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  • 1
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    Sema3A regulates bone-mass accrual through sensory innervations (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-05-07
    Description: Semaphorin 3A (Sema3A) is a diffusible axonal chemorepellent that has an important role in axon guidance. Previous studies have demonstrated that Sema3a(-/-) mice have multiple developmental defects due to abnormal neuronal innervations. Here we show in mice that Sema3A is abundantly expressed in bone, and cell-based assays showed that Sema3A affected osteoblast differentiation in a cell-autonomous fashion. Accordingly, Sema3a(-/-) mice had a low bone mass due to decreased bone formation. However, osteoblast-specific Sema3A-deficient mice (Sema3acol1(-/-) and Sema3aosx(-/-) mice) had normal bone mass, even though the expression of Sema3A in bone was substantially decreased. In contrast, mice lacking Sema3A in neurons (Sema3asynapsin(-/-) and Sema3anestin(-/-) mice) had low bone mass, similar to Sema3a(-/-) mice, indicating that neuron-derived Sema3A is responsible for the observed bone abnormalities independent of the local effect of Sema3A in bone. Indeed, the number of sensory innervations of trabecular bone was significantly decreased in Sema3asynapsin(-/-) mice, whereas sympathetic innervations of trabecular bone were unchanged. Moreover, ablating sensory nerves decreased bone mass in wild-type mice, whereas it did not reduce the low bone mass in Sema3anestin(-/-) mice further, supporting the essential role of the sensory nervous system in normal bone homeostasis. Finally, neuronal abnormalities in Sema3a(-/-) mice, such as olfactory development, were identified in Sema3asynasin(-/-) mice, demonstrating that neuron-derived Sema3A contributes to the abnormal neural development seen in Sema3a(-/-) mice, and indicating that Sema3A produced in neurons regulates neural development in an autocrine manner. This study demonstrates that Sema3A regulates bone remodelling indirectly by modulating sensory nerve development, but not directly by acting on osteoblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukuda, Toru -- Takeda, Shu -- Xu, Ren -- Ochi, Hiroki -- Sunamura, Satoko -- Sato, Tsuyoshi -- Shibata, Shinsuke -- Yoshida, Yutaka -- Gu, Zirong -- Kimura, Ayako -- Ma, Chengshan -- Xu, Cheng -- Bando, Waka -- Fujita, Koji -- Shinomiya, Kenichi -- Hirai, Takashi -- Asou, Yoshinori -- Enomoto, Mitsuhiro -- Okano, Hideyuki -- Okawa, Atsushi -- Itoh, Hiroshi -- NS065048/NS/NINDS NIH HHS/ -- England -- Nature. 2013 May 23;497(7450):490-3. doi: 10.1038/nature12115. Epub 2013 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, School of Medicine, Keio University, Shinanomachi 35, Shinjyuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23644455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Remodeling ; Bone and Bones/anatomy & histology/*innervation/*metabolism ; Cell Differentiation ; Cells, Cultured ; Female ; Male ; Mice ; Organ Size ; Osteoblasts/cytology/metabolism ; Semaphorin-3A/deficiency/genetics/*metabolism ; Sensory Receptor Cells/cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-11-01
    Description: Adiponectin secreted from adipocytes binds to adiponectin receptors AdipoR1 and AdipoR2, and exerts antidiabetic effects via activation of AMPK and PPAR-alpha pathways, respectively. Levels of adiponectin in plasma are reduced in obesity, which causes insulin resistance and type 2 diabetes. Thus, orally active small molecules that bind to and activate AdipoR1 and AdipoR2 could ameliorate obesity-related diseases such as type 2 diabetes. Here we report the identification of orally active synthetic small-molecule AdipoR agonists. One of these compounds, AdipoR agonist (AdipoRon), bound to both AdipoR1 and AdipoR2 in vitro. AdipoRon showed very similar effects to adiponectin in muscle and liver, such as activation of AMPK and PPAR-alpha pathways, and ameliorated insulin resistance and glucose intolerance in mice fed a high-fat diet, which was completely obliterated in AdipoR1 and AdipoR2 double-knockout mice. Moreover, AdipoRon ameliorated diabetes of genetically obese rodent model db/db mice, and prolonged the shortened lifespan of db/db mice on a high-fat diet. Thus, orally active AdipoR agonists such as AdipoRon are a promising therapeutic approach for the treatment of obesity-related diseases such as type 2 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada-Iwabu, Miki -- Yamauchi, Toshimasa -- Iwabu, Masato -- Honma, Teruki -- Hamagami, Ken-ichi -- Matsuda, Koichi -- Yamaguchi, Mamiko -- Tanabe, Hiroaki -- Kimura-Someya, Tomomi -- Shirouzu, Mikako -- Ogata, Hitomi -- Tokuyama, Kumpei -- Ueki, Kohjiro -- Nagano, Tetsuo -- Tanaka, Akiko -- Yokoyama, Shigeyuki -- Kadowaki, Takashi -- England -- Nature. 2013 Nov 28;503(7477):493-9. doi: 10.1038/nature12656. Epub 2013 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan [2] Department of Integrated Molecular Science on Metabolic Diseases, 22nd Century Medical and Research Center, The University of Tokyo, Tokyo 113-0033, Japan [3] Department of Molecular Medicinal Sciences on Metabolic Regulation, 22nd Century Medical and Research Center, The University of Tokyo, Tokyo 113-0033, Japan [4].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24172895" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylate Kinase/metabolism ; Adiponectin/metabolism/pharmacology ; Adipose Tissue, White/drug effects/metabolism/pathology ; Administration, Oral ; Animals ; Diabetes Mellitus, Type 2/complications/*drug therapy/metabolism/prevention & ; control ; Diet, High-Fat ; Drug Evaluation, Preclinical ; Dyslipidemias/drug therapy ; Enzyme Activation/drug effects ; Glucose Intolerance/drug therapy ; Inflammation/drug therapy ; Insulin Resistance ; Liver/drug effects/metabolism/pathology ; Longevity/*drug effects ; Mice ; Mitochondria/drug effects/metabolism ; Muscle Fibers, Skeletal/cytology/drug effects ; Muscles/cytology ; Obesity/complications/drug therapy/genetics/*physiopathology ; Oxidative Stress/drug effects ; PPAR alpha/metabolism ; Piperidines/administration & dosage/metabolism/*pharmacology/therapeutic use ; Receptors, Adiponectin/*agonists/deficiency/genetics/metabolism ; Signal Transduction/drug effects ; Small Molecule Libraries/chemistry ; Transcription Factors/biosynthesis ; Triglycerides/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Meis1 regulates postnatal cardiomyocyte cell cycle arrest (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-04-19
    Description: The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal day 7 and the mechanisms of cardiomyocyte cell cycle arrest remain unclear. The homeodomain transcription factor Meis1 is required for normal cardiac development but its role in cardiomyocytes is unknown. Here we identify Meis1 as a critical regulator of the cardiomyocyte cell cycle. Meis1 deletion in mouse cardiomyocytes was sufficient for extension of the postnatal proliferative window of cardiomyocytes, and for re-activation of cardiomyocyte mitosis in the adult heart with no deleterious effect on cardiac function. In contrast, overexpression of Meis1 in cardiomyocytes decreased neonatal myocyte proliferation and inhibited neonatal heart regeneration. Finally, we show that Meis1 is required for transcriptional activation of the synergistic CDK inhibitors p15, p16 and p21. These results identify Meis1 as a critical transcriptional regulator of cardiomyocyte proliferation and a potential therapeutic target for heart regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159712/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159712/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahmoud, Ahmed I -- Kocabas, Fatih -- Muralidhar, Shalini A -- Kimura, Wataru -- Koura, Ahmed S -- Thet, Suwannee -- Porrello, Enzo R -- Sadek, Hesham A -- 1R01HL115275-01/HL/NHLBI NIH HHS/ -- R01 HL115275/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 May 9;497(7448):249-53. doi: 10.1038/nature12054. Epub 2013 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23594737" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Animals, Newborn ; *Cell Cycle Checkpoints ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p15/metabolism ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Female ; Heart/anatomy & histology/physiology ; Homeodomain Proteins/genetics/*metabolism ; Male ; Mice ; Myocardial Infarction/metabolism/pathology ; Myocytes, Cardiac/*cytology/*metabolism ; Neoplasm Proteins/deficiency/genetics/*metabolism ; Regeneration ; Transcriptional Activation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Vascularized and functional human liver from an iPSC-derived organ bud transplant (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-07-05
    Description: A critical shortage of donor organs for treating end-stage organ failure highlights the urgent need for generating organs from human induced pluripotent stem cells (iPSCs). Despite many reports describing functional cell differentiation, no studies have succeeded in generating a three-dimensional vascularized organ such as liver. Here we show the generation of vascularized and functional human liver from human iPSCs by transplantation of liver buds created in vitro (iPSC-LBs). Specified hepatic cells (immature endodermal cells destined to track the hepatic cell fate) self-organized into three-dimensional iPSC-LBs by recapitulating organogenetic interactions between endothelial and mesenchymal cells. Immunostaining and gene-expression analyses revealed a resemblance between in vitro grown iPSC-LBs and in vivo liver buds. Human vasculatures in iPSC-LB transplants became functional by connecting to the host vessels within 48 hours. The formation of functional vasculatures stimulated the maturation of iPSC-LBs into tissue resembling the adult liver. Highly metabolic iPSC-derived tissue performed liver-specific functions such as protein production and human-specific drug metabolism without recipient liver replacement. Furthermore, mesenteric transplantation of iPSC-LBs rescued the drug-induced lethal liver failure model. To our knowledge, this is the first report demonstrating the generation of a functional human organ from pluripotent stem cells. Although efforts must ensue to translate these techniques to treatments for patients, this proof-of-concept demonstration of organ-bud transplantation provides a promising new approach to study regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takebe, Takanori -- Sekine, Keisuke -- Enomura, Masahiro -- Koike, Hiroyuki -- Kimura, Masaki -- Ogaeri, Takunori -- Zhang, Ran-Ran -- Ueno, Yasuharu -- Zheng, Yun-Wen -- Koike, Naoto -- Aoyama, Shinsuke -- Adachi, Yasuhisa -- Taniguchi, Hideki -- England -- Nature. 2013 Jul 25;499(7459):481-4. doi: 10.1038/nature12271. Epub 2013 Jul 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Regenerative Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa 236-0004, Japan. (ttakebe@yokohama-cu.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23823721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Drug-Induced Liver Injury/therapy ; Endothelial Cells/cytology/metabolism/transplantation ; Gene Expression Profiling ; Humans ; Induced Pluripotent Stem Cells/*cytology/metabolism/transplantation ; Liver/*blood supply/embryology/metabolism/*physiology ; Liver Failure/therapy ; Liver Transplantation ; Mesoderm/cytology/metabolism/transplantation ; Mice ; Regenerative Medicine/*methods ; Tissue Culture Techniques
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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