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Impact of Retrotransposons in Pluripotent Stem Cells
Yoshiaki Tanaka,In-Hyun Park,Leeyup Chung 한국분자세포생물학회 2012 Molecules and cells Vol.34 No.6
Retrotransposons, which constitute approximately 40% of the human genome, have the capacity to ‘jump’ across the genome. Their mobility contributes to oncogenesis, evolution, and genomic plasticity of the host genome. Induced pluripotent stem cells as well as embryonic stem cells are more susceptible than differentiated cells to genomic aberrations including insertion, deletion and duplication. Recent studies have revealed specific behaviors of retrotransposons in pluripotent cells. Here, we review recent progress in understanding retrotransposons and provide a perspective on the relationship between retrotransposons and genomic variation in pluripotent stem cells.
Yoshiaki Oda,Tomoyuki Takigawa,Ryo Ugawa,Yasuyuki Shiozaki,Haruo Misawa,Yoshihisa Sugimoto,Masato Tanaka,Toshifumi Ozaki 대한척추외과학회 2018 Asian Spine Journal Vol.12 No.2
Study Design: Cross sectional study. Purpose: To clarify the difference in position of the psoas muscle between adult spinal deformity (ASD) and lumbar spinal stenosis (LSS). Overview of Literature: Although it is known that the psoas major muscle deviates in ASD patients, no report is available regarding the difference in comparison with LSS patients. Methods: This study investigates 39 patients. For evaluating spinal alignment, pelvic tilt (PT), pelvic incidence (PI), sacral slope, lumbar lordosis (LL), PI–LL, Cobb angle, and the convex side, the lumbar curves were measured. For measuring the position of the psoas major at the L4/5 disk level, magnetic resonance imaging was used. The displacements of psoas major muscle were measured separately in the anterior–posterior and lateral directions. We examined the relationship between the radiographic parameters and anterior displacement (AD) and lateral displacement (LD) of the psoas major muscle. Results: AD was demonstrated in 15 cases with ASD and nine cases with LSS (p >0.05). LD was observed in 13 cases with ASD and no cases with LSS (p <0.01). The Cobb angle was significantly greater in cases with AD than in those without AD (p =0.04). PT, LL, PI– LL, and Cobb angle were significantly greater in cases with LD (p <0.05). All cases with LD had AD, but no case without AD had LD (p <0.001). The side of greater displacement at L4/5 and the convex side of the lumbar curve were consistent in all cases. Conclusions: Despite AD being observed in LSS as well, LD was observed only in the ASD group. Radiographic parameters were worse when LD was seen, rather than AD.
Foxf2 represses bone formation via Wnt2b/β-catenin signaling
Tanaka Tomoyuki,Takahashi Akira,Kobayashi Yutaka,Saito Masanori,Xiaolong Sun,Jingquan Chen,Ito Yoshiaki,Kato Tsuyoshi,Ochi Hiroki,Sato Shingo,Yoshii Toshitaka,Okawa Atsushi,Carlsson Peter,Inose Hiroyu 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Differentiation of mesenchymal stem cells (MSCs) into osteoblasts is a critical process for proper skeletal development and acquisition/maintenance of bone mass. However, since this regulatory mechanism has not yet been fully elucidated, the treatment of severe osteoporosis and fractures is a challenge. Here, through a comprehensive analysis of gene expression during the differentiation of MSCs into osteoblasts, we show that the forkhead transcription factor Foxf2 is a crucial regulator of this process. Foxf2 expression transiently increased during MSC osteoblastic differentiation. Overexpression of Foxf2 in MSCs inhibited osteoblastic differentiation, and conversely, knockdown of Foxf2 expression promoted this process. Osteoprogenitor-specific Foxf2 knockout mice developed a high bone mass phenotype due to increased bone formation. RNA-seq analysis and molecular experiments revealed that Foxf2 regulation of bone formation is mediated by Wnt2b. Knockdown of Foxf2 in mouse femurs enhanced bone regeneration in vivo. FOXF2 expression was correlated with hip bone mineral density in postmenopausal women with low bone mass. Finally, inhibition of FOXF2 promoted osteoblastic differentiation of human MSCs. This study uncovers a critical role of Foxf2 in the differentiation of MSCs into osteoblasts and provides insight into the pathogenesis associated with bone-related diseases such as osteoporosis and nonunion after fracture
Yoshiaki Kubota,Masaaki Miyamoto,Gen Takagi,Takeshi Ikeda,Sonoko Kirinoki-Ichikawa,Kotoko Tanaka,Kyoichi Mizuno 대한의학회 2012 Journal of Korean medical science Vol.27 No.11
The vascular endothelial function is impaired in the very early stage of atherosclerosis in diabetic patients. The goal of this study was to identify the mechanism underlying the improvement in vascular endothelial function by sitagliptin in type 2 diabetes mellitus patients. This study was an open-labeled prospective observational single arm trial. Forty patients were treated with 50 mg of sitagliptin once daily for 12-weeks. The flowmediated dilation (FMD) and plasma adiponectin were measured at baseline and 12 weeks after initiating treatment. The %FMD was significantly increased after treatment (4.13 ± 1.59 vs 5.12 ± 1.55, P < 0.001), whereas the nitroglycerin-mediated dilation (NMD) did not change. The plasma adiponectin levels significantly increased (13.0 ± 11.3vs 14.3 ± 12.8, P < 0.001). The changes in the FMD were significantly correlated with those of the plasma adiponectin (r = 0.322, P < 0.05). A multivariate linear regression analysis demonstrated that the improvement in the FMD is associated with the plasma adiponectin (P < 0.05). The treatment of type 2 diabetes mellitus patients with sitagliptin reverses vascular endothelial dysfunction, as evidenced by increase in the FMD, and improvement of the adiponectin levels (UMIN Clinical Trials Registry System as trial ID UMIN000004236).
Yoshiaki Yamanaka,Kunitaka Menuki,Yukichi Zenke,Satoshi Ikeda,Eiji Hatakeyama,Kimiaki Kawano,Satoshi Nishida,Hiroaki Tanaka,Keiichi Yumisashi,Akinori Sakai 대한골다공증학회 2019 Osteoporosis and Sarcopenia Vol.5 No.4
Objectives: To assess the vitamin D status in postmenopausal women with osteoporotic fractures, determine its concentration by fracture site at the clinical setting, and compare the proportion of vitamin D deficiency with that reported in literature. Methods: The prospective study included 317 postmenopausal women with osteoporotic fractures who were treated consecutively from 2016 to 2018. After obtaining informed consent for participation in the seamless treatment of osteoporosis against fractures study, which is our initiative to prevent secondary osteoporotic fractures, we registered the patients, examined bone mineral density (BMD) at the unfractured femoral neck and lumbar spine, serum 25-hydroxyvitamin D (25(OH)D) concentration, blood chemistry, and bone turnover markers. Results: The mean age of the patients was 80.7 years. Moreover, 78% of patients of all fractures had 25(OH)D concentration < 20 ng/mL, whereas 12% of patients had 25(OH)D concentration 30 ng/mL 25(OH)D concentration in hip fractures was significantly lower than that in vertebral or distal radius fractures (P < 0.05). Multiple regression analysis revealed that 25(OH)D concentration is significantly associated with femoral neck BMD (b ¼ 0.16; 95% confidence interval [CI], 0.78e12.17, P ¼ 0.03) and serum albumin concentration (b ¼ 0.21; 95% CI, 0.62e2.96, P < 0.001) in patients with 25(OH)D concentration < 30 ng/mL. Conclusions: The results of this study show that the proportion of postmenopausal women with osteoporotic fractures who had vitamin D deficiency was higher than the proportion in previous reports that examined general postmenopausal women (35.2%e52.0%).
Hiroki Tanaka,Shimpei Matsusaki,Youichirou Baba,Yoshiaki Isono,Tomohiro Sase,Hiroshi Okano,Tomonori Saito,Katsumi Mukai,Tetsuya Murata,Hiroki Taoka 대한소화기내시경학회 2018 Clinical Endoscopy Vol.51 No.2
Background/Aims: It is sometimes difficult to distinguish between malignant and benign biliary strictures using imaging studiesalone, and pathological diagnosis is necessary. The aim of this study was to determine the usefulness of endoscopic transpapillary tissuesampling and factors predictive of diagnostic accuracy. Methods: From April 2008 to December 2014, 136 patients underwent endoscopic transpapillary tissue sampling for malignantbiliary strictures. The cytological and histological findings were reported as negative, suspicious, or positive. Suspicious and positivefindings were defined as pathologically positive. Results: The sensitivity was 65.0% for forceps biopsy, 49.5% for brush cytology, 46.2% for bile aspiration cytology, and 21.9% forendoscopic nasobiliary drainage cytology. The combination of these procedures improved the sensitivity (72.8%). Endoscopictranspapillary tissue sampling was more sensitive for lesions of biliary origin (91.4%) than for extrabiliary lesions (66.3%). In surgicalcases, the sensitivity for tumors with an infiltrative growth pattern (53.3%) was significantly lower than for a tumor with an expandingor intermediate growth pattern (87.5%). Conclusions: Combining procedures can improve diagnostic accuracy. It may be possible to predict the sensitivity of endoscopictranspapillary tissue sampling by evaluating the etiology and tumor growth pattern using preoperative imaging studies.
New Advances in Human X Chromosome Status from a Developmental and Stem Cell Biology
Benjamin Patterson,Yoshiaki Tanaka,박인현 한국조직공학과 재생의학회 2017 조직공학과 재생의학 Vol.14 No.6
Recent advances in stem cell biology have dramatically increased the understanding of molecular and cellular mechanism of pluripotency and cell fate determination. Additionally, pluripotent stem cells (PSCs), including embryonic stem cells and induced pluripotent stem cells, arose as essential resources for disease modeling and cellular therapeutics. Despite these advancements, the epigenetic dysregulation in pluripotency such as the imprinting status, and X chromosome dosage compensation, and its consequences on future utility of PSCs yet remain unresolved. In this review, we will focus on the X chromosome regulation in human PSCs (hPSCs). We will introduce the previous findings in the dosage compensation process on mouse model, and make comparison with those of human systems. Particularly, the X chromosome activation status of human preimplantation embryos, and the regulation of the active X chromosome by human specific lincRNA, X Active Coating Transcript (XACT), will be discussed. We will also discuss the recent findings on higher order X chromosome architecture, and abnormal X chromosome status in hPSCs.