010

We previously showed that cultured rat dermal papilla cells (DPCs) retain their hair-inducing capacity on afollicular epidermal cell (EPCs). Here, we examined the hair growth-inducing capacity of differently subcultured DPCs by transplanting them, along with rat EPCs, onto the backs of nude mice (graft chamber assay). DPCs at passage (p)≥ 6 (DPCs p6≥ or, more generally, low-passage DPCs) induced hair formation. However, DPCs p>30 (high-passage DPCs) had no such activity and induced only subepidermal hair follicles (HFs) that were not encapsulated by the dermal sheath (DS). Thus, we examined the effect of DS cells (DSCsp=1) on the ability of DPCsp=60 to induce hair growth by testing a mixture of these two cell types (cotransplant) in the graft chamber assay, in which DSCs p=1 and DPCsp=60 were labeled with enhanced green fluorescent protein (EGFP) and 1,1-dioctadecyl-3,3,3,3-tetramethylindocarbocyanine perchlorate (DiI), respectively. These cotransplants generated hairs as actively as did DPCsp=6 transplants. Their HFs were encapsulated with EGFP-DS and had DPs consisting largely of EGFP-DPCs (47%) and DiI-DPCs (43%), indicating a major contribution of DSCp1-derived DPCs to HF induction. In addition, the results of in vitro coculture of DPCsp=60 and DSCsp=1 suggest that high-passage DPCs stimulate the expression of certain trichogenic genes in DSCs. © 2010 The Society for Investigative Dermatology.


Yamazaki M.,Tokyo Medical University | Sato A.,Tokyo Memorial Clinic Hirayama | Toyoshima K.-E.,Phoenixbio | Kojima Y.,Phoenixbio | And 5 more authors.
Journal of Dermatology | Year: 2011

Female pattern hair loss (FPHL) is frequently referred to as female androgenetic alopecia (FAGA). However, the role of androgen in this type of hair loss remains uncertain. We previously reported greater therapeutic efficacy of finasteride in Japanese male androgenetic alopecia (MAGA) patients in cases where the CAG repeats of the androgen receptor (AR) gene were short. To examine the correlation between CAG repeat numbers and the therapeutic efficacy of finasteride in FPHL patients, the efficacy of finasteride (1 mg/day) was evaluated macroscopically. Because women have two X-chromosomes, the shorter and longer CAG repeat numbers were analyzed in 37 Japanese FPHL patients, then the correlation of these factors was statistically analyzed by anova. No statistical significance in terms of the differences in CAG repeat numbers was detected among the four groups classified on the basis of the efficacy of finasteride. From these results, it may be concluded that the efficacy of this medicine in each FPHL patient cannot be predicted by the CAG repeat numbers in the AR gene. © 2010 Japanese Dermatological Association.


PubMed | PhoenixBio
Type: Comparative Study | Journal: The Journal of investigative dermatology | Year: 2010

We previously showed that cultured rat dermal papilla cells (DPCs) retain their hair-inducing capacity on afollicular epidermal cell (EPCs). Here, we examined the hair growth-inducing capacity of differently subcultured DPCs by transplanting them, along with rat EPCs, onto the backs of nude mice (graft chamber assay). DPCs at passage (p) 6 (DPCs(p6) or, more generally, low-passage DPCs) induced hair formation. However, DPCs(p>30) (high-passage DPCs) had no such activity and induced only subepidermal hair follicles (HFs) that were not encapsulated by the dermal sheath (DS). Thus, we examined the effect of DS cells (DSCs(p=1)) on the ability of DPCs(p=60) to induce hair growth by testing a mixture of these two cell types (cotransplant) in the graft chamber assay, in which DSCs(p=1) and DPCs(p=60) were labeled with enhanced green fluorescent protein (EGFP) and 1,1-dioctadecyl-3,3,3,3-tetramethylindocarbocyanine perchlorate (DiI), respectively. These cotransplants generated hairs as actively as did DPCs(p=6) transplants. Their HFs were encapsulated with EGFP(+)-DS and had DPs consisting largely of EGFP(+)-DPCs (47%) and DiI(+)-DPCs (43%), indicating a major contribution of DSC(p=1)-derived DPCs to HF induction. In addition, the results of in vitro coculture of DPCs(p=60) and DSCs(p=1) suggest that high-passage DPCs stimulate the expression of certain trichogenic genes in DSCs.

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