巻号一覧
107 巻 (1996)
- 6 号 p. 259-
- 5 号 p. 213-
- 4 号 p. 173-
- 3 号 p. 97-
- 2 号 p. 47-
- 1 号 p. 1-
前身誌
107 巻, 3 号
選択された号の論文の8件中1～8を表示しています
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血管形成と再構築の基礎眞崎 知生1996 年 107 巻 3 号 p. 97
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーPDF形式でダウンロード (882K) -
血管形成と再構築の基礎豊田 淑江, 森田 育男, 室田 誠逸1996 年 107 巻 3 号 p. 99-107
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーAngiogenesis, a process of new blood vessel formation, is an integral part of development, wound repair and tumor growth. The formation of capillary networks requires a complex series of cellular events, in which endothelial cells locally degrade their basement membrane, migrate into the connective tissue stroma, proliferate at the migrating tip, elongate and organize into capillary loops. In response to angiogenic stimuli, endothelial cells in culture develop networks of capillarylike tubes. In this paper, we showed the relationship between angiogenesis and diseases, the assay systems of angiogenesis and the reports of angiogenesis published recently.抄録全体を表示PDF形式でダウンロード (8400K) -
血管形成と再構築の基礎佐藤 靖史1996 年 107 巻 3 号 p. 109-117
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーEndothelial cells lining the lumen of vessels are maintained in the quiescent state and play important physiological roles. Yet, they can be de-differentiated and become one of the most rapidly proliferating of all cell types when stimulated. Angiogenesis or neovascularization is defined as the formation of new capillary vessels from existent microvessels, which plays a major role in the evolvement of a vascular supply in tissue during development or remodeling and disease. Angiogenesis is believed to be regulated by the balance between inducers and inhibitors. In this review article, I will summarize the molecules that regulate the process of angiogenesis.抄録全体を表示PDF形式でダウンロード (8050K) -
血管形成と再構築の基礎渋谷 正史1996 年 107 巻 3 号 p. 119-131
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーAngiogenesis is important not only in normal embryogenesis, tissue organization and its maintenance but also in pathological processes such as ocular disease in diabetes mellitus and rapid growth of tumors in vivo. Recently, endothelial cell-specific growth factor (VEGF) and its receptors (Flt family) has been characterized, and this ligand-tyrosine kinase receptor is considered to be one of the most important systems involved in angiogenesis. VEGF is induced by a variety of normal or tumor cells under conditions such as hypoxia and hypoglycemia and in the presence of substances such as hormones and growth factors. On the other hand, receptors of the Flt family (Flt-1, KDR/Flk-1, Flt-4) are basically strictly expressed only on vascular endothelial cells with a rare exception. Thus, the stimulation of VEGF-Flt towards angiogenesis is through a paracrine mechanism. A direct involvement of Flt-1 and KDR/Flk-1 in vasculogenesis/angiogenesis has recently been demonstrated by gene targetting studies. Blocking of this system might be a useful tool for suppression of solid tumors in vivo.抄録全体を表示PDF形式でダウンロード (10612K) -
血管形成と再構築の基礎宮園 浩平1996 年 107 巻 3 号 p. 133-140
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーTransforming growth factor-β (TGF-β) is a family of multifunctional proteins that inhibit the growth of most cell types, and these proteins induce the deposition of extracellular matrix. TGF-β inhibits the growth and migration of endothelial cells in vitro, but induces angiogenesis in vivo. TGF-β belongs to a larger superfamily known as the TGF-β superfamily, which includes activins and bone morphogenetic proteins. TGF-β is produced as latent high molecular weight complexes from producer cells and is then activated by plasmin or thrombospondin. Latent TGF-β binding protein (LTBP) is a component of the latent TGF-β complex produced from platelets and many other cell types; LTBP plays an important role for the interaction of the latent TGF-β complex with extracellular matrix components. TGF-, 3 binds several cell surface receptors, including type III receptor (betaglycan), endoglin, type II receptor and type I receptor. The type III receptor and endoglin are indirectly involved in the signal transduction. The type II and type I receptors have intracellular serine/threonine kinase domains. They form a heteromeric complex after ligand binding and are most important for signal transduction; the type II receptor transactivates the type I receptor, which transduces various signals.抄録全体を表示PDF形式でダウンロード (6631K) -
血管形成と再構築の基礎安藤 譲二1996 年 107 巻 3 号 p. 141-152
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーBlood flow plays important roles in the morphogenesis of blood vessels. For instance, increases in blood flow induce dilatation of the blood vessels, while decreases in blood flow cause reduction of vessel diameter. Blood flow also stimulates angiogenesis. In these blood flow-dependent phenomena, wall shear stress generated by flowing blood that acts on vascular endothelial cells works as a key factor. Numerous in vivo and in vitro studies have demonstrated that mechanical forces, shear stress, actually modulate the morphology and many functions of endothelial cells, and these forces also alter their gene expressions. More recently, a cis-acting shear stress responsive element was identified in the promoters of endothelial genes that respond to shear stress, suggesting a common mechanism linking biomechanical forces to gene expression. Details of the process in which shear stress-mediated changes in endothelial cell functions lead to vascular remodeling and angiogenesis, however, are not entirely clear. Elucidation of this problem will give us not only a better understanding of the morphogenesis of blood vessels but also new therapies that can help manage or prevent cardiovascular diseases including atherosclerosis.抄録全体を表示PDF形式でダウンロード (10264K) -
血管形成と再構築の基礎今村 道博1996 年 107 巻 3 号 p. 153-160
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーAngiogenesis, the formation of new capillaries, is critical for normal physiological processes such as embryonic development and wound repair. However, it also facilitates pathological processes including tumor growth, metastases, proliferative diabetic retinopathy and pannus formation in rheumatoid arthritis. It has been described that the angiogenesis occurs through a series of events that include endothelial cell protease production, migration and proliferation, tubule formation, and basement membrane incorporation. Within the last two decades, with in vivo assay systems, various kinds of growth factors were identified as angiogenic factors that promote endothelial cell proliferation and migration, while an in vitro model for angiogenesis indicated that extracellular matrix (ECM) proteins stimulated endothelial cells to organize into a capillary-like tubular network and suggested that the ECM proteins are involved in the tubule formation process of antiogenesis. Recent papers reported the identification of the specific receptors on endothelial cells involved in the ECM-induced capillary tube formation. This article will focus on papers describing the in vitro analyses of tube formation of endothelial cells.抄録全体を表示PDF形式でダウンロード (9206K) -
血管形成と再構築の基礎森 聖二郎, 斎藤 康1996 年 107 巻 3 号 p. 161-170
発行日: 1996年
公開日: 2007/02/06
ジャーナル フリーPhenotypic change of the smooth muscle cell (SMC) is implicated in normal development as well as several pathological processes including atherosclerosis. In general, differentiated SMCs show contractile responses to different exogenous stimuli and are inactive in mitosis, while undifferentiated or dedifferentiated SMCs show a mitogenic response and are not contractible. In the present review, we describe structural and functional aspects of the phenotypic change of SMCs with special reference to their role in atherogenesis. SMCs derived from atherosclerotic intimal lesions (intimal SMCs) show more amplified growth potential and chemotactic activity than medial SMCs; and, furthermore, they acquire a macrophage-like phenotype: uptake of modified low density lipoproteins through the scavenger receptor, which leads to high tendency toward foam cell formation. Platelet-derived growth factor, secreted from most of the cells existing in atherosclerotic plaques, is one of candidates that promote the formation of such a highly dedifferentiated intimal SMC. Clinical and experimental evidence supports the concept that an appearance of the pathological intimal SMCs is a key step for their abnormal proliferation in atheromatous lesions. Recent advances in characterization of the phenotype-specific molecular markers for SMC, such as myosin heavy chain, caldesmon, and calponin, are also described.抄録全体を表示PDF形式でダウンロード (8290K)
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