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1. 先天性性腺刺激ホルモン放出ホルモン欠乏症（特発性低ゴナドトロピン性性腺機能低下） congenital gonadotropin releasing hormone deficiency idiopathic hypogonadotropic hypogonadism
2. 待機的経皮的冠動脈インターベンションのための抗血栓療法：臨床研究 antithrombotic therapy for elective percutaneous coronary intervention clinical studies
3. 待機的経皮的冠動脈インターベンションのための抗血栓療法：一般的使用 antithrombotic therapy for elective percutaneous coronary intervention general use
4. 急性心臓同種移植拒絶反応：治療 acute cardiac allograft rejection treatment
5. エプスタインバーウイルス（EBウイルス）のウイルス学 virology of epstein barr virus

English Journal

The Role of Neuropilin-1/Semaphorin 3A Signaling in Lymphatic Vessel Development and Maturation.

Ochsenbein AM, Karaman S, Jurisic G, Detmar M.Author information Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Wolfgang Pauli-Str. 10, HCI H303, 8093, Zurich, Switzerland.AbstractDuring development, the lymphatic and the blood vascular system form highly branched networks that show extensive architectural similarities with the peripheral nervous system. Increasing evidence suggests that the vascular and the nervous systems share signaling pathways to overcome common challenges such as guidance of growth and patterning. Semaphorins, a large group of proteins originally identified as axon guidance molecules with repelling function, and their receptors, neuropilins and plexins, have recently also been implicated in vascular development. Here, we summarize the role of semaphorins and their receptors in angiogenesis and lymphangiogenesis, with an emphasis on neuropilin-1/semaphorin 3A interactions in lymphatic vessel maturation and valve formation. Understanding the basic principles of lymphatic vessel development and maturation might facilitate the development of therapies for the treatment of human diseases associated with lymphedema.
Advances in anatomy, embryology, and cell biology.Adv Anat Embryol Cell Biol.2014;214:143-52. doi: 10.1007/978-3-7091-1646-3_11.
During development, the lymphatic and the blood vascular system form highly branched networks that show extensive architectural similarities with the peripheral nervous system. Increasing evidence suggests that the vascular and the nervous systems share signaling pathways to overcome common challeng
PMID 24276892

Impeding Macrophage Entry into Hypoxic Tumor Areas by Sema3A/Nrp1 Signaling Blockade Inhibits Angiogenesis and Restores Antitumor Immunity.

Casazza A1, Laoui D2, Wenes M1, Rizzolio S3, Bassani N1, Mambretti M1, Deschoemaeker S1, Van Ginderachter JA2, Tamagnone L3, Mazzone M4.Author information 1Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, 3000 Leuven, Belgium; Laboratory of Molecular Oncology and Angiogenesis, Department of Oncology, Vesalius Research Center, KU Leuven, 3000 Leuven, Belgium.2Laboratory of Myeloid Cell Immunology, VIB, 1050 Brussels, Belgium; Laboratory of Cellular and Molecular Immunology, Department of Molecular and Cellular Interactions, Vrije Universiteit Brussel, 1050 Brussels, Belgium.3Institute for Cancer Research at Candiolo, Department of Oncology, University of Torino, 10060 Candiolo, Torino, Italy.4Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, 3000 Leuven, Belgium; Laboratory of Molecular Oncology and Angiogenesis, Department of Oncology, Vesalius Research Center, KU Leuven, 3000 Leuven, Belgium. Electronic address: massimiliano.mazzone@vib-kuleuven.be.AbstractRecruitment of tumor-associated macrophages (TAMs) into avascular areas sustains tumor progression; however, the underlying guidance mechanisms are unknown. Here, we report that hypoxia-induced Semaphorin 3A (Sema3A) acts as an attractant for TAMs by triggering vascular endothelial growth factor receptor 1 phosphorylation through the associated holoreceptor, composed of Neuropilin-1 (Nrp1) and PlexinA1/PlexinA4. Importantly, whereas Nrp1 levels are downregulated in the hypoxic environment, Sema3A continues to regulate TAMs in an Nrp1-independent manner by eliciting PlexinA1/PlexinA4-mediated stop signals, which retain them inside the hypoxic niche. Consistently, gene deletion of Nrp1 in macrophages favors TAMs' entrapment in normoxic tumor regions, which abates their pro-angiogenic and immunosuppressive functions, hence inhibiting tumor growth and metastasis. This study shows that TAMs' heterogeneity depends on their localization, which is tightly controlled by Sema3A/Nrp1 signaling.
Cancer cell.Cancer Cell.2013 Dec 9;24(6):695-709. doi: 10.1016/j.ccr.2013.11.007.
Recruitment of tumor-associated macrophages (TAMs) into avascular areas sustains tumor progression; however, the underlying guidance mechanisms are unknown. Here, we report that hypoxia-induced Semaphorin 3A (Sema3A) acts as an attractant for TAMs by triggering vascular endothelial growth factor rec
PMID 24332039

Location, Location, Location: Macrophage Positioning within Tumors Determines Pro- or Antitumor Activity.

Rivera LB1, Bergers G2.Author information 1Department of Neurological Surgery, Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA.2Department of Neurological Surgery, Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: gabriele.bergers@ucsf.edu.AbstractMacrophages infiltrate hypoxic tumor regions, where they promote angiogenesis and immunosuppression. In this issue of Cancer Cell, Casazza and colleagues report that tumor-associated macrophage (TAM) entry into avascular tumor areas is regulated by Semaphorin 3A/Neuropilin-1 signaling; interference with this pathway entraps TAMs in oxygenated areas, preventing their tumorigenic function.
Cancer cell.Cancer Cell.2013 Dec 9;24(6):687-9. doi: 10.1016/j.ccr.2013.11.014.
Macrophages infiltrate hypoxic tumor regions, where they promote angiogenesis and immunosuppression. In this issue of Cancer Cell, Casazza and colleagues report that tumor-associated macrophage (TAM) entry into avascular tumor areas is regulated by Semaphorin 3A/Neuropilin-1 signaling; interference
PMID 24332035

Japanese Journal

抗疲労性筋線維の形成機構の解明と食品機能学的制御

辰巳隆一
上原記念生命科学財団研究報告集 32, 9p, 2018
NAID 40021786887

筋幹細胞の新たな性質を見出す

鈴木貴弘
食肉の科学 59(1), 33-38, 2018
NAID 40021637798

Characterization of Konjac Ceramide (kCer) Binding to Sema3A Receptor Nrp1

Usuki Seigo,Tamura Noriko,Tamura Tomohiro,Mukai Katsuyuki,Igarashi Yasuyuki
日本油化学会誌 67(1), 87-94, 2018
… Thus prepared kCer showed an activation effect on Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerizaion, resulting in opposing NGF-induced neurite outgrowth. … In the present study, we have shown that kCer is a potential Sema3A-like ligand that has a competitive effect on Sema3A binding to a cell surface receptor Nrp1, but animal-type ceramides have no effect on Sema3A binding to Nrp1. …
NAID 130006301048

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