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  1. Article ; Online: Upregulation of Mineralocorticoid Receptor Contributes to Development of Salt-Sensitive Hypertension after Ischemia-Reperfusion Injury in Rats.

    Matsumoto, Takumi / Doi, Shigehiro / Nakashima, Ayumu / Ike, Takeshi / Sasaki, Kensuke / Masaki, Takao

    International journal of molecular sciences

    2022  Volume 23, Issue 14

    Abstract: The ischemia-reperfusion injury (IRI) of rat kidneys is used as a model of acute kidney injury. Salt-sensitive hypertension occurs in rats after IRI, and the distal nephrons play important roles in the development of this condition. We investigated the ... ...

    Abstract The ischemia-reperfusion injury (IRI) of rat kidneys is used as a model of acute kidney injury. Salt-sensitive hypertension occurs in rats after IRI, and the distal nephrons play important roles in the development of this condition. We investigated the role of the mineralocorticoid receptor (MR) in the progression of IRI-induced salt-sensitive hypertension in rats. Fourteen days after right-side nephrectomy, IRI was induced by clamping the left renal artery, with sham surgery performed as a control. IRI rats were provided with normal water or water with 1.0% NaCl (IRI/NaCl), or they were implanted with an osmotic mini-pump to infuse vehicle or aldosterone (IRI/Aldo). Esaxerenone, a non-steroidal MR blocker (MRB), was administered to IRI/NaCl and IRI/Aldo rats for 6 weeks. MR expression increased by day 7 post-IRI. Blood pressure and urinary protein excretion increased in IRI/NaCl and IRI/Aldo rats over the 6-week period, but these effects were negated by MRB administration. The MRB attenuated the expression of the gamma-epithelial sodium channel (ENaC) and renal damage. The ENaC inhibitor, amiloride, ameliorated hypertension and renal damage in IRI/NaCl and IRI/Aldo rats. Our findings thus showed that MR upregulation may play a pivotal role in ENaC-mediated sodium uptake in rats after IRI, resulting in the development of salt-sensitive hypertension in response to salt overload or the activation of the renin-angiotensin-aldosterone system.
    MeSH term(s) Aldosterone/metabolism ; Animals ; Blood Pressure ; Hypertension/metabolism ; Kidney/metabolism ; Rats ; Receptors, Mineralocorticoid/metabolism ; Reperfusion Injury/complications ; Reperfusion Injury/metabolism ; Sodium Chloride/pharmacology ; Sodium Chloride, Dietary/metabolism ; Up-Regulation ; Water/metabolism
    Chemical Substances Receptors, Mineralocorticoid ; Sodium Chloride, Dietary ; Water (059QF0KO0R) ; Sodium Chloride (451W47IQ8X) ; Aldosterone (4964P6T9RB)
    Language English
    Publishing date 2022-07-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23147831
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The hypoxia-inducible factor-α prolyl hydroxylase inhibitor FG4592 ameliorates renal fibrosis by inducing the H3K9 demethylase JMJD1A.

    Ike, Takeshi / Doi, Shigehiro / Nakashima, Ayumu / Sasaki, Kensuke / Ishiuchi, Naoki / Asano, Tomoichiro / Masaki, Takao

    American journal of physiology. Renal physiology

    2022  Volume 323, Issue 5, Page(s) F539–F552

    Abstract: The transcription factors hypoxia-inducible factor-1α and -2α (HIF-1α/2α) are the major regulators of the cellular response to hypoxia and play a key role in renal fibrosis associated with acute and chronic kidney disease. Jumonji domain-containing 1a ( ... ...

    Abstract The transcription factors hypoxia-inducible factor-1α and -2α (HIF-1α/2α) are the major regulators of the cellular response to hypoxia and play a key role in renal fibrosis associated with acute and chronic kidney disease. Jumonji domain-containing 1a (JMJD1A), a histone H3 lysine 9 (H3K9) demethylase, is reported to be an important target gene of HIF-α. However, whether JMJD1A and H3K9 methylation status play a role in renal fibrosis is unclear. Here, we investigated the involvement of HIF-α, JMJD1A, and monomethylated/dimethylated H3K9 (H3K9me1/H3K9me2) levels in unilateral ureteral obstruction (UUO)-induced renal fibrosis in mice. Intraperitoneal administration of FG4592, an inhibitor of HIF-α prolyl hydroxylase, which controls HIF-α protein stability, significantly attenuated renal fibrosis on
    MeSH term(s) Rats ; Animals ; Transforming Growth Factor beta1/metabolism ; Prolyl-Hydroxylase Inhibitors/pharmacology ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Histones/metabolism ; Lysine/metabolism ; RNA, Small Interfering ; Actins/metabolism ; Fibrosis ; Ureteral Obstruction/complications ; Ureteral Obstruction/drug therapy ; Kidney Diseases/complications ; Hypoxia/metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Histone-Lysine N-Methyltransferase/metabolism ; Erythropoietin/metabolism
    Chemical Substances Transforming Growth Factor beta1 ; Prolyl-Hydroxylase Inhibitors ; Hypoxia-Inducible Factor 1, alpha Subunit ; Histones ; Lysine (K3Z4F929H6) ; RNA, Small Interfering ; Actins ; Procollagen-Proline Dioxygenase (EC 1.14.11.2) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Erythropoietin (11096-26-7)
    Language English
    Publishing date 2022-09-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00083.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Klotho protects chromosomal DNA from radiation-induced damage.

    Nakayama, Shinya / Sun, Jiying / Horikoshi, Yasunori / Kamimura, Yoshitaka / Ike, Takeshi / Fujino, Shu / Kinugasa, Yasuha / Sasaki, Kensuke / Nakashima, Ayumu / Masaki, Takao / Tashiro, Satoshi

    Journal of biochemistry

    2023  Volume 173, Issue 5, Page(s) 375–382

    Abstract: Klotho is an anti-aging, single-pass transmembrane protein found mainly in the kidney. Although aging is likely to be associated with DNA damage, the involvement of Klotho in protecting cells from DNA damage is still unclear. In this study, we examined ... ...

    Abstract Klotho is an anti-aging, single-pass transmembrane protein found mainly in the kidney. Although aging is likely to be associated with DNA damage, the involvement of Klotho in protecting cells from DNA damage is still unclear. In this study, we examined DNA damage in human kidney cells and mouse kidney tissue after ionizing radiation (IR). The depletion and overexpression of Klotho in human kidney cells reduced and increased the cell survival rates after IR, respectively. The formation of γ-H2AX foci, representing DNA damage, was significantly elevated immediately after IR in cells with Klotho depletion and decreased in cells overexpressing Klotho. These results were confirmed in mouse renal tissues after IR. Quantification of DNA damage by a comet assay revealed that the Klotho knockdown significantly increased the amount of DNA damage immediately after IR, suggesting that Klotho protects chromosomal DNA from the induction of damage, rather than facilitating DNA repair. Consistent with this notion, Klotho was detected in both the nucleus and cytoplasm. In the nucleus, Klotho may serve to protect chromosomal DNA from damage, leading to its anti-aging effects.
    MeSH term(s) Animals ; Humans ; Mice ; Aging/genetics ; DNA ; DNA Damage ; DNA Repair ; Histones/metabolism ; Klotho Proteins/genetics ; Klotho Proteins/metabolism
    Chemical Substances DNA (9007-49-2) ; Histones ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2023-01-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 218073-x
    ISSN 1756-2651 ; 0021-924X
    ISSN (online) 1756-2651
    ISSN 0021-924X
    DOI 10.1093/jb/mvad001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Klotho overexpression protects against renal aging along with suppression of transforming growth factor-β1 signaling pathways.

    Oishi, Hiroaki / Doi, Shigehiro / Nakashima, Ayumu / Ike, Takeshi / Maeoka, Yujiro / Sasaki, Kensuke / Doi, Toshiki / Masaki, Takao

    American journal of physiology. Renal physiology

    2021  Volume 321, Issue 6, Page(s) F799–F811

    Abstract: Klotho is an antiaging protein reported to suppress transforming growth factor-β1 (TGF-β1) signaling. Aging kidneys are characterized by interstitial fibrosis, accumulation of cell cycle-arrested cells, and increased levels of oxidative stress. TGF-β1 ... ...

    Abstract Klotho is an antiaging protein reported to suppress transforming growth factor-β1 (TGF-β1) signaling. Aging kidneys are characterized by interstitial fibrosis, accumulation of cell cycle-arrested cells, and increased levels of oxidative stress. TGF-β1 signaling is involved in these processes. In this study, we investigated whether klotho overexpression improves these features in the kidneys of aging mice and examined the inhibitory effect of klotho on signaling molecules related to transforming growth of TGF-β1. Klotho transgenic (KLTG) and wild-type (WT) mice were used, and 8-wk-old and 24-mo-old mice were defined as young and aging, respectively. We found that klotho expression was decreased in aging WT mice, but it was maintained in aging KLTG mice. Klotho overexpression improved the survival of 24-mo-old mice. Although the serum Ca
    MeSH term(s) Aging/drug effects ; Animals ; Fibrosis/drug therapy ; Kidney/drug effects ; Kidney/metabolism ; Kidney Diseases/drug therapy ; Kidney Diseases/pathology ; Mice, Transgenic ; Protective Agents/pharmacology ; Signal Transduction/drug effects ; Transforming Growth Factor beta1/metabolism ; Transforming Growth Factor beta1/pharmacology
    Chemical Substances Protective Agents ; Transforming Growth Factor beta1
    Language English
    Publishing date 2021-11-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00609.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Klotho deficiency intensifies hypoxia-induced expression of IFN-α/β through upregulation of RIG-I in kidneys.

    Urabe, Asako / Doi, Shigehiro / Nakashima, Ayumu / Ike, Takeshi / Morii, Kenichi / Sasaki, Kensuke / Doi, Toshiki / Arihiro, Koji / Masaki, Takao

    PloS one

    2021  Volume 16, Issue 10, Page(s) e0258856

    Abstract: Hypoxia is a common pathway to the progression of end-stage kidney disease. Retinoic acid-inducible gene I (RIG-I) encodes an RNA helicase that recognizes viruses including SARS-CoV2, which is responsible for the production of interferon (IFN)-α/β to ... ...

    Abstract Hypoxia is a common pathway to the progression of end-stage kidney disease. Retinoic acid-inducible gene I (RIG-I) encodes an RNA helicase that recognizes viruses including SARS-CoV2, which is responsible for the production of interferon (IFN)-α/β to prevent the spread of viral infection. Recently, RIG-I activation was found under hypoxic conditions, and klotho deficiency was shown to intensify the activation of RIG-I in mouse brains. However, the roles of these functions in renal inflammation remain elusive. Here, for in vitro study, the expression of RIG-I and IFN-α/β was examined in normal rat kidney (NRK)-52E cells incubated under hypoxic conditions (1% O2). Next, siRNA targeting RIG-I or scramble siRNA was transfected into NRK52E cells to examine the expression of RIG-I and IFN-α/β under hypoxic conditions. We also investigated the expression levels of RIG-I and IFN-α/β in 33 human kidney biopsy samples diagnosed with IgA nephropathy. For in vivo study, we induced renal hypoxia by clamping the renal artery for 10 min in wild-type mice (WT mice) and Klotho-knockout mice (Kl-/- mice). Incubation under hypoxic conditions increased the expression of RIG-I and IFN-α/β in NRK52E cells. Their upregulation was inhibited in NRK52E cells transfected with siRNA targeting RIG-I. In patients with IgA nephropathy, immunohistochemical staining of renal biopsy samples revealed that the expression of RIG-I was correlated with that of IFN-α/β (r = 0.57, P<0.001, and r = 0.81, P<0.001, respectively). The expression levels of RIG-I and IFN-α/β were upregulated in kidneys of hypoxic WT mice and further upregulation was observed in hypoxic Kl-/- mice. These findings suggest that hypoxia induces the expression of IFN-α/β through the upregulation of RIG-I, and that klotho deficiency intensifies this hypoxia-induced expression in kidneys.
    MeSH term(s) Animals ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Hypoxia/genetics ; Hypoxia/metabolism ; Interferon-alpha/metabolism ; Kidney/metabolism ; Mice ; Mice, Knockout ; RNA Helicases/metabolism ; RNA, Small Interfering ; Rats ; Up-Regulation
    Chemical Substances Interferon-alpha ; RNA, Small Interfering ; interferon-alpha 8 ; RIG-I protein, rat (EC 2.7.7.-) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31) ; RNA Helicases (EC 3.6.4.13)
    Language English
    Publishing date 2021-10-21
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0258856
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  6. Article ; Online: A Combination of Iohexol Treatment and Ionizing Radiation Exposure Enhances Kidney Injury in Contrast-Induced Nephropathy by Increasing DNA Damage.

    Fujino, Shu / Sun, Jying / Nakayama, Shinya / Horikoshi, Yasunori / Kinugasa, Yasuha / Ishida, Mari / Sakai, Chiemi / Ike, Takeshi / Doi, Shigehiro / Masaki, Takao / Tashiro, Satoshi

    Radiation research

    2022  Volume 197, Issue 4, Page(s) 384–395

    Abstract: Contrast media has been shown to induce nephropathy (i.e., contrast-induced nephropathy) after various types of radiological examinations. The molecular mechanism of contrast-induced nephropathy has been unclear. In this study, we investigated the ... ...

    Abstract Contrast media has been shown to induce nephropathy (i.e., contrast-induced nephropathy) after various types of radiological examinations. The molecular mechanism of contrast-induced nephropathy has been unclear. In this study, we investigated the mechanism of contrast-induced nephropathy by examining the effects of combined treatment of contrast medium and ionizing radiation on kidney cells in vitro and kidney tissue in vivo. In human renal tubular epithelium cells, immunofluorescence analysis revealed that iohexol increased the numbers of radiation-induced γH2AX nuclear foci. The numbers of γH2AX nuclear foci remained high at 24 h, suggesting that some radiation-induced double-strand breaks remain unrepaired in the presence of iohexol. We established a mouse model of contrast-induced nephropathy, then showed that iohexol and ionizing radiation synergistically reduced renal function and induced double-strand breaks. Importantly, iohexol induced significant macrophage accumulation and oxidative DNA damage in the kidneys of contrast-induced nephropathy model mice in the absence of ionizing radiation; these effects were amplified by ionizing radiation. The results suggest that underlying inflammation and oxidative DNA damage caused by iohexol contribute to the enhancement of radiation-induced double-strand breaks, leading to contrast-induced nephropathy.
    MeSH term(s) Animals ; Contrast Media/adverse effects ; DNA Damage ; Iohexol/adverse effects ; Kidney/physiology ; Kidney Diseases/chemically induced ; Mice ; Radiation, Ionizing
    Chemical Substances Contrast Media ; Iohexol (4419T9MX03)
    Language English
    Publishing date 2022-01-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80322-4
    ISSN 1938-5404 ; 0033-7587
    ISSN (online) 1938-5404
    ISSN 0033-7587
    DOI 10.1667/RADE-21-00178.1
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  7. Article ; Online: Interferon-γ enhances the therapeutic effect of mesenchymal stem cells on experimental renal fibrosis.

    Kanai, Ryo / Nakashima, Ayumu / Doi, Shigehiro / Kimura, Tomoe / Yoshida, Ken / Maeda, Satoshi / Ishiuchi, Naoki / Yamada, Yumi / Ike, Takeshi / Doi, Toshiki / Kato, Yukio / Masaki, Takao

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 850

    Abstract: Mesenchymal stem cells (MSCs) administered for therapeutic purposes can be activated by interferon-γ (IFN-γ) secreted from natural killer cells in injured tissues and exert anti-inflammatory effects. These processes require a substantial period of time, ... ...

    Abstract Mesenchymal stem cells (MSCs) administered for therapeutic purposes can be activated by interferon-γ (IFN-γ) secreted from natural killer cells in injured tissues and exert anti-inflammatory effects. These processes require a substantial period of time, leading to a delayed onset of MSCs' therapeutic effects. In this study, we investigated whether pretreatment with IFN-γ could potentiate the anti-fibrotic ability of MSCs in rats with ischemia-reperfusion injury (IRI) and unilateral ureter obstruction. Administration of MSCs treated with IFN-γ strongly reduced infiltration of inflammatory cells and ameliorated interstitial fibrosis compared with control MSCs without IFN-γ treatment. In addition, conditioned medium obtained from IFN-γ-treated MSCs decreased fibrotic changes in cultured cells induced by transforming growth factor-β1 more efficiently than that from control MSCs. Most notably, secretion of prostaglandin E2 from MSCs was significantly increased by treatment with IFN-γ. Increased prostaglandin E2 in conditioned medium obtained from IFN-γ-treated MSCs induced polarization of immunosuppressive CD163 and CD206-positive macrophages. In addition, knockdown of prostaglandin E synthase weakened the anti-fibrotic effects of MSCs treated with IFN-γ in IRI rats, suggesting the involvement of prostaglandin E2 in the beneficial effects of IFN-γ. Administration of MSCs treated with IFN-γ might represent a promising therapy to prevent the progression of renal fibrosis.
    MeSH term(s) Animals ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; Cells, Cultured ; Culture Media, Conditioned ; Dinoprostone/metabolism ; Fibrosis/therapy ; Interferon-gamma/pharmacology ; Kidney/pathology ; Kidney Diseases/drug therapy ; Kidney Diseases/therapy ; Killer Cells, Natural/metabolism ; Macrophages/metabolism ; Male ; Mesenchymal Stem Cell Transplantation/methods ; Mesenchymal Stem Cells/cytology ; Rats ; Rats, Sprague-Dawley ; Receptors, Cell Surface/metabolism ; Reperfusion Injury/physiopathology ; Reperfusion Injury/therapy ; Ureteral Obstruction/physiopathology ; Ureteral Obstruction/therapy
    Chemical Substances Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; CD163 antigen ; Culture Media, Conditioned ; Receptors, Cell Surface ; Interferon-gamma (82115-62-6) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2021-01-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-79664-6
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  8. Article ; Online: Hypoxia-preconditioned mesenchymal stem cells prevent renal fibrosis and inflammation in ischemia-reperfusion rats.

    Ishiuchi, Naoki / Nakashima, Ayumu / Doi, Shigehiro / Yoshida, Ken / Maeda, Satoshi / Kanai, Ryo / Yamada, Yumi / Ike, Takeshi / Doi, Toshiki / Kato, Yukio / Masaki, Takao

    Stem cell research & therapy

    2020  Volume 11, Issue 1, Page(s) 130

    Abstract: Background: Mesenchymal stem cells (MSCs) have been reported to promote the regeneration of injured tissue via their paracrine abilities, which are enhanced by hypoxic preconditioning. In this study, we examined the therapeutic efficacy of hypoxia- ... ...

    Abstract Background: Mesenchymal stem cells (MSCs) have been reported to promote the regeneration of injured tissue via their paracrine abilities, which are enhanced by hypoxic preconditioning. In this study, we examined the therapeutic efficacy of hypoxia-preconditioned MSCs on renal fibrosis and inflammation in rats with ischemia-reperfusion injury (IRI).
    Methods: MSCs derived from rats and humans were incubated in 1% O
    Results: Administration of rat 1%O
    Conclusions: Our results indicate that hypoxia-preconditioned MSCs are useful as an allogeneic transplantation cell therapy to prevent renal fibrosis and inflammation.
    MeSH term(s) Animals ; Cell Hypoxia ; Cells, Cultured ; Fibrosis ; Humans ; Inflammation ; Ischemia ; Kidney/blood supply ; Kidney/pathology ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells ; Rats ; Reperfusion ; Reperfusion Injury/therapy ; Vascular Endothelial Growth Factor A
    Chemical Substances Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2020-03-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2548671-8
    ISSN 1757-6512 ; 1757-6512
    ISSN (online) 1757-6512
    ISSN 1757-6512
    DOI 10.1186/s13287-020-01642-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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