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497 results on '"Nishinakamura, Ryuichi"'

105. A Novel Chordin-like Protein Inhibitor for Bone Morphogenetic Proteins Expressed Preferentially in Mesenchymal Cell Lineages

Author

Nakayama, Naoki, Han, Chun-ya E., Scully, Sheila, Nishinakamura, Ryuichi, He, Ching, Zeni, Lisa, Yamane, Harvey, Chang, David, Yu, Dongyin, Yokota, Takashi, and Wen, Duanzhi

Subjects
Bone morphogenetic proteins -- Physiological aspects, Cartilage cells -- Physiological aspects, Xenopus -- Physiological aspects, Biological sciences
Abstract

Chordin is a bone morphogenetic protein (BMP) inhibitor that has been identified as a factor dorsalizing the Xenopus embryo. A novel secreted protein, CHL (for chordin-like), with significant homology to chordin, was isolated from mouse bone marrow stromal cells. Injection of CHL RNA into Xenopus embryos induced a secondary axis. Recombinant CHL protein inhibited the BMP4-dependent differentiation of embryonic stem cells in vitro and interacted directly with BMPs, similar to chordin. However, CHL also weakly bound to TGF[Beta]s. In situ hybridization revealed that the mouse CHL gene, located on the X chromosome, was expressed predominantly in mesenchyme-derived cell types: (1) the dermatome and limb bud mesenchyme and, later, the subdermal mesenchyme and the chondrocytes of the developing skeleton during embryogenesis and (2) a layer of fibroblasts/connective tissue cells in the gastrointestinal tract, the thick straight segments of kidney tubules, and the marrow stromal cells in adults. An exception was expression in the neural cells of the olfactory bulb and cerebellum. Interestingly, the spatiotemporal expression patterns of CHL were distinct from those of chordin in many areas examined. Thus, CHL may serve as an important BMP regulator for differentiating mesenchymal cells, especially during skeletogenesis, and for developing specific neurons. Key Words: secreted protein; chordin; BMP inhibitor; embryogenesis; embryonic stem cell; dorsalizing factor; skeletogenesis; mesenchymal cell; chondrocyte; organogenesis.

Published
2001

106. The pluripotency factor Nanog regulates pericentromeric heterochromatin organization in mouse embryonic stem cells

Author

Novo, Clara Lopes, primary, Tang, Calvin, additional, Ahmed, Kashif, additional, Djuric, Ugljesa, additional, Fussner, Eden, additional, Mullin, Nicholas P., additional, Morgan, Natasha P., additional, Hayre, Jasvinder, additional, Sienerth, Arnold R., additional, Elderkin, Sarah, additional, Nishinakamura, Ryuichi, additional, Chambers, Ian, additional, Ellis, James, additional, Bazett-Jones, David P., additional, and Rugg-Gunn, Peter J., additional

Published
2016
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112. <italic>Dullard</italic> deficiency causes hemorrhage in the adult ovarian follicles.

Author

Hayata, Tadayoshi, Chiga, Masahiko, Ezura, Yoichi, Asashima, Makoto, Katabuchi, Hidetaka, Nishinakamura, Ryuichi, and Noda, Masaki

Subjects
HEMORRHAGE, OVARIAN follicle, BONE morphogenetic proteins, PHOSPHATASES, ADULTS, CELL communication, PHYSIOLOGY
Abstract

In mammals, the ovarian follicles are regulated at least in part by bone morphogenetic protein (BMP) family members. Dullard (also known as Ctdnep1) gene encodes a phosphatase that suppresses BMP signaling by inactivating or degrading BMP receptors. Here we report that the Col1a1‐Cre‐induced Dullard mutant mice displayed hemorrhagic ovarian cysts, with red blood cells accumulated in the follicles, resulting in infertility. Cells expressing Cre driven by Col1a1 2.3‐kb promoter and their descendants were found in granulosa cells in the ovary and in Sertoli cells in the testis. DullardmRNA was localized to granulosa cells in the ovary. Genes involved in steroid hormone genesis including Cyp11a1, Hsd3b1 and Star were reduced, whereas expression of Smad6 and Smad7, BMP‐inducible inhibitory Smads, was up‐regulated in the Dullard mutant ovaries. Tamoxifen‐inducible Dullard deletion in the whole body using Rosa26‐CreER mice also resulted in hemorrhagic ovarian cysts in 2 weeks, which was rescued by administration of LDN‐193189, a chemical inhibitor of BMP receptor kinase, suggesting that the hemorrhage in the Dullard‐deficient ovarian follicles might be caused by increased BMP signaling. Thus, we conclude that Dullard is essential for ovarian homeostasis at least in part via suppression of BMP signaling. [ABSTRACT FROM AUTHOR]

Published
2018
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120. Sall1 Maintains Nephron Progenitors and Nascent Nephrons by Acting as Both an Activator and a Repressor

Author

Kanda, Shoichiro, primary, Tanigawa, Shunsuke, additional, Ohmori, Tomoko, additional, Taguchi, Atsuhiro, additional, Kudo, Kuniko, additional, Suzuki, Yutaka, additional, Sato, Yuki, additional, Hino, Shinjiro, additional, Sander, Maike, additional, Perantoni, Alan O., additional, Sugano, Sumio, additional, Nakao, Mitsuyoshi, additional, and Nishinakamura, Ryuichi, additional

Published
2014
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126. Re-expression of Sall1in podocytes protects against adriamycin-induced nephrosis

Author

Hosoe-Nagai, Yoshiko, Hidaka, Teruo, Sonoda, Ayano, Sasaki, Yu, Yamamoto-Nonaka, Kanae, Seki, Takuto, Asao, Rin, Tanaka, Eriko, Oliva Trejo, Juan Alejandro, Kodama, Fumiko, Takagi, Miyuki, Tada, Nobuhiro, Ueno, Takashi, Nishinakamura, Ryuichi, Tomino, Yasuhiko, and Asanuma, Katsuhiko

Abstract

The highly conserved spalt (sal) gene family members encode proteins characterized by multiple double zinc finger motifs of the C2H2 type. Humans and mice each have four known Sal-like genes (SALL1–4in humans and Sall1–4in mice). Sall1is known to have a crucial role in kidney development. To explore the significance of Sall1in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1knockdown (Sall1KD) podocytes. Under physiological conditions, Sall1KOp°d°/p°d°mice exhibited no proteinuria during their lifetime, but foot-process effacement was detected in some of the podocytes. To elucidate the role of Sall1in injured podocytes, we used an adriamycin (ADR)-induced model of nephrosis and glomerulosclerosis. Surprisingly, the expression of Sall1was elevated in control mice on day 14 after ADR injection. On day 28 after ADR injection, Sall1KOp°d°/p°d°mice exhibited significantly higher levels of proteinuria and higher numbers of sclerotic glomeruli. Differentiated Sall1KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration. In addition, the loss of Sall1increased the number of apoptotic podocytes following ADR treatment. These results indicated that Sall1has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78. GRP78 expression was higher in ADR-treated Sall1KOp°d°/p°d°mice than in control mice. Sall1appeared to influence the expression of GRP78 in injured podocytes. These results suggest that Sall1is associated with actin reorganization, endoplasmic reticulum stress, and apoptosis in injured podocytes. These protective aspects of Sall1re-expression in injured podocytes may have the potential to reduce apoptosis and possibly glomerulosclerosis.

Published
2017
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128. Histone Lysine-specific Demethylase 1 (LSD1) Protein Is Involved in Sal-like Protein 4 (SALL4)-mediated Transcriptional Repression in Hematopoietic Stem Cells

Author

Liu, Li, primary, Souto, Joseph, additional, Liao, Wenbin, additional, Jiang, Yongping, additional, Li, Yangqiu, additional, Nishinakamura, Ryuichi, additional, Huang, Suming, additional, Rosengart, Todd, additional, Yang, Vincent W., additional, Schuster, Michael, additional, Ma, Yupo, additional, and Yang, Jianchang, additional

Published
2013
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133. The phosphatase Dullard negatively regulates BMP signalling and is essential for nephron maintenance after birth

Author

Sakaguchi, Masaji, primary, Sharmin, Sazia, additional, Taguchi, Atsuhiro, additional, Ohmori, Tomoko, additional, Fujimura, Sayoko, additional, Abe, Takaya, additional, Kiyonari, Hiroshi, additional, Komatsu, Yoshihiro, additional, Mishina, Yuji, additional, Asashima, Makoto, additional, Araki, Eiichi, additional, and Nishinakamura, Ryuichi, additional

Published
2013
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134. A mouse model of Townes-Brocks syndrome expressing a truncated mutant Sall1 protein is protected from acute kidney injury.

Author

Hirsch, Sara, Rauchman, Michael, El-Achkar, Tarek, Heitmeier, Monique, Robbins, Lynn, Basta, Jeannine, and Nishinakamura, Ryuichi

Subjects
ACUTE kidney failure, MUTANT proteins, NEPHROTOXICOLOGY, GENETICS
Abstract

It has been postulated that developmental pathways are reutilized during repair and regeneration after injury, but functional analysis of many genes required for kidney formation has not been performed in the adult organ. Mutations in SALL1 cause Townes-Brocks syndrome (TBS) and nonsyndromic congenital anomalies of the kidney and urinary tract, both of which lead to childhood kidney failure. Sall1 is a transcriptional regulator that is expressed in renal progenitor cells and developing nephrons in the embryo. However, its role in the adult kidney has not been investigated. Using a mouse model of TBS (Sall1TBS), we investigated the role of Sall1 in response to acute kidney injury. Our studies revealed that Sall1 is expressed in terminally differentiated renal epithelia, including the S3 segment of the proximal tubule, in the mature kidney. Sall1TBS mice exhibited significant protection from ischemia-reperfusion injury and aristolochic acid-induced nephrotoxicity. This protection from acute injury is seen despite the presence of slowly progressive chronic kidney disease in Sall1TBS mice. Mice containing null alleles of Sall1 are not protected from acute kidney injury, indicating that expression of a truncated mutant protein from the Sall1TBS allele, while causative of congenital anomalies, protects the adult kidney from injury. Our studies further revealed that basal levels of the preconditioning factor heme oxygenase-1 are elevated in Sall1TBS kidneys, suggesting a mechanism for the relative resistance to injury in this model. Together, these studies establish a functional role for Sall1 in the response of the adult kidney to acute injury. [ABSTRACT FROM AUTHOR]

Published
2015
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148. Sall4 Is Essential for Stabilization, But Not for Pluripotency, of Embryonic Stem Cells by Repressing Aberrant Trophectoderm Gene Expression

Author

Yuri, Shunsuke, primary, Fujimura, Sayoko, additional, Nimura, Keisuke, additional, Takeda, Naoki, additional, Toyooka, Yayoi, additional, Fujimura, Yu-Ichi, additional, Aburatani, Hiroyuki, additional, Ura, Kiyoe, additional, Koseki, Haruhiko, additional, Niwa, Hitoshi, additional, and Nishinakamura, Ryuichi, additional

Published
2009
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