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  1. Article ; Online: Independent regulation of renin-angiotensin-aldosterone system in the kidney.

    Nishiyama, Akira / Kobori, Hiroyuki

    Clinical and experimental nephrology

    2018  Volume 22, Issue 6, Page(s) 1231–1239

    Abstract: Renin-angiotensin-aldosterone system (RAAS) plays important roles in regulating renal hemodynamics and functions, as well as in the pathophysiology of hypertension and renal disease. In the kidney, angiotensin II (Ang II) production is controlled by ... ...

    Abstract Renin-angiotensin-aldosterone system (RAAS) plays important roles in regulating renal hemodynamics and functions, as well as in the pathophysiology of hypertension and renal disease. In the kidney, angiotensin II (Ang II) production is controlled by independent multiple mechanisms. Ang II is compartmentalized in the renal interstitial fluid with much higher concentrations than those existing in the circulation. Inappropriate activation of the intrarenal RAAS is an important contributor to the pathogenesis of hypertension and renal injury. It has been revealed that intrarenal Ang II levels are predominantly regulated by angiotensinogen and therefore, urinary angiotensinogen could be a biomarker for intrarenal Ang II generation. In addition, recent studies have demonstrated that aldosterone contributes to the progression of renal injury via direct actions on glomerular podocytes, mesangial cells, proximal tubular cells and tubulo-interstitial fibroblasts through the activation of locally expressed mineralocorticoid receptor. Thus, it now appears that intrarenal RAAS is independently regulated and its inappropriate activation contributes to the pathogenesis of the development of hypertension and renal disease. This short review article will focus on the independent regulation of the intrarenal RAAS with an emphasis on the specific role of angiotensinogen.
    MeSH term(s) Angiotensin II/biosynthesis ; Angiotensin II/blood ; Angiotensinogen/physiology ; Angiotensinogen/urine ; Enzyme-Linked Immunosorbent Assay ; Humans ; Hypertension/etiology ; Kidney/physiology ; Kidney Diseases/etiology ; Renin/blood ; Renin-Angiotensin System/physiology
    Chemical Substances Angiotensinogen (11002-13-4) ; Angiotensin II (11128-99-7) ; Renin (EC 3.4.23.15)
    Language English
    Publishing date 2018-03-29
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 1338768-6
    ISSN 1437-7799 ; 1342-1751
    ISSN (online) 1437-7799
    ISSN 1342-1751
    DOI 10.1007/s10157-018-1567-1
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  2. Article ; Online: Intrarenal renin-angiotensin system activation in end-stage renal disease.

    Urushihara, Maki / Kobori, Hiroyuki

    Hypertension research : official journal of the Japanese Society of Hypertension

    2017  Volume 40, Issue 4, Page(s) 351–352

    MeSH term(s) Angiotensin II ; Angiotensinogen ; Humans ; Kidney ; Kidney Failure, Chronic ; Renin ; Renin-Angiotensin System
    Chemical Substances Angiotensinogen (11002-13-4) ; Angiotensin II (11128-99-7) ; Renin (EC 3.4.23.15)
    Language English
    Publishing date 2017
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 1175297-x
    ISSN 1348-4214 ; 0916-9636
    ISSN (online) 1348-4214
    ISSN 0916-9636
    DOI 10.1038/hr.2017.7
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    Zs.A 3898: Show issues Location:
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  3. Article ; Online: Melatonin in chronic kidney disease: a promising chronotherapy targeting the intrarenal renin-angiotensin system.

    Rahman, Asadur / Hasan, Arif Ul / Kobori, Hiroyuki

    Hypertension research : official journal of the Japanese Society of Hypertension

    2019  Volume 42, Issue 6, Page(s) 920–923

    MeSH term(s) Animals ; Antioxidants/therapeutic use ; Chronotherapy/methods ; Humans ; Kidney/drug effects ; Melatonin/therapeutic use ; Renal Insufficiency, Chronic/drug therapy ; Renin-Angiotensin System/drug effects
    Chemical Substances Antioxidants ; Melatonin (JL5DK93RCL)
    Language English
    Publishing date 2019-02-13
    Publishing country England
    Document type Editorial
    ZDB-ID 1175297-x
    ISSN 1348-4214 ; 0916-9636
    ISSN (online) 1348-4214
    ISSN 0916-9636
    DOI 10.1038/s41440-019-0223-9
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  4. Article: [Intrarenal mechanisms of angiotensin II formation].

    Kobori, Hiroyuki

    Nihon Jinzo Gakkai shi

    2010  Volume 52, Issue 2, Page(s) 92–100

    MeSH term(s) Angiotensin II/biosynthesis ; Angiotensin-Converting Enzyme 2 ; Angiotensinogen/metabolism ; Animals ; Biomarkers ; Humans ; Hypertension/etiology ; Kidney/metabolism ; Kidney Diseases/etiology ; Peptidyl-Dipeptidase A/physiology ; Receptors, Cell Surface ; Renin/physiology ; Renin-Angiotensin System ; Serine Proteases/physiology
    Chemical Substances Biomarkers ; Receptors, Cell Surface ; prorenin receptor ; Angiotensinogen (11002-13-4) ; Angiotensin II (11128-99-7) ; Serine Proteases (EC 3.4.-) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Renin (EC 3.4.23.15)
    Language Japanese
    Publishing date 2010-04-22
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 1195538-7
    ISSN 0385-2385
    ISSN 0385-2385
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  5. Article ; Online: Interactions between Host PPARs and Gut Microbiota in Health and Disease.

    Hasan, Arif Ul / Rahman, Asadur / Kobori, Hiroyuki

    International journal of molecular sciences

    2019  Volume 20, Issue 2

    Abstract: The human gastrointestinal tract is inhabited by many types of microbiota, including bacteria, viruses, and fungi. Dysregulations of their microenvironment are associated with various health problems, not only limited to gastrointestinal disorders, such ... ...

    Abstract The human gastrointestinal tract is inhabited by many types of microbiota, including bacteria, viruses, and fungi. Dysregulations of their microenvironment are associated with various health problems, not only limited to gastrointestinal disorders, such as inflammatory bowel disease, but to impacts beyond the intestine. For example, intestinal microbiota can affect the liver in non-alcoholic fatty liver disease, visceral adipose tissue during adipogenesis, and the heart in atherosclerosis. The factors contributing to these pathogeneses involve the gut microbiota and the effector organs of the host, and everything in between. The nuclear receptor peroxisome proliferator-activated receptors (PPARs) are pivotal for the modulation of many of the pathogeneses mentioned above. It is, therefore, conceivable that, in the process of host-microbiota interactions, PPARs play important roles. In this review, we focus on the interactions between host PPARs in different organs and gut microbiota and their impacts on maintaining health and various diseases.
    MeSH term(s) Adaptation, Biological ; Animals ; Disease Susceptibility ; Energy Metabolism ; Gastrointestinal Microbiome ; Gene Expression Regulation ; Host-Pathogen Interactions ; Humans ; Immunomodulation ; Peroxisome Proliferator-Activated Receptors/genetics ; Peroxisome Proliferator-Activated Receptors/metabolism ; Signal Transduction
    Chemical Substances Peroxisome Proliferator-Activated Receptors
    Language English
    Publishing date 2019-01-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20020387
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  6. Article ; Online: Interactions between Host PPARs and Gut Microbiota in Health and Disease

    Arif Ul Hasan / Asadur Rahman / Hiroyuki Kobori

    International Journal of Molecular Sciences, Vol 20, Iss 2, p

    2019  Volume 387

    Abstract: The human gastrointestinal tract is inhabited by many types of microbiota, including bacteria, viruses, and fungi. Dysregulations of their microenvironment are associated with various health problems, not only limited to gastrointestinal disorders, such ... ...

    Abstract The human gastrointestinal tract is inhabited by many types of microbiota, including bacteria, viruses, and fungi. Dysregulations of their microenvironment are associated with various health problems, not only limited to gastrointestinal disorders, such as inflammatory bowel disease, but to impacts beyond the intestine. For example, intestinal microbiota can affect the liver in non-alcoholic fatty liver disease, visceral adipose tissue during adipogenesis, and the heart in atherosclerosis. The factors contributing to these pathogeneses involve the gut microbiota and the effector organs of the host, and everything in between. The nuclear receptor peroxisome proliferator-activated receptors (PPARs) are pivotal for the modulation of many of the pathogeneses mentioned above. It is, therefore, conceivable that, in the process of host-microbiota interactions, PPARs play important roles. In this review, we focus on the interactions between host PPARs in different organs and gut microbiota and their impacts on maintaining health and various diseases.
    Keywords atherosclerosis ; inflammatory bowel disease ; irritable bowel syndrome ; metabolic syndrome ; non-alcoholic liver diseases ; obesity ; type 2 diabetes mellitus ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Knee Alignment Correction by High Tibial Osteotomy Reduces Symptoms and Synovial Inflammation in Knee Osteoarthritis Accompanied by Macrophage Phenotypic Change From M1 to M2.

    Yoshida, Shigeo / Nishitani, Kohei / Yoshitomi, Hiroyuki / Kuriyama, Shinichi / Nakamura, Shinichiro / Fujii, Takayuki / Saito, Motoo / Kobori, Yu / Murakami, Akinori / Murata, Koichi / Ito, Hiromu / Ueno, Hideki / Matsuda, Shuichi

    Arthritis & rheumatology (Hoboken, N.J.)

    2023  Volume 75, Issue 6, Page(s) 950–960

    Abstract: Objective: This study aimed to determine whether alignment correction by high tibial osteotomy (HTO) can change the biologic intraarticular microenvironment of osteoarthritic (OA) knees.: Methods: Synovial tissue (ST) and fluid (SF) were collected ... ...

    Abstract Objective: This study aimed to determine whether alignment correction by high tibial osteotomy (HTO) can change the biologic intraarticular microenvironment of osteoarthritic (OA) knees.
    Methods: Synovial tissue (ST) and fluid (SF) were collected from the affected knees of 31 OA patients during initial HTO and plate removal surgeries. Changes in gene expression in ST were investigated by microarray and real-time polymerase chain reaction (PCR). ST specimens were also evaluated histologically using synovitis scores and immunofluorescence staining to determine macrophage polarity. Cytokines and chemokines in SF were analyzed by enzyme-linked immunosorbent assays. The mechanism of macrophage polarization was investigated in human peripheral blood mononuclear cell-derived macrophages and fibroblast-like synoviocytes (FLS) stimulated with cartilage fragments. We also evaluated Spearman correlations between Knee Injury and Osteoarthritis Outcome scores (KOOS) and macrophage-related gene expression.
    Results: The microarray results indicated down-regulated inflammatory genes and pathways. Real-time PCR determined that genes expressing proinflammatory IL1B and IL6 were down-regulated and M2 macrophage-related IL1RA, IL10, CCL18, and CD206 were up-regulated. Histologic findings revealed attenuated synovitis scores and a shift from M1 to M2 macrophages. Interleukin-1β (IL-1β) concentrations in SF decreased after HTO. Cartilage fragments were responsible for M1 macrophage polarization and proinflammatory gene and protein expression in macrophages, whereas cartilage fragments up-regulated only IL-6 protein in FLS. Postoperative KOOS positively correlated with the expression of the M2-related genes CCL18 and CD206.
    Conclusion: Correction of lower limb alignment with HTO attenuated synovial inflammation and changed macrophage polarization from M1 to M2, suggesting an improved intraarticular environment in knee OA.
    MeSH term(s) Humans ; Osteoarthritis, Knee/genetics ; Osteoarthritis, Knee/surgery ; Osteoarthritis, Knee/metabolism ; Leukocytes, Mononuclear/metabolism ; Macrophages/metabolism ; Synovitis/surgery ; Synovitis/metabolism ; Inflammation/metabolism ; Lower Extremity ; Osteotomy/methods
    Language English
    Publishing date 2023-03-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42424
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    Zs.A 24: Show issues Location:
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  8. Article ; Online: Klotho supplementation attenuates blood pressure and albuminuria in murine model of IgA nephropathy.

    Takenaka, Tsuneo / Hasan, Arif / Marumo, Takeshi / Kobori, Hiroyuki / Inoue, Tsutomu / Miyazaki, Takashi / Suzuki, Hiromichi / Nishiyama, Akira / Ishii, Naohito / Hayashi, Matsuhiko

    Journal of hypertension

    2021  Volume 39, Issue 8, Page(s) 1567–1576

    Abstract: Background: Klotho interacts with various membrane proteins, such as transforming growth factor-β (TGFβ) and insulin-like growth factor (IGF) receptors. The renal expression of klotho is diminished in chronic kidney disease.: Method: In this study, ... ...

    Abstract Background: Klotho interacts with various membrane proteins, such as transforming growth factor-β (TGFβ) and insulin-like growth factor (IGF) receptors. The renal expression of klotho is diminished in chronic kidney disease.
    Method: In this study, we assessed the effects of klotho supplementation on a murine model of IgA nephropathy. Twenty-four-week-old hyper serum IgA (HIGA) mice were subcutaneously injected daily with recombinant human klotho protein (20 μg/kg per day) or the vehicle. After 2 months, the mice were killed using an anesthesia overdose and their kidneys were harvested for analysis.
    Results: Supplementation of exogenous klotho protein reduced SBP, albuminuria, 8-epi-prostaglandin F2α excretion, glomerular filtration rate, renal angiotensin II concentration, and angiotensinogen expression in HIGA mice. Additionally, it enhanced renal expression of superoxide dismutase (SOD) and renal klotho itself. The findings using laser-manipulated microdissection demonstrated that klotho supplementation reduced the glomerular expression of TGFβ, fibronectin, and IGF, and increased the glomerular expression of connexin (Cx) 40.
    Conclusion: These results indicate that klotho supplementation reduces blood pressure by suppressing the renin--angiotensin system in HIGA mice. Klotho inhibits IGF signaling to preserve glomerular Cx40 levels, ameliorating albuminuria in HIGA mice. Klotho protein supplementation attenuates mesangial expansion by inhibiting TGFβ signaling in HIGA mice.
    MeSH term(s) Albuminuria ; Animals ; Blood Pressure ; Dietary Supplements ; Disease Models, Animal ; Glomerulonephritis, IGA/drug therapy ; Glucuronidase ; Klotho Proteins ; Mice
    Chemical Substances Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2021-05-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605532-1
    ISSN 1473-5598 ; 0263-6352 ; 0952-1178
    ISSN (online) 1473-5598
    ISSN 0263-6352 ; 0952-1178
    DOI 10.1097/HJH.0000000000002845
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    Zs.A 1885: Show issues Location:
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    Zs.MO 614: Show issues

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  9. Article ; Online: Development of 7SK snRNA Mimics That Inhibit HIV Transcription.

    Yamayoshi, Asako / Fukumoto, Hiroyuki / Hayashi, Rie / Kishimoto, Kyosuke / Kobori, Akio / Koyanagi, Yoshio / Komano, Jun A / Murakami, Akira

    ChemMedChem

    2021  Volume 16, Issue 20, Page(s) 3181–3184

    Abstract: The 332-nucleotide small nuclear RNA (snRNA) 7SK is a highly conserved non-coding RNA that regulates transcriptional elongation. By binding with positive transcriptional elongation factor b (P-TEFb) via HEXIM1, 7SK snRNA decreases the kinase activity of ... ...

    Abstract The 332-nucleotide small nuclear RNA (snRNA) 7SK is a highly conserved non-coding RNA that regulates transcriptional elongation. By binding with positive transcriptional elongation factor b (P-TEFb) via HEXIM1, 7SK snRNA decreases the kinase activity of P-TEFb and inhibits transcriptional elongation. Additionally, it is reported that 7SK inhibition results in the stimulation of human immunodeficiency virus (HIV)-specific transcription. These reports suggest that 7SK is a naturally occurring functional molecule as negative regulator of P-TEFb and HIV transcription. In this study, we developed functional oligonucleotides that mimic the function of 7SK (7SK mimics) as novel inhibitors of HIV replication. We defined the essential region of 7SK regarding its suppressive effects on transcriptional downregulation using an antisense strategy. Based on the results, we designed 7SK mimics containing the defined region. The inhibitory effects of 7SK mimics on HIV-1 long terminal repeat promoter specific transcription was drastic compared with those of the control mimic molecule. Notably, these effects were found to be more enhanced by co-transfection with Tat-expressing plasmids. From these results, it is indicated that 7SK mimics may have great therapeutic potential for HIV/AIDS treatment.
    MeSH term(s) Dose-Response Relationship, Drug ; Drug Development ; Molecular Structure ; RNA, Small Nuclear/chemical synthesis ; RNA, Small Nuclear/chemistry ; RNA, Small Nuclear/pharmacology ; Structure-Activity Relationship ; Transcription, Genetic/drug effects ; Transcription, Genetic/genetics ; tat Gene Products, Human Immunodeficiency Virus/antagonists & inhibitors ; tat Gene Products, Human Immunodeficiency Virus/genetics
    Chemical Substances RNA, Small Nuclear ; tat Gene Products, Human Immunodeficiency Virus
    Language English
    Publishing date 2021-07-26
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2218496-X
    ISSN 1860-7187 ; 1860-7179
    ISSN (online) 1860-7187
    ISSN 1860-7179
    DOI 10.1002/cmdc.202100422
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  10. Article ; Online: Altered Circadian Timing System-Mediated Non-Dipping Pattern of Blood Pressure and Associated Cardiovascular Disorders in Metabolic and Kidney Diseases.

    Rahman, Asadur / Hasan, Arif Ul / Nishiyama, Akira / Kobori, Hiroyuki

    International journal of molecular sciences

    2018  Volume 19, Issue 2

    Abstract: The morning surge in blood pressure (BP) coincides with increased cardiovascular (CV) events. This strongly suggests that an altered circadian rhythm of BP plays a crucial role in the development of CV disease (CVD). A disrupted circadian rhythm of BP, ... ...

    Abstract The morning surge in blood pressure (BP) coincides with increased cardiovascular (CV) events. This strongly suggests that an altered circadian rhythm of BP plays a crucial role in the development of CV disease (CVD). A disrupted circadian rhythm of BP, such as the non-dipping type of hypertension (i.e., absence of nocturnal BP decline), is frequently observed in metabolic disorders and chronic kidney disease (CKD). The circadian timing system, controlled by the central clock in the suprachiasmatic nucleus of the hypothalamus and/or by peripheral clocks in the heart, vasculature, and kidneys, modulates the 24 h oscillation of BP. However, little information is available regarding the molecular and cellular mechanisms of an altered circadian timing system-mediated disrupted dipping pattern of BP in metabolic disorders and CKD that can lead to the development of CV events. A more thorough understanding of this pathogenesis could provide novel therapeutic strategies for the management of CVD. This short review will address our and others' recent findings on the molecular mechanisms that may affect the dipping pattern of BP in metabolic dysfunction and kidney disease and its association with CV disorders.
    MeSH term(s) Blood Pressure ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/physiopathology ; Cardiovascular Diseases/therapy ; Circadian Rhythm ; Humans ; Kidney Diseases/pathology ; Kidney Diseases/physiopathology ; Kidney Diseases/therapy
    Language English
    Publishing date 2018-01-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19020400
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