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Prohibitins, novel vitamin K2 target factors in osteoblast

Journal of Biosciences and Medicines 2013年第3期1卷 1-4页

作者： Tatsuya Uebi Makoto Umeda Naoya Maekawa Satoshi Karasawa Hiroshi Handa Takeshi Imai Department of Aging Intervention National Center for Geriatrics and Gerontology (NCGG) Obu Japan Faculty of Bioscience and Biotechnology Tokyo Institute of Technology Yokohama Japan

Vitamin K2 (VK2, menaquinone) is a drug for osteoporosis. VK2 acts as a cofactor for γ-glutamyl carboxylase, which catalyzes the carboxylation of specific glutamic acid residues (γ-carboxylation) of substrate proteins. Here we demonstrate that VK2 also regulate osteoblastgenic marker gene expression. Using VK2-immobilzed nanobeads new target proteins were purified and identified from osteoblastic cell line. They are prohibitin 1 and 2 (PHB1 & 2), respectively. To confirm the PHBs function on VK2-dependent transcription, PHB1 & 2 were knock-down and osteocalcin gene 2 transcriptions were analyzed, indicating that PHBs regulate VK2-dependent transcription. Taken together PHBs are VK2 target proteins for osteoblastgenic transcription.

关键词： Vitamin K2 Prohibitin Osteoblast runt-related Transcription Factor 2 (Runx2)

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Cancer detection by ubiquitin carboxyl-terminal esterase L1 methylation in pancreatobiliary fluids

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World Journal of Gastroenterology 2013年第11期19卷 1718-1727页

作者： Norihiro Kato Hiroyuki Yamamoto Yasushi Adachi Hirokazu Ohashi Hiroaki Taniguchi Hiromu Suzuki Mayumi Nakazawa Hiroyuki Kaneto Shigeru Sasaki Kohzoh Imai Yasuhisa Shinomura First Department of Internal Medicine Sapporo Medical University School of MedicineSapporo 060-8543Japan The Section of Antibody Vaccine and Molecular Targeted Therapy ResearchThe Institute of Medical ScienceThe University of TokyoTokyo 108-8639Japan Department of Molecular Biology Sapporo Medical University School of MedicineSapporo 060-8556Japan Division of Gastroenterology Muroran City General HospitalMuroran 051-8512Japan

AIM:To evaluate the utility of measuring epigenetic alterations in pancreatic and biliary fluids in determining molecular markers for pancreatobiliary ***:DNA was extracted from undiluted pancreatic and biliary *** a surrogate for a genomewide hypomethylation assay,levels of long interspersed nuclear element-1(LINE-1) methylation were analyzed using bisulfite *** island hypermethylation of 10 tumor-associated genes,aryl-hydrocarbon receptor repressor,adenomatous polyposis coli,calcium channel,voltage dependent,T type α1G subunit,insulin-like growth factor 2,O-6-methyl-guanine-DNA methyltransferase,neurogenin 1,CDKN2A,runt-related transcription factor 3(RUNX3),secreted frizzled-related protein 1,and ubiquitin carboxyl-terminal esterase L1(UCHL1),was analyzed using *** examine the role of CpG methylation and histone deacetylation in the silencing of UCHL1,human gallbladder carcinoma cell lines and pancreatic carcinoma cell lines were treated with 2 or 5 μmol/L 5-AZA-dC for 72 h or 100 nmol/L Trichostatin A for 24 *** the treatment,UCHL1 expression was analyzed by real-time reverse transcription-polymerase chain ***:Pancreatobiliary cancers exhibited significantly lower LINE-1 methylation levels in pancreatic and biliary fluids than did noncancerous pancreatobiliary disease(58.7% ± 4.3% vs 61.7% ± 2.2%,P = 0.027;53.8% ± 6.6% vs 57.5% ± 1.7%,P = 0.007);however,LINE-1 hypomethylation was more evident in pancreatic cancer tissues than in pancreatic fluids(45.4% ± 5.5% vs 58.7% ± 4.3%,P related with LINE-1 *** of the UCHL1 gene was cancer-specific and most frequently detected in pancreatic(67%) or biliary(70%) fluids from patients with pancreatobiliary *** a single marker,hypermethylation of the UCHL1 gene in pancreatic and biliary fluids was most useful for the de

关键词： Pancreatobiliary cancers DNA methylation Pancreatobiliary fluids Ubiquitin carboxyl-terminal esterase L1 runt-related transcription factor 3

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Molecular mechanisms of mesenchymal stem cell differentiation towards osteoblasts

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World Journal of Stem Cells 2013年第4期5卷 136-148页

作者： Maya Fakhry René Buchet David Magne Eva Hamade Bassam Badran ICBMS UMR CNRS 5246 University of Lyon 1 Genomic and Health laboratory/PRASE-EDST Campus Rafic Hariri-HadathBeirut-Liban Faculty of Sciences Lebanese university

Bone is a dynamic tissue that is constantly renewed by the coordinated action of two cell types, i.e., the bone-resorbing osteoclasts and the bone-forming osteoblasts. However, in some circumstances, bone regeneration exceeds bone self repair capacities. This is notably often the case after bone fractures, osteolytic bone tumor surgery, or osteonecrosis. In this regard,bone tissue engineering with autologous or allogenic mesenchymal stem cells(MSCs) is been widely developed. MSCs can be isolated from bone marrow or other tissues such as adipose tissue or umbilical cord, and can be implanted in bone defects with or without prior amplification and stimulation. However, the outcome of most pre-clinical studies remains relatively disappointing. A better understanding of the successive steps and molecular mechanisms involved in MSC-osteoblastic differentiation appears to be crucial to optimize MSC-bone therapy. In this review, we first present the important growth factors that stimulate osteoblastogenesis. Then we review the main transcription factors that modulate osteoblast differentiation, and the microRNAs(miRs)that inhibit their expression. Finally, we also discuss articles dealing with the use of these factors and miRs in the development of new bone MSC therapy strategies. We particularly focus on the studies using human MSCs, since significant differences exist between osteoblast differentiation mechanisms in humans and mice for instance.

关键词： Mesenchymal stem cells Osteogenesis runt-related 2 Wnt MicroRNAs

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