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4. Intermittent hypoxia increased the expression of ESM1 and ICAM‐1 in vascular endothelial cells via the downregulation of microRNA‐181a1.

Author

Takasawa, Shin, Makino, Mai, Yamauchi, Akiyo, Sakuramoto‐Tsuchida, Sumiyo, Hirota, Rina, Fujii, Ryusei, Asai, Keito, Takeda, Yoshinori, Uchiyama, Tomoko, Shobatake, Ryogo, and Ota, Hiroyo

Subjects
VASCULAR endothelial cells, VASCULAR cell adhesion molecule-1, SLEEP apnea syndromes, HYPOXEMIA, CELL adhesion, DOWNREGULATION
Abstract

Sleep apnea syndrome (SAS) exposes cells throughout the body to intermittent hypoxia (IH). Intermittent hypoxia is a risk factor not only for hypertension and insulin resistance but also for vascular dysfunction. We have reported correlations between IH, insulin resistance and hypertension. However, the details of why IH leads to vascular dysfunction remain unclear. In this study, we investigated inflammation‐related transcripts in vascular endothelial cells (human HUEhT‐1 and mouse UV2) exposed to IH by real‐time RT‐PCR and found that intercellular adhesion molecule‐1 (ICAM‐1) and endothelial cell‐specific molecule‐1 (ESM1) mRNAs were significantly increased. ELISA confirmed that, in the UV2 cell medium, ICAM‐1 and ESM1 were significantly increased by IH. However, the promoter activities of ICAM‐1 and ESM1 were not upregulated. On the other hand, IH treatment significantly decreased microRNA (miR)‐181a1 in IH‐treated cells. The introduction of miR‐181a1 mimic but not miR‐181a1 mimic NC abolished the IH‐induced upregulation of Ican‐1 and ESM1. These results indicated that ICAM‐1 and ESM1 were upregulated by IH via the IH‐induced downregulation of miR‐181a1 in vascular endothelial cells and suggested that SAS patients developed atherosclerosis via the IH‐induced upregulation of ICAM‐1 and ESM1. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Expression of REG family genes in human inflammatory bowel diseases and its regulation.

Author

Tsuchida, Chikatsugu, Sakuramoto-Tsuchida, Sumiyo, Takeda, Maiko, Itaya-Hironaka, Asako, Yamauchi, Akiyo, Misu, Masayasu, Shobatake, Ryogo, Uchiyama, Tomoko, Makino, Mai, Pujol-Autonell, Irma, Vives-Pi, Marta, Ohbayashi, Chiho, Takasawa, Shin, Tsuchida, Chikatsugu, Sakuramoto-Tsuchida, Sumiyo, Takeda, Maiko, Itaya-Hironaka, Asako, Yamauchi, Akiyo, Misu, Masayasu, Shobatake, Ryogo, Uchiyama, Tomoko, Makino, Mai, Pujol-Autonell, Irma, Vives-Pi, Marta, Ohbayashi, Chiho, and Takasawa, Shin

Abstract

The pathophysiology of inflammatory bowel disease (IBD) reflects a balance between mucosal injury and reparative mechanisms. Some regenerating gene (Reg) family members have been reported to be expressed in Crohn's disease (CD) and ulcerative colitis (UC) and to be involved as proliferative mucosal factors in IBD. However, expression of all REG family genes in IBD is still unclear. Here, we analyzed expression of all REG family genes (REG Iα, REG Iβ, REG III, HIP/PAP, and REG IV) in biopsy specimens of UC and CD by real-time RT-PCR. REG Iα, REG Iβ, and REG IV genes were overexpressed in CD samples. REG IV gene was also overexpressed in UC samples. We further analyzed the expression mechanisms of REG Iα, REG Iβ, and REG IV genes in human colon cells. The expression of REG Iα was significantly induced by IL-6 or IL-22, and REG Iβ was induced by IL-22. Deletion analyses revealed that three regions (- 220 to - 211, - 179 to - 156, and - 146 to - 130) in REG Iα and the region (- 274 to- 260) in REG Iβ promoter were responsible for the activation by IL-22/IL-6. The promoters contain consensus transcription factor binding sequences for MZF1, RTEF1/TEAD4, and STAT3 in REG Iα, and HLTF/FOXN2F in REG Iβ, respectively. The introduction of siRNAs for MZF1, RTEF1/TEAD4, STAT3, and HLTF/FOXN2F abolished the transcription of REG Iα and REG Iβ. The gene activation mechanisms of REG Iα/REG Iβ may play a role in colon mucosal regeneration in IBD., 博士（医学）・乙第1438号・令和元年9月27日, © 2017 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).

Published
2020

17. Up-regulation of POMC and CART mRNAs by intermittent hypoxia via GATA transcription factors in human neuronal cells

Author

Shobatake, Ryogo, Takasawa, Ken, Ota, Hiroyo, Itaya-Hironaka, Asako, Yamauchi, Akiyo, Sakuramoto-Tsuchida, Sumiyo, Uchiyama, Tomoko, Makino, Mai, Sugie, Kazuma, Takasawa, Shin, and Ueno, Satoshi

Subjects
endocrine system, Sleep apnea syndrome, CART (cocaine- and amphetamine-regulated transcript), nervous system, Intermittent hypoxia, GATA, POMC (proopiomelanocortin), digestive, oral, and skin physiology, Appetite, hormones, hormone substitutes, and hormone antagonists
Abstract

Sleep apnea syndrome (SAS) is characterized by intermittent hypoxia (IH) during sleep. SAS and obesity are strongly related to each other. Here, we investigated the effect of IH on the expression of major appetite regulatory genes in human neuronal cells. We exposed NB-1, SH-SY5Y, and SK-N-SH human neuronal cells to IH (64 cycles of 5 min hypoxia and 10 min normoxia), normoxia, or sustained hypoxia for 24 h and measured the mRNA levels of proopiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), galanin, galanin-like peptide, ghrelin, pyroglutamylated RFamide peptide, agouti-related peptide, neuropeptide Y, and melanocortin 4 receptor by real-time RT-PCR. IH significantly increased the mRNA levels of POMC and CART in all the neuronal cells. Deletion analysis revealed that the -705 to -686 promoter region of POMC and the -950 to -929 region of CART were essential for the IH-induced promoter activity. As possible GATA factor binding sequences were found in the two regions, we performed real-time RT-PCR to determine which GATA family members were expressed and found that GATA2 and GATA3 mRNAs were predominantly expressed. Therefore, we introduced siRNAs against GATA2 and GATA3 into NB-1 cells and found that GATA2 and GATA3 siRNAs abolished the IH-induced up-regulation of both POMC and CART mRNAs. These results indicate that IH stress up-regulates the mRNA levels of anorexigenic peptides, POMC and CART, in human neuronal cells via GATA2 and GATA3. IH can have an anorexigenic effect on SAS patients through the transcriptional activation of POMC and CART in the central nervous system., 博士（医学）・甲第685号・平成30年6月27日, © 2017 Elsevier Ltd. All rights reserved.

Published
2018

19. Expression of REG family genes in human inflammatory bowel diseases and its regulation

Author

Tsuchida, Chikatsugu, Sakuramoto-Tsuchida, Sumiyo, Takeda, Maiko, Itaya-Hironaka, Asako, Yamauchi, Akiyo, Misu, Masayasu, Shobatake, Ryogo, Uchiyama, Tomoko, Makino, Mai, Pujol-Autonell, Irma, Vives-Pi, Marta, Ohbayashi, Chiho, and Takasawa, Shin

Subjects
Crohn's disease, Ulcerative colitis, immune system diseases, REG family genes, hemic and lymphatic diseases, Celiac disease, hemic and immune systems, chemical and pharmacologic phenomena, Transcription
Abstract

The pathophysiology of inflammatory bowel disease (IBD) reflects a balance between mucosal injury and reparative mechanisms. Some regenerating gene (Reg) family members have been reported to be expressed in Crohn's disease (CD) and ulcerative colitis (UC) and to be involved as proliferative mucosal factors in IBD. However, expression of all REG family genes in IBD is still unclear. Here, we analyzed expression of all REG family genes (REG Iα, REG Iβ, REG III, HIP/PAP, and REG IV) in biopsy specimens of UC and CD by real-time RT-PCR. REG Iα, REG Iβ, and REG IV genes were overexpressed in CD samples. REG IV gene was also overexpressed in UC samples. We further analyzed the expression mechanisms of REG Iα, REG Iβ, and REG IV genes in human colon cells. The expression of REG Iα was significantly induced by IL-6 or IL-22, and REG Iβ was induced by IL-22. Deletion analyses revealed that three regions (- 220 to - 211, - 179 to - 156, and - 146 to - 130) in REG Iα and the region (- 274 to- 260) in REG Iβ promoter were responsible for the activation by IL-22/IL-6. The promoters contain consensus transcription factor binding sequences for MZF1, RTEF1/TEAD4, and STAT3 in REG Iα, and HLTF/FOXN2F in REG Iβ, respectively. The introduction of siRNAs for MZF1, RTEF1/TEAD4, STAT3, and HLTF/FOXN2F abolished the transcription of REG Iα and REG Iβ. The gene activation mechanisms of REG Iα/REG Iβ may play a role in colon mucosal regeneration in IBD., 博士（医学）・乙第1438号・令和元年9月27日, © 2017 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).

Published
2017

20. 妊娠高血圧症候群におけるRAGEの関与

Author

Akasaka, Juria, Naruse, Katsuhiko, Sado, Toshiyuki, Uchiyama, Tomoko, Makino, Mai, Yamauchi, Akiyo, Ota, Hiroyo, Sakuramoto-Tsuchida, Sumiyo, Itaya-Hironaka, Asako, Takasawa, Shin, and Kobayashi, Hiroshi

Subjects
IL-6, AGE, LPS, hypertensive disorders of pregnancy, adipocyte, RAGE, CCL2
Abstract

Preeclampsia/hypertensive disorders of pregnancy (PE/HDP) is a serious and potentially life-threatening disease. Recently, PE/HDP has been considered to cause adipose tissue inflammation, but the detailed mechanism remains unknown. We exposed human primary cultured adipocytes with serum from PE/HDP and healthy controls for 24 h, and analyzed mRNA expression of several adipokines, cytokines, and ligands of the receptor for advanced glycation endproducts (RAGE). We found that the mRNA levels of interleukin-6 (IL-6), C-C motif chemokine ligand 2 (CCL2), high mobility group box 1 (HMGB1), and RAGE were significantly increased by the addition of PE/HDP serum. Among RAGE ligands, advanced glycation endproducts (AGE) and HMGB1 increased mRNA levels of IL-6 and CCL2 in SW872 human adipocytes and mouse 3T3-L1 cells. The introduction of small interfering RNA for RAGE (siRAGE) into SW872 cells abolished the AGE- and HMGB1-induced up-regulation of IL-6 and CCL2. In addition, lipopolysaccharide (LPS), a ligand of RAGE, increased the expression of IL-6 and CCL2 and siRAGE attenuated the LPS-induced expression of IL-6 and CCL2. These results strongly suggest that the elevated AGE, HMGB1, and LPS in pregnant women up-regulate the expression of IL-6 and CCL2 via the RAGE system, leading to systemic inflammation such as PE/HDP., 博士（医学）・乙第1451号・令和2年3月16日, © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

Published
2019

25. Intermittent Hypoxia Up-Regulates Gene Expressions of Peptide YY (PYY), Glucagon-like Peptide-1 (GLP-1), and Neurotensin (NTS) in Enteroendocrine Cells

Author

Shobatake, Ryogo, primary, Itaya-Hironaka, Asako, additional, Yamauchi, Akiyo, additional, Makino, Mai, additional, Sakuramoto-Tsuchida, Sumiyo, additional, Uchiyama, Tomoko, additional, Ota, Hiroyo, additional, Takahashi, Nobuyuki, additional, Ueno, Satoshi, additional, Sugie, Kazuma, additional, and Takasawa, Shin, additional

Published
2019
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30. Up-regulation of selenoprotein P and HIP/PAP mRNAs in hepatocytes by intermittent hypoxia via down-regulation of miR-203

Author

Uchiyama, Tomoko, primary, Ota, Hiroyo, additional, Itaya-Hironaka, Asako, additional, Shobatake, Ryogo, additional, Yamauchi, Akiyo, additional, Sakuramoto-Tsuchida, Sumiyo, additional, Makino, Mai, additional, Kimura, Hiroshi, additional, Takeda, Maiko, additional, Ohbayashi, Chiho, additional, and Takasawa, Shin, additional

Published
2017
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32. Expression of REGfamily genes in human inflammatory bowel diseases and its regulation

Author

Tsuchida, Chikatsugu, Sakuramoto-Tsuchida, Sumiyo, Taked, Maiko, Itaya-Hironaka, Asako, Yamauchi, Akiyo, Misu, Masayasu, Shobatake, Ryogo, Uchiyama, Tomoko, Makino, Mai, Pujol-Autonell, Irma, Vives-Pi, Marta, Ohbayashi, Chiho, and Takasawa, Shin

Abstract

The pathophysiology of inflammatory bowel disease (IBD) reflects a balance between mucosal injury and reparative mechanisms. Some regenerating gene (Reg) family members have been reported to be expressed in Crohn's disease (CD) and ulcerative colitis (UC) and to be involved as proliferative mucosal factors in IBD. However, expression of all REGfamily genes in IBD is still unclear. Here, we analyzed expression of all REGfamily genes (REG Iα, REG Iβ, REG III, HIP/PAP, and REG IV) in biopsy specimens of UC and CD by real-time RT-PCR. REG Iα, REG Iβ, and REG IVgenes were overexpressed in CD samples. REG IVgene was also overexpressed in UC samples. We further analyzed the expression mechanisms of REG Iα, REG Iβ, and REG IVgenes in human colon cells. The expression of REG Iαwas significantly induced by IL-6 or IL-22, and REG Iβwas induced by IL-22. Deletion analyses revealed that three regions (− 220 to − 211, − 179 to − 156, and − 146 to − 130) in REG Iαand the region (− 274 to− 260) in REG Iβpromoter were responsible for the activation by IL-22/IL-6. The promoters contain consensus transcription factor binding sequences for MZF1, RTEF1/TEAD4, and STAT3 in REG Iα, and HLTF/FOXN2F in REG Iβ, respectively. The introduction of siRNAs for MZF1, RTEF1/TEAD4, STAT3, and HLTF/FOXN2F abolished the transcription of REG Iαand REG Iβ. The gene activation mechanisms of REG Iα/REG Iβmay play a role in colon mucosal regeneration in IBD.

Published
2017
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33. Up-regulation of selenoprotein Pand HIP/PAPmRNAs in hepatocytes by intermittent hypoxia via down-regulation of miR-203

Author

Uchiyama, Tomoko, Ota, Hiroyo, Itaya-Hironaka, Asako, Shobatake, Ryogo, Yamauchi, Akiyo, Sakuramoto-Tsuchida, Sumiyo, Makino, Mai, Kimura, Hiroshi, Takeda, Maiko, Ohbayashi, Chiho, and Takasawa, Shin

Abstract

Sleep apnea syndrome is characterized by recurrent episodes of oxygen desaturation and reoxygenation (intermittent hypoxia [IH]) and is a risk factor for insulin resistance/type 2 diabetes. However, the mechanisms linking IH stress and insulin resistance remain elusive. We exposed human hepatocytes (JHH5, JHH7, and HepG2) to experimental IH or normoxia for 24h, measured mRNA levels by real-time reverse transcription polymerase chain reaction (RT-PCR), and found that IH significantly increased the mRNA levels of selenoprotein P(SELENOP) — a hepatokine — and hepatocarcinoma-intestine-pancreas/pancreatitis-associated protein(HIP/PAP) — one of REG(Regenerating gene) family. We next investigated promoter activities of both genes and discovered that they were not increased by IH. On the other hand, a target mRNA search of micro RNA (miRNA) revealed that both mRNAs have a potential target sequence for miR-203. The miR-203 level of IH-treated cells was significantly lower than that of normoxia-treated cells. Thus, we introduced miR-203 inhibitor and a non-specific control RNA (miR-203 inhibitor NC) into HepG2 cells and measured the mRNA levels of SELENOPand HIP/PAP. The IH-induced expression of SELENOPand HIP/PAPwas abolished by the introduction of miR-203 inhibitor but not by miR-203 inhibitor NC. These results demonstrate that IH stress up-regulates the levels of SELENOPin human hepatocytes to accelerate insulin resistance and up-regulates the levels of HIP/PAPmRNAs to proliferate such hepatocytes, via the miR-203 mediated mechanism.

Published
2017
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34. Involvement of Receptor for Advanced Glycation Endproducts in Hypertensive Disorders of Pregnancy.

Author

Akasaka, Juria, Naruse, Katsuhiko, Sado, Toshiyuki, Uchiyama, Tomoko, Makino, Mai, Yamauchi, Akiyo, Ota, Hiroyo, Sakuramoto-Tsuchida, Sumiyo, Itaya-Hironaka, Asako, Takasawa, Shin, and Kobayashi, Hiroshi

Subjects
ADIPOKINES, SMALL interfering RNA, INTERLEUKIN-6, ADIPOSE tissue physiology, PREGNANT women, ADIPOSE tissues, PREGNANCY
Abstract

Preeclampsia/hypertensive disorders of pregnancy (PE/HDP) is a serious and potentially life-threatening disease. Recently, PE/HDP has been considered to cause adipose tissue inflammation, but the detailed mechanism remains unknown. We exposed human primary cultured adipocytes with serum from PE/HDP and healthy controls for 24 h, and analyzed mRNA expression of several adipokines, cytokines, and ligands of the receptor for advanced glycation endproducts (RAGE). We found that the mRNA levels of interleukin-6 (IL-6), C-C motif chemokine ligand 2 (CCL2), high mobility group box 1 (HMGB1), and RAGE were significantly increased by the addition of PE/HDP serum. Among RAGE ligands, advanced glycation endproducts (AGE) and HMGB1 increased mRNA levels of IL-6 and CCL2 in SW872 human adipocytes and mouse 3T3-L1 cells. The introduction of small interfering RNA for RAGE (siRAGE) into SW872 cells abolished the AGE- and HMGB1-induced up-regulation of IL-6 and CCL2. In addition, lipopolysaccharide (LPS), a ligand of RAGE, increased the expression of IL-6 and CCL2 and siRAGE attenuated the LPS-induced expression of IL-6 and CCL2. These results strongly suggest that the elevated AGE, HMGB1, and LPS in pregnant women up-regulate the expression of IL-6 and CCL2 via the RAGE system, leading to systemic inflammation such as PE/HDP. [ABSTRACT FROM AUTHOR]

Published
2019
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