Yasuteru Muragaki

Wakayama Medical University, Wakayama, Wakayama, Japan

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Publications (121)465.29 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Arterial medial calcification is a major complication in patients with chronic kidney disease and diabetes. It has been hypothesized that a high concentration of inorganic phosphate (Pi) induces calcification in vascular smooth muscle cells (vSMCs). However, the role of transforming growth factor-β (TGF-β)/Smad3 signaling in Pi-induced vascular calcification remains controversial. The aim of this study was to investigate the possible involvement of Smad3 in Pi-induced vascular calcification. We compared the degree of Pi-induced vSMC calcification between vSMCs isolated from wild-type (Smad3+/+) and Sma3-deficient (Smad3−/−) mice. We found that vSMCs from Smad3+/+ mice had less calcium (Ca) than those from Smad3−/− mice when they were exposed to high concentrations of Pi and Ca (Pi + Ca). The phosphorylation of Smad3 was induced in Smad3+/+ vSMCs by exposure to Pi + Ca. The concentration of extracellular pyrophosphate (ePPi) was lower in Smad3−/− vSMCs than in Smad3+/+ vSMCs and was significantly increased in Smad3+/+ vSMCs by treatment with TGF-β1. Also, the addition of a small amount of PPi to culture medium significantly decreased the deposition of Ca in both Smad3+/+ and Smad3−/− vSMCs. Extracellular nucleotide phosphatase/phosphodiesterase1 (Enpp1) was decreased at the mRNA, protein, and enzymatic activity levels in Smad3−/− vSMCs compared with Smad3+/+ vSMCs. A ChIP assay showed that phosphorylated Smad3 directly binds to the Enpp1 gene. Furthermore, the calcification of aortic segments was attenuated by treatment with TGF-β1 only in Smad3+/+ mice. Taken together, we conclude that Pi-induced vSMC calcification is suppressed by Smad3 via an increase in ePPi.
    Experimental and Molecular Pathology 10/2014; · 2.13 Impact Factor
  • Yuta Tsugeno, Fuyuki Sato, Yasuteru Muragaki, Yukio Kato
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    ABSTRACT: The majority of cells are cultured with Dulbecco's modified Eagle's medium (DMEM) or RPMI supplemented with fetal bovine serum (FBS), which contains numerous factors, including cytokines, nutrients and unknown growth factors. These factors may affect cell growth, apoptosis and differentiation. The serum-free medium, STK2, has been previously reported as suitable for the cell culture of human mesenchymal stem cells. However, how STK1 or STK2 affect the cell proliferation of normal and cancer cells remains unknown. The present study examined the growth of the human gingival fibroblast (HGF-1) cell-line and the HSC-3, CA9-22 and MSTO cancer cell-lines, cultured with STK1 and STK2. STK1 increased the cell proliferation of HGF-1 compared to DMEM by assessment with the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)- 2H-tetrazolium (MTS) assay, whereas STK1 and STK2 markedly inhibited the cell proliferation of HSC-3 and MSTO. The cell proliferation rate of CA9-22 cultured with STK1 or STK2 for 96 h was ~2-fold higher than the rate for 24 h culture. The shape of the HSC-3 cells was also found to have changed to round when cultured with STK2. These results indicate that STK1 increased the cell proliferation of HGF-1 compared to DMEM, whereas the proliferation of HSC-3 and MSTO was inhibited by STK1 and STK2. Thus, STK1 and STK2 had different affects on the cell growth of HGF-1, CA9-22, HSC-3 and MSTO.
    Biomedical reports. 09/2014; 2(5):644-648.
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    ABSTRACT: Previous studies have suggested that Klotho provides reno-protection against unilateral ureteral obstruction (UUO)-induced renal tubulointerstitial fibrosis (RTF). Because the existing studies are mainly performed using heterozygous Klotho mutant (HT) mice, we focused on the effect of UUO on homozygous Klotho mutant (kl/kl) mice. UUO kidneys from HT mice showed a significantly higher level of RTF and TGF-β/Smad3 signaling than wild-type (WT) mice, whereas both were greatly suppressed in kl/kl mice. Primary proximal tubular epithelial culture cells isolated from kl/kl mice showed no suppression in TGF-β1-induced epithelial mesenchymal transition (EMT) compared to those from HT mice. In the renal epithelial cell line NRK52E, a large amount of inorganic phosphate (Pi), FGF23, or calcitriol was added to the medium to mimic the in vivo homeostasis of kl/kl mice. Neither Pi nor FGF23 antagonized TGF-β1-induced EMT. In contrast, calcitriol ameliorated TGF-β1-induced EMT in a dose dependent manner. A vitamin D3-deficient diet normalized the serum 1,25 (OH)2 vitamin D3 level in kl/kl mice and enhanced UUO-induced RTF and TGF-β/Smad3 signaling. In conclusion, the alleviation of UUO-induced RTF in kl/kl mice was due to the TGF-β1 signaling suppression caused by an elevated serum 1, 25(OH)2 vitamin D3.
    Scientific reports. 01/2014; 4:6563.
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    ABSTRACT: To compare the degree of uterine damage caused by uterine artery embolization (UAE) with gelatin sponge particles (GSPs) and N-butyl cyanoacrylate (NBCA) in swine. Fifteen swine were divided into three groups of five according to embolic material: group A (1-mm GSPs), group B (NBCA:Lipiodol = 1:1), and group C (NBCA:Lipiodol = 1:7). The uterine arteries were completely occluded bilaterally. The uteri were removed 3 days after embolization, and radiographs of the removed specimens were obtained in groups B and C to evaluate the distribution of the NBCA. The macroscopic necrosis rates of the uteri were calculated, and the uteri were evaluated histologically. Uterine necrosis rates were 4.9 ± 6.1, 1.3 ± 3.3, and 41.4 ± 28.8 % in groups A, B, and C, respectively, and were significantly higher in group C than in groups A (p = 0.0014) and B (p < 0.001). Uterine necroses were found in all 9 of the uteri with distal distributions of NBCA, and in only 1 of the 11 uteri with proximal distributions of NBCA. Dilute NBCA caused more damage to the uteri than GSPs and concentrated NBCA did. Distal embolization using NBCA caused large necroses. Therefore, proximal UAE using concentrated NBCA should be considered in clinical situations.
    Japanese journal of radiology 08/2013; · 0.73 Impact Factor
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    ABSTRACT: In a previous study, we demonstrated that Trps1-deficient (KO) mice show an expanded renal interstitium compared to wild-type (WT) mice because the loss of Trps1 affects the mesenchymal-epithelial transition (MET) in the cap mesenchyme and ureteric bud (UB) branching. Although we previously elucidated the mechanism underlying the impact of Trps1 on the MET, how Trps1 is involved in UB branching remains unknown. In the present study, we unveil the molecular mechanisms by which the loss of Trps1 suppresses UB branching. When we compared gene expression patterns via DNA microarray analysis using cultured ureteric buds isolated from E11.5 kidneys of WT and KO embryos, we found aberrant expression of genes associated with the transforming growth factor (TGF)-β⧸Smad3 signaling pathway in the KO UBs. Western blot and immunohistochemistry analyses showed increased levels of Rb1cc1, Arkadia1, and phosphorylated Smad3 and decreased levels of Smurf2, Smad7, and c-Ski in the KO embryonic kidneys. In addition, TUNEL staining and immunohistochemical detection of PCNA revealed that the apoptosis of UB cells was upregulated and, conversely, that cell proliferation was suppressed. Finally, we demonstrated that the suppression of UB branching in the KO UBs was restored via the exogenous addition of the Smad3 inhibitor SIS3, whereas the addition of TGF-β1 accelerated the suppression of UB branching in organ cultures of both isolated UBs and whole embryonic kidneys. Considering these results, we conclude that UB branching is suppressed through increased activation of the TGF-β⧸Smad3 signaling pathway when Trps1 is lost.
    Developmental Biology 03/2013; · 3.87 Impact Factor
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    Yujing Sun, Ting Gui, Aiko Shimokado, Yasuteru Muragaki
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    ABSTRACT: TRPS1 is a GATA-type transcription factor that is closely related to human tricho-rhino-phalangeal syndrome (TRPS) types I and III, variants of an autosomal dominant skeletal disorder. During embryonic development, Trps1 represses Sox9 expression and regulates Wnt signaling pathways that determine the number of hair follicles and their normal morphogenesis. In the growth plate, Trps1 regulates chondrocytes condensation, proliferation, and maturation and phalangeal joint formation by functioning downstream of Gdf5 signaling and by targeting at Pthrp, Stat3 and Runx2. Also, Trps1 protein directly interacts with an activated form of Gli3. In embryonic kidneys, Trps1 functions downstream of BMP7 promoting the mesenchymal-to-epithelial transition, and facilitating tubule morphogenesis and ureteric bud branching. Moreover, Trps1 has been found to be closely related to tumorigenesis, invasion, and metastasis in prostate and breast cancers. It is interesting to note that during the development of hair follicles, bones, and kidneys, mutations in Trps1 cause, either directly or through crosstalk with other regulators, a notable change in cell proliferation and cell death. In this review, we will summarize the most recent studies on Trps1 and seek to elucidate the role for Trps1 in apoptotic regulation.
    Cells. 01/2013; 2(3):496-505.
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    Masaaki Iwahashi, Yasuteru Muragaki, Kazuhiko Ino
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    ABSTRACT: BACKGROUND: To investigate the role of prolyl hydroxylase (PH), a key enzyme of collagen synthesis, in human uterine leiomyoma, PH expression was determined in the normal uterine myometrium and the leiomyoma tissues during the menstrual cycle. METHODS: The tissues were obtained from 40 regularly cycling women (aged 29 to 53 yr) who were undergoing abdominal hysterectomy for symptomatic uterine leiomyoma. Immunohistochemistry for human PH with specific monoclonal antibody was used for analysis. RESULTS: Immunohistochemical staining for PH revealed intense staining of leiomyoma cells in the uterine leiomyoma throughout the menstrual cycle, as compared with the adjacent normal myometrium. In the secretory phase, weak or no immunostaining for PH was detected in the normal myometrial tissues. CONCLUSIONS: These results suggest that increased expression of PH might play an role in the physiology of uterine leiomyoma during the menstrual cycle.
    Reproductive Biology and Endocrinology 12/2012; 10(1):111. · 2.14 Impact Factor
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    ABSTRACT: Overexpression of the Snail gene transcriptional repressor promotes an epithelial-to-mesenchymal transition (EMT) in epithelial tumor cell lines. In this study, we aimed to determine the correlation between Snail protein expression and clinicopathological features and to test whether Snail can be used as a marker to distinguish gastric carcinomas from benign tissues in biopsy samples. The results of immunohistochemistry with an antibody against Snail showed that most adenocarcinomas had positive Snail expression, whereas weak Snail expression was detected in a small number of gastritis and gastric adenomas. Snail-positive cells were detected in the stroma as well as in the glandular epithelium in some adenocarcinomas. In addition to Snail immunostaining, immunostaining of the EMT-related molecules, E-cadherin and vimentin, was performed. E-cadherin was not detected in adenocarcinomas that expressed Snail, whereas gastritis and adenomas stained positively for E-cadherin. Vimentin expression was seen in adenocarcinomas with positive Snail expression, whereas gastritis and adenomas did not express vimentin. In conclusion, we propose that Snail is a useful biomarker to distinguish gastric adenocarcinomas from benign lesions in biopsy samples.
    ISRN Pathology. 07/2012; 2012.
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    ABSTRACT: The role of microRNAs (miRNAs) in vascular calcification is currently unclear. To examine how miRNAs are involved in vascular smooth muscle cell (VSMC) calcification, we explored the alteration of miRNAs in VSMC calcification in vitro and in vivo. Klotho homozygous mutant mice (kl/kl) display vascular calcification and have perturbations of calcium handling. We therefore hypothesized that the calcium perturbations in VSMCs could be mediated by miRNAs. Using an miRNA array analysis, we demonstrated that miRNAs are aberrantly expressed in the aortic media of 3-week-old kl/kl mice compared with wild-type (WT) mice. The expression levels of miR-135a(*), miR-762, miR-714, and miR-712(*) in the aortic media of kl/kl mice were significantly higher than in WT mice. We used quantitative real-time reverse transcriptase polymerase chain reaction to further confirm that these miRNAs were increased in the aortic media of kl/kl mice and in cultured VSMCs treated with high phosphate and calcium. A search of the miRNA database indicated that the Ca(2+) efflux proteins NCX1, PMCA1, and NCKX4 frequently appeared as potential targets of these miRNAs. The transfection of miRNA mimics into cultured VSMCs reduced the protein levels of each potential target. Conversely, miRNA inhibitors reduced phosphate and calcium-induced VSMC calcification. Furthermore, these inhibitors decreased the intracellular Ca(2+) concentration in cultured VSMCs after treatment with phosphate and calcium. Our results suggest that increased expression of miR-135a(*), miR-762, miR-714, and miR-712(*) in VSMCs may be involved in VSMC calcification by disrupting Ca(2+) efflux proteins.
    Laboratory Investigation 06/2012; 92(9):1250-9. · 3.96 Impact Factor
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    ABSTRACT: Translocated in liposarcoma-CCAAT/enhancer binding protein homologous protein (TLS-CHOP) (also known as FUS-DDIT3) chimeric oncoprotein is found in the majority of human myxoid liposarcoma (MLS), but its molecular function remains unclear. We knockdowned TLS-CHOP expression in MLS-derived cell lines by a specific small interfering RNA, and analysed the gene expression profiles with microarray. TLS-CHOP knockdown inhibited growth of MLS cells, and induced an anticancer cytokine, melanoma differentiation-associated gene 7 (MDA-7)/interleukin-24 (IL-24) expression. However, double knockdown of TLS-CHOP and MDA-7/IL-24 did not inhibit MLS cell growth. Repression of MDA-7/IL-24 expression by TLS-CHOP is required for MLS tumour growth, and TLS-CHOP may become a promising therapeutic target for MLS treatment.
    British Journal of Cancer 05/2012; 106(12):1976-9. · 5.08 Impact Factor
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    ABSTRACT: Mutation of the human TRPS1 gene leads to trichorhinophalangeal syndrome (TRPS), which is characterized by an abnormal development of various organs including the craniofacial skeleton. Trps1 has recently been shown to be expressed in the jaw joints of zebrafish; however, whether Trps1 is expressed in the mammalian temporomandibular joint (TMJ), or whether it is necessary for TMJ development is unknown. We have analyzed (1) the expression pattern of Trps1 during TMJ development in mice and (2) TMJ development in Trps1 knockout animals. Trps1 is expressed in the maxillo-mandibular junction at embryonic day (E) 11.5. At E15.5, expression is restricted to the developing condylar cartilage and to the surrounding joint disc progenitor cells. In Trps1 knockout mice, the glenoid fossa of the temporal bone forms relatively normally but the condylar process is extremely small and the joint disc and cavities do not develop. The initiation of condyle formation is slightly delayed in the mutants at E14.5; however, at E18.5, the flattened chondrocyte layer is narrowed and most of the condylar chondrocytes exhibit precocious chondrocyte maturation. Expression of Runx2 and its target genes is expanded toward the condylar apex in the mutants. These observations underscore the indispensable role played by Trps1 in normal TMJ development in supporting the differentiation of disc and synoviocyte progenitor cells and in coordinating condylar chondrocyte differentiation.
    Cell and Tissue Research 03/2012; 348(1):131-40. · 3.68 Impact Factor
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    Ting Gui, Yujing Sun, Aiko Shimokado, Yasuteru Muragaki
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    ABSTRACT: The mitogen-activated protein kinase (MAPK) pathway allows cells to interpret external signals and respond appropriately, especially during the epithelial-mesenchymal transition (EMT). EMT is an important process during embryonic development, fibrosis, and tumor progression in which epithelial cells acquire mesenchymal, fibroblast-like properties and show reduced intercellular adhesion and increased motility. TGF-β signaling is the first pathway to be described as an inducer of EMT, and its relationship with the Smad family is already well characterized. Studies of four members of the MAPK family in different biological systems have shown that the MAPK and TGF-β signaling pathways interact with each other and have a synergistic effect on the secretion of additional growth factors and cytokines that in turn promote EMT. In this paper, we present background on the regulation and function of MAPKs and their cascades, highlight the mechanisms of MAPK crosstalk with TGF-β signaling, and discuss the roles of MAPKs in EMT.
    Journal of signal transduction. 01/2012; 2012:289243.
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    ABSTRACT: To clarify whether fibulins-5 is associated with primary spontaneous pneumothorax (PSP) in young PSP patients. Forty-six surgically resected, fresh lung specimens were used. Patients were divided into 3 groups: younger than 25 years with pneumothorax (group Y), 25 years or older with pneumothorax (group O), and without pneumothorax (group C). Chest X-ray, computed tomography data, height/width ratio (H/W) and anteroposterior/transverse diameter ratio (a/b) were measured. Elastica van Gieson staining and immunofluorescence staining for fibulin-5 were performed. Fibulin-5 mRNA expression and protein levels were measured by real-time PCR and western blotting. Direct sequences of the fibulin-5 gene in PSP patients were performed. The mean H/W ratio in group Y was significantly larger than that in the other groups (p <0.01). The mean a/b ratio in group Y was significantly smaller than that in the other groups (p = 0.02). Fibulin-5 mRNA expression was not significantly different among the groups (p = 0.64). The relative intensity of fibulin-5 protein in group Y was significantly lower than that in group O (p = 0.006), with no significant differences between groups O and C (p = 0.14). We showed that fibulin-5 is reduced in patients with PSP who are younger than 25 years.
    Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia. 01/2012; 18(3):200-5.
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    ABSTRACT: Cardiovascular disease, a leading cause of mortality in developed countries, is mainly caused by atherosclerosis, a chronic inflammatory disease. Macrophages, which differentiate from monocytes that are recruited from the blood, account for the majority of leukocytes in atherosclerotic plaques. Apoptosis and the suppressed clearance of apoptotic macrophages (efferocytosis) are associated with vulnerable plaques that are prone to rupture, leading to thrombosis. Based on the central functions of macrophages in atherogenesis, cytokines, chemokines, enzymes, or microRNAs related to or produced by macrophages have become important clinical prognostic or diagnostic biomarkers. This paper discusses the impact of monocyte-derived macrophages in early atherogenesis and advanced disease. The role and possible future development of macrophage inflammatory biomarkers are also described.
    Mediators of Inflammation 01/2012; 2012:693083. · 3.88 Impact Factor
  • Zhibo Gai, Ting Gui, Yasuteru Muragaki
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    ABSTRACT: TRPS1 is a gene involved in Tricho-rhino-phalangeal syndrome (TRPS), an autosomal dominant skeletal disorder. TRPS1 encodes a GATA-type transcription factor that has nine zinc-finger motifs. A variety of mutations in TRPS1 including deletions and insertions, have been found in patients with TRPS type I and III. The functions of each domain of TRPS1 have been clarified from study of these mutations. Further studies on the localization and the function of TRPS1 have been performed using TRPS1Δgt and Trps1-deficient mice, which allow examination of the development and differentiation of all tissues with Trps1 expression. These studies suggest that TRPS1 exhibits a variety of functions in cartilage, kidneys, and hair follicles. In the growth plate cartilage, TRPS1 regulates the differentiation, proliferation, and apoptosis of chondrocytes through interaction of several signaling molecules. In addition, TRPS1 has a function downstream of BMP7, which regulates the mesenchymal-epithelial transition when nephrons are formed in renal development. Furthermore, TRPS1 suppresses the epithelial-mesenchymal transition and renal fibrosis induced by unilateral ureteral obstruction by decreasing Arkadia expression. Finally, TRPS1 is expressed in the dermal papillae and the mesenchymal cells surrounding the hair pegs, and the loss of TRPS1 largely influences the development of hair follicles. The molecular mechanisms of the function of TRPS1 in cartilage, kidneys, and hair follicles are discussed in this review.
    Histology and histopathology 07/2011; 26(7):915-21. · 2.28 Impact Factor
  • Masaaki Iwahashi, Yasuteru Muragaki
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    ABSTRACT: The precise mechanism of prolapse uteri is not fully understood. There is evidence to suggest that abnormalities of collagen, the main component of extracellular matrix, or its repair mechanism, may predispose women to prolapse. To investigate the characteristic structure of human uterine cervix of patients with prolapse uteri, various types of collagen expression in the uterine cervix tissues of the prolapse uteri were compared to those of normal uterine cervix. After informed consent, 36 specimens of uterine cervical tissues were obtained at the time of surgery from 16 postmenopausal women with prolapse uteri (stage III-IV by the Pelvic Organ Prolapse Quantification examination) and 20 postmenopausal women without prolapse uteri (control group). Collagens were extracted from the uterine cervix tissues by salt precipitation methods. The relative levels of various collagens were evaluated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The uterine cervix was longer in the patients with prolapse uteri than those of postmenopausal controls without prolapse uteri. The ratios of type III to type I collagen in the uterine cervical tissues were significantly decreased in the prolapse uteri, as compared to those of the postmenopausal uterine cervix without prolapse. These results suggest that decreased type III collagen expression may play an important role in determing the physiology and structure of the uterine cervix tissues of prolapse uteri.
    Experimental and therapeutic medicine 01/2011; 2(2):271-274. · 0.34 Impact Factor
  • Masaaki Iwahashi, Yasuteru Muragaki
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    ABSTRACT: Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis showed that the ratios of type I and type V collagen expression were significantly increased in the leiomyoma tissues at the protein level, as compared with those in the normal myometrium tissues through the menstrual cycle. These results suggest that increased expression of type I and type V collagen might play a role in the pathogenesis of uterine leiomyoma.
    Fertility and sterility 01/2011; 95(6):2137-9. · 3.97 Impact Factor
  • Masaaki Iwahashi, Yasuteru Muragaki
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    ABSTRACT: Immunohistochemical staining for human prolyl hydroxylase revealed intense staining of the human corpora lutea (CL) parencyma during early pregnancy compared with those in the menstrual cycle. These results suggest that human prolyl hydroxylase might play an important role in determining the physiology and structure of the CL during the menstrual cycle and early pregnancy.
    Fertility and sterility 01/2011; 95(1):345-8. · 3.97 Impact Factor
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    ABSTRACT: To investigate the possible involvement of collagen in the characteristic features of human leiomyoma, type I, III and IV collagen expression was determined at the protein level in normal myometrium and leiomyoma tissues throughout the menstrual cycle. The tissues were obtained from 40 pre-menopausal women (29-53 years of age) at various stages of the menstrual cycle who were undergoing abdominal hysterectomy for symptomatic uterine leiomyoma. Immunohistochemical staining was performed with specific monoclonal antibodies against type I, III and IV collagen in the leiomyoma and the myometrial tissues. Immunohistochemical analysis revealed that type I collagen expression was increased in the leiomyoma tissues at the protein level as compared to that in the normal myometrium tissues throughout the menstrual cycle. These results suggest that increased expression of type I collagen plays a key role in the pathogenesis of uterine leiomyoma.
    Experimental and therapeutic medicine 01/2011; 2(2):287-290. · 0.34 Impact Factor
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    ABSTRACT: Tricho-rhino-phalangeal syndrome (TRPS) is an autosomal dominant skeletal disorder caused by mutations of the Trps1 gene, which encodes a GATA type transcriptional repressor. To investigate the genes that act downstream of Trps1, we performed a DNA array using ATDC5 cells. One of the target genes identified from the DNA array was Runx1, which is essential for hematopoiesis and like Runx2 plays a significant role in chondrogenesis. A luciferase promoter assay and a chromosome immunoprecipitation assay showed that Runx1 expression in mouse epiphyseal cartilage was repressed by Trps1 binding to the GATA domain of the P2 promoter; the proximal segment of two promoters of the Runx1 gene. The aberrant expression of P2 transcripts was detected in growth plate chondrocytes from Trps1-null mice by in situ hybridization. In conclusion, Trps1 binds to the P2 promoter of the Runx1 gene and down-regulates Runx1 expression, which is necessary for normal cartilage formation.
    Experimental and Molecular Pathology 11/2010; 90(2):143-8. · 2.13 Impact Factor

Publication Stats

3k Citations
465.29 Total Impact Points

Institutions

  • 1986–2014
    • Wakayama Medical University
      • • Department of Obstetrics and Gynaecology
      • • Second Department of Surgery
      • • Department of Cardiovascular Medicine
      • • Department of Ophthalmology
      • • Department of Pathology
      Wakayama, Wakayama, Japan
  • 2010
    • University of Jinan (Jinan, China)
      Chi-nan-shih, Shandong Sheng, China
  • 2008
    • Kinki University
      • Department of Plastic and Reconstructive Surgery
      Ōsaka, Ōsaka, Japan
  • 2007
    • Yamagata University
      • Department of Orthopaedic Surgery
      Yamagata-shi, Yamagata-ken, Japan
  • 2005
    • Tenri Yorozu Hospital
      Тэнри, Nara, Japan
  • 1989–1996
    • Harvard Medical School
      • Department of Cell Biology
      Boston, MA, United States
  • 1988–1993
    • Toyama Medical and Pharmaceutical University
      Тояма, Toyama, Japan