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Volume 42 (2009)
- Issue 6 Pages 159-
- Issue 5 Pages 129-
- Issue 4 Pages 95-
- Issue 3 Pages 65-
- Issue 2 Pages 15-
- Issue 1 Pages 1-
Volume 42, Issue 4
Displaying 1-4 of 4 articles from this issue
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REVIEW
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Robert Y. Osamura, Noboru Egashira, Hanako Kajiya, Mao Takei, Maya Tob ...2009 Volume 42 Issue 4 Pages 95-104
Published: 2009
Released on J-STAGE: August 29, 2009
Advance online publication: August 11, 2009JOURNAL FREE ACCESSGrowth hormone (GH)-producing adenomas (GHomas) are one of the most frequently-occurring pituitary adenomas. Differentiation of hormone-producing cells in the pituitary gland is regulated by transcription factors and co-factors. The transcription factors include Pit-1, Prop-1, NeuroD1, Tpit, GATA-2, SF-1. Aberrant expression of transcription factors such as Pit-1 results in translineage expression of GH in adrenocorticotropic hormone-producing adenomas (ACTHomas). This situation has been substantiated by GFP-Pit-1 transfection expression in the AtT20 cell line. Experimentally, GHomas have been induced in GH-releasing hormone (GHRH) or Prop-1 transgenic animals. Immunohistochemical detection of somatostatin receptor (SSTR2a) has recently emphasized their role in the response of GHomas to somatostatin analogue therapy. In this review, the advances in technology and their contribution to cell biology and medical practice are discussed.
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REGULAR ARTICLE
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Yoko Omi, Noriyuki Shibata, Takahiro Okamoto, Takao Obara, Makio Kobay ...2009 Volume 42 Issue 4 Pages 105-109
Published: 2009
Released on J-STAGE: August 29, 2009
Advance online publication: July 14, 2009JOURNAL FREE ACCESSMicrosomal prostaglandin E2 synthase-1 (mPGES-1) is an inducible enzyme that catalyzes the conversion of prostaglandin (PG) H2 to PGE2 in downstream of cyclooxygenase-2 (COX-2). Recent studies have obtained in vitro evidence that PGE2 participates in carcinogenesis, angiogenesis, and induction of matrix metalloproteinase-9 (MMP-9), which plays a crucial role in cancer invasion. However, implications for mPGES-1 in thyroid carcinomas remain to be determined. To address this issue, we performed an immunohistochemical analysis for mPGES-1, COX-2 and MMP-9 in 20 papillary thyroid carcinoma (PTC) patients. mPGES-1 immunoreactivity was localized in the cytoplasm of carcinoma cells in 19 cases, with an intensity that tended to be distinct at the interface between the tumor and the surrounding non-neoplastic tissue. Staining was more intense in regions with papillary arrangement, while it was less intense in regions with trabecular or solid arrangement. In many cases, immunohistochemical localization of COX-2 and MMP-9 resemble that of mPGES-1. Taken together, our results suggest the involvement of mPGES-1 in proliferation and differentiation of PTC as well as local invasion of PTC.
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Hiroshi Sakamoto, Toyoko Kawate, Yongnan Li, Saoko Atsumi2009 Volume 42 Issue 4 Pages 111-119
Published: 2009
Released on J-STAGE: August 29, 2009
Advance online publication: July 15, 2009JOURNAL FREE ACCESSSynaptic glomeruli that involve tachykinin-containing primary afferent central terminals are numerous in lamina II of the chicken spinal cord. Therefore, a certain amount of noxious information is likely to be modulated in these structures in chickens. In this study, we used immunohistochemistry with confocal and electron microscopy to investigate whether neurokinin-1 receptor (NK-1R)-expressing neuronal elements are in contact with the central primary afferent terminals in synaptic glomeruli of the chicken spinal cord. We also investigated which neuronal elements (axon terminals, dendrites, cell bodies) and which neurons in the spinal cord possess NK-1R, and are possibly influenced by tachykinin in the glomeruli. By confocal microscopy, NK-1R immunoreactivities were seen in a variety of neuronal cell bodies, their dendrites and smaller fibers of unknown origin. Some of the NK-1R immunoreactive profiles also expressed GABA immunoreactivities. A close association was observed between the NK-1R-immunoreactive neurons and tachykinin-immunoreactive axonal varicosities. By electron microscopy, NK-1R immunoreactivity was seen in cell bodies, conventional dendrites and vesicle-containing dendrites in laminae I and II. Among these elements, dendrites and vesicle-containing dendrites made contact with tachykinin-containing central terminals in the synaptic glomeruli. These results indicate that tachykinin-containing central terminals in the chicken spinal cord can modulate second-order neuronal elements in the synaptic glomeruli.
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Yasunori Tamagawa, Tomoyuki Saino, Makoto Matsuura, Yoh-ichi Satoh2009 Volume 42 Issue 4 Pages 121-128
Published: 2009
Released on J-STAGE: August 29, 2009
Advance online publication: August 11, 2009JOURNAL FREE ACCESSThe regulation of cytosolic Ca2+ homeostasis is essential for cells, including vascular smooth muscle cells. Arterial tone, which underlies the maintenance of peripheral resistance in the circulation, is a major contributor to the control of blood pressure. Diuretics may regulate intracellular Ca2+ concentration ([Ca2+]i) and have an effect on vascular tone. In order to investigate the influence of diuretics on peripheral resistance in circulation, we investigated the alteration of [Ca2+]i in testicular arterioles with respect to several categories of diuretics using real-time confocal laser scanning microscopy. In this study, hydrochlorothiazide (100 μM) and furosemide (100 μM) had no effect on the [Ca2+]i dynamics. However, when spironolactone (300 μM) was applied, the [Ca2+]i of smooth muscles increased. The response was considerably inhibited under either extracellular Ca2+-free conditions, the presence of Gd3+, or with a treatment of diltiazem. After the thapsigargin-induced depletion of internal Ca2+ store, the spironolactone-induced [Ca2+]i dynamics was slightly inhibited. Therefore, the spironolactone-induced dynamics of [Ca2+]i can be caused by either a Ca2+ influx from extracellular fluid or Ca2+ mobilization from internal Ca2+ store, with the former being dominant. As tetraethylammonium, an inhibitor of the K+ channel, slightly inhibited the spironolactone-induced [Ca2+]i dynamics, the K+ channel might play a minor role in those dynamics. Tetrodotoxin, a neurotoxic Na+ channel blocker, had no effect, therefore the spironolactone-induced dynamics is a direct effect to smooth muscles, rather than an indirect effect via vessel nerves.
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