Nagoya-shi, Japan
Nagoya-shi, Japan

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PubMed | Center for Neurological Diseases and Cancer, Mano Womens Clinic and 65 Tsurumai cho
Type: | Journal: Free radical biology & medicine | Year: 2016

Oxidative stress plays an important role in the pathogenesis of preeclampsia. Recently, molecular hydrogen (H


Ishikawa J.,65 Tsurumai cho | Takahashi N.,Orthopedic Surgery and Rheumatology | Matsumoto T.,Orthopedic Surgery and Rheumatology | Yoshioka Y.,Orthopedic Surgery and Rheumatology | And 7 more authors.
Bone | Year: 2016

Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial hyperplasia and chronic inflammation, which lead to the progressive destruction of cartilage and bone in the joints. Numerous studies have reported that administrations of various types of MSCs improve arthritis symptoms in animal models, by paracrine mechanisms. However, the therapeutic effects of the secreted factors alone, without the cell graft, have been uncertain. Here, we show that a single intravenous administration of serum-free conditioned medium (CM) from human deciduous dental pulp stem cells (SHED-CM) into anti-collagen type II antibody-induced arthritis (CAIA), a mouse model of rheumatoid arthritis (RA), markedly improved the arthritis symptoms and joint destruction. The therapeutic efficacy of SHED-CM was associated with an induction of anti-inflammatory M2 macrophages in the CAIA joints and the abrogation of RANKL expression. SHED-CM specifically depleted of an M2 macrophage inducer, the secreted ectodomain of sialic acid-binding Ig-like lectin-9 (ED-Siglec-9), exhibited a reduced ability to induce M2-related gene expression and attenuate CAIA. SHED-CM also inhibited the RANKL-induced osteoclastogenesis in vitro. Collectively, our findings suggest that SHED-CM provides multifaceted therapeutic effects for treating CAIA, including the ED-Siglec-9-dependent induction of M2 macrophage polarization and inhibition of osteoclastogenesis. Thus, SHED-CM may represent a novel anti-inflammatory and reparative therapy for RA. © 2015 Elsevier Inc.


Hirata A.,65 Tsurumai cho | Fukaya M.,65 Tsurumai cho | Yokoyama Y.,65 Tsurumai cho | Miyahara R.,Nagoya University | And 2 more authors.
Digestive Surgery | Year: 2016

Background: It is unclear which reconstructive route (retrocolic or antecolic) is more effective in preventing postoperative gastroesophageal reflux disease (GERD) in Roux-en-Y reconstruction following distal gastrectomy. Methods: Eighty-one eligible patients (retrocolic, n = 39; antecolic, n = 42) underwent endoscopies before surgery and 1 year after surgery to evaluate reflux esophagitis according to the Los Angeles classifications. The relative anatomical position of gastrojejunostomy to the cardia was measured by CT imaging. Results: The proportion of patients with reflux esophagitis was also significantly higher in the antecolic group than in the retrocolic group (38.1 vs. 10.3%, p = 0.005). Multivariate analysis revealed that antecolic reconstruction and body mass index (BMI) were independent risk factors for reflux esophagitis. The relative position of gastrojejunostomy to the cardia in the antecolic group was shifted to the left laterally (59.0 vs. 28.8 degree, p < 0.001) and ventrally (65.4 vs. 39.8 degree, p < 0.001) than in the retrocolic group. There was a positive correlation between BMI and left lateral and ventral shifts of gastrojejunostomy in the antecolic group. Conclusion: Retrocolic reconstruction may be superior to antecolic reconstruction in preventing postoperative GERD, especially in obese patients. The left lateral and ventral shifts of gastrojejunostomy after antecolic reconstruction may aggravate the occurrence of GERD. © 2016 S. Karger AG, Basel.


PubMed | Orthopedic Surgery and Rheumatology, 65 Tsurumai cho and Nagoya University
Type: | Journal: Bone | Year: 2016

Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial hyperplasia and chronic inflammation, which lead to the progressive destruction of cartilage and bone in the joints. Numerous studies have reported that administrations of various types of MSCs improve arthritis symptoms in animal models, by paracrine mechanisms. However, the therapeutic effects of the secreted factors alone, without the cell graft, have been uncertain. Here, we show that a single intravenous administration of serum-free conditioned medium (CM) from human deciduous dental pulp stem cells (SHED-CM) into anti-collagen type II antibody-induced arthritis (CAIA), a mouse model of rheumatoid arthritis (RA), markedly improved the arthritis symptoms and joint destruction. The therapeutic efficacy of SHED-CM was associated with an induction of anti-inflammatory M2 macrophages in the CAIA joints and the abrogation of RANKL expression. SHED-CM specifically depleted of an M2 macrophage inducer, the secreted ectodomain of sialic acid-binding Ig-like lectin-9 (ED-Siglec-9), exhibited a reduced ability to induce M2-related gene expression and attenuate CAIA. SHED-CM also inhibited the RANKL-induced osteoclastogenesis in vitro. Collectively, our findings suggest that SHED-CM provides multifaceted therapeutic effects for treating CAIA, including the ED-Siglec-9-dependent induction of M2 macrophage polarization and inhibition of osteoclastogenesis. Thus, SHED-CM may represent a novel anti-inflammatory and reparative therapy for RA.


PubMed | Nagoya University, 65 Tsurumai cho and The Francis Crick Institute
Type: | Journal: Scientific reports | Year: 2016

Bone marrow-derived mesenchymal stromal cells (BM-MSCs) in culture are derived from BM stromal cells or skeletal stem cells. Whereas MSCs have been exploited in clinical medicine, the identification of MSC-specific markers has been limited. Here, we report that a cell surface and secreted protein, Meflin, is expressed in cultured MSCs, fibroblasts and pericytes, but not other types of cells including epithelial, endothelial and smooth muscle cells. In vivo, Meflin is expressed by immature osteoblasts and chondroblasts. In addition, Meflin is found on stromal cells distributed throughout the BM, and on pericytes and perivascular cells in multiple organs. Meflin maintains the undifferentiated state of cultured MSCs and is downregulated upon their differentiation, consistent with the observation that Meflin-deficient mice exhibit increased number of osteoblasts and accelerated bone development. In the bone and BM, Meflin is more highly expressed in primitive stromal cells that express platelet-derived growth factor receptor and Sca-1 than the Sca-1-negative adipo-osteogenic progenitors, which create a niche for hematopoiesis. Those results are consistent with a decrease in the number of clonogenic colony-forming unit-fibroblasts within the BM of Meflin-deficient mice. These preliminary data suggest that Meflin is a potential marker for cultured MSCs and their source cells in vivo.

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