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Artikel: A method for phenylalanine self-monitoring using phenylalanine ammonia-lyase and a pre-existing portable ammonia detection system.

Wada, Yoichi / Totsune, Eriko / Mikami-Saito, Yasuko / Kikuchi, Atsuo / Miyata, Toshio / Kure, Shigeo

Molecular genetics and metabolism reports

2023 Band 35, Seite(n) 100970

Abstract: Phenylketonuria is an inborn error of phenylalanine metabolism caused by a phenylalanine hydroxylase deficiency. To prevent the occurrence of neurological symptoms and maternal complications resulting from phenylketonuria, patients must adhere to a ... ...

Abstract	Phenylketonuria is an inborn error of phenylalanine metabolism caused by a phenylalanine hydroxylase deficiency. To prevent the occurrence of neurological symptoms and maternal complications resulting from phenylketonuria, patients must adhere to a strict diet therapy, tetrahydrobiopterin supplementation, or pegvaliase injection to maintain blood phenylalanine levels within a recommended range throughout their lives. Therefore, monitoring blood phenylalanine levels is necessary to determine the recent metabolic status of phenylalanine in patients with PKU; however, there are no available instruments for individuals to monitor their own blood phenylalanine levels using whole fingertip blood. We developed a phenylalanine monitoring system (designated as PheCheck) that included a pre-existing portable ammonia detection device and phenylalanine ammonia-lyase, which converts phenylalanine to trans-cinnamic acid and ammonia. This system was able to remove 86.7% ± 0.03% of the ammonia contained in fingertip blood and successfully reduce background ammonia levels. A good correlation was found between the estimated plasma phenylalanine levels detected by PheCheck and plasma phenylalanine levels detected by high-performance liquid chromatography (R
Sprache	Englisch
Erscheinungsdatum	2023-03-21
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2821908-9
ISSN	2214-4269
ISSN	2214-4269
DOI	10.1016/j.ymgmr.2023.100970
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: [Drug discovery and development in academia].

Miyata, Toshio

Rinsho shinkeigaku = Clinical neurology

2012 Band 51, Heft 11, Seite(n) 1084

Mesh-Begriff(e)	Drug Discovery ; Universities
Sprache	Japanisch
Erscheinungsdatum	2012-01-03
Erscheinungsland	Japan
Dokumenttyp	Journal Article
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
DOI	10.5692/clinicalneurol.51.1084
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: A PAI-1 antagonist ameliorates hypophosphatemia in the Hyp vitamin D-resistant rickets model mouse.

Qian, Cheng / Ito, Nobuaki / Tsuji, Kunikazu / Sato, Shingo / Kikuchi, Katsushi / Yoshii, Toshitaka / Miyata, Toshio / Asou, Yoshinori

FEBS open bio

2023 Band 14, Heft 2, Seite(n) 290–299

Abstract: Congenital fibroblast growth factor 23 (FGF23)-related hypophosphatemic rickets/osteomalacia is a rare bone metabolism disorder characterized by hypophosphatemia and caused by genetic abnormalities that result in excessive secretion of FGF23. Hyp mice ... ...

Abstract	Congenital fibroblast growth factor 23 (FGF23)-related hypophosphatemic rickets/osteomalacia is a rare bone metabolism disorder characterized by hypophosphatemia and caused by genetic abnormalities that result in excessive secretion of FGF23. Hyp mice are a model of X-linked hypophosphatemia (XLH) caused by deletion of the PHEX gene and excessive production of FGF23. The purpose of this study was to investigate the potential of TM5614 as a therapeutic agent for the treatment of congenital FGF23-related hypophosphatemic rickets and osteomalacia in humans by administering TM5614 to Hyp mice and examining its curative effect on hypophosphatemia. After a single oral administration of TM5614 10 mg·kg
Mesh-Begriff(e)	Mice ; Female ; Humans ; Animals ; Familial Hypophosphatemic Rickets/drug therapy ; Familial Hypophosphatemic Rickets/metabolism ; Plasminogen Activator Inhibitor 1 ; Osteomalacia/drug therapy ; Osteomalacia/metabolism ; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase/therapeutic use ; Hypophosphatemia/drug therapy ; Hypophosphatemia/metabolism ; RNA, Messenger/metabolism
Chemische Substanzen	Plasminogen Activator Inhibitor 1 ; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase (EC 1.14.15.18) ; RNA, Messenger
Sprache	Englisch
Erscheinungsdatum	2023-12-25
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2651702-4
ISSN	2211-5463 ; 2211-5463
ISSN (online)	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13745
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Pharmacological inhibition of plasminogen activator inhibitor-1 prevents memory deficits and reduces neuropathology in APP/PS1 mice.

Rodriguez, Guadalupe / Eren, Mesut / Haupfear, Isabel / Viola, Kirsten L / Cline, Erika N / Miyata, Toshio / Klein, William L / Vaughan, Douglas E / Dong, Hongxin

Psychopharmacology

2023 Band 240, Heft 12, Seite(n) 2641–2655

Abstract: Rationale: Extracellular proteolytic activity plays an important role in memory formation and the preservation of cognitive function. Previous studies have shown increased levels of plasminogen activator inhibitor-1 (PAI-1) in the brain of mouse models ... ...

Abstract	Rationale: Extracellular proteolytic activity plays an important role in memory formation and the preservation of cognitive function. Previous studies have shown increased levels of plasminogen activator inhibitor-1 (PAI-1) in the brain of mouse models of Alzheimer's disease (AD) and plasma of AD patients, associated with memory and cognitive decline; however, the exact function of PAI-1 in AD onset and progression is largely unclear. Objective: In this study, we evaluated a novel PAI-1 inhibitor, TM5A15, on its ability to prevent or reverse memory deficits and decrease Aβ levels and plaque deposition in APP/PS1 mice. Methods: We administered TM5A15 mixed in a chow diet to 3-month and 9-month-old APP/PS1 mice before and after neuropathological changes were distinguishable. We then evaluated the effects of TM5A15 on memory function and neuropathology at 9 months and 18 months of age. Results: In the younger mice, 6 months of TM5A15 treatment protected against recognition and short-term working memory impairment. TM5A15 also decreased oligomer levels and amyloid plaques, and increased mBDNF expression in APP/PS1 mice at 9 months of age. In aged mice, 9 months of TM5A15 treatment did not significantly improve memory function nor decrease amyloid plaques. However, TM5A15 treatment showed a trend in decreasing oligomer levels in APP/PS1 mice at 18 months of age. Conclusion: Our results suggest that PAI-1 inhibition could improve memory function and reduce the accumulation of amyloid levels in APP/PS1 mice. Such effects are more prominent when TM5A15 is administered before advanced AD pathology and memory deficits occur.
Mesh-Begriff(e)	Mice ; Humans ; Animals ; Infant ; Amyloid beta-Peptides/metabolism ; Mice, Transgenic ; Plaque, Amyloid/metabolism ; Plasminogen Activator Inhibitor 1/metabolism ; Plasminogen Activator Inhibitor 1/therapeutic use ; Alzheimer Disease/metabolism ; Memory Disorders/drug therapy ; Memory Disorders/prevention & control ; Memory Disorders/complications ; Disease Models, Animal ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Presenilin-1/genetics
Chemische Substanzen	Amyloid beta-Peptides ; Plasminogen Activator Inhibitor 1 ; Amyloid beta-Protein Precursor ; Presenilin-1
Sprache	Englisch
Erscheinungsdatum	2023-09-12
Erscheinungsland	Germany
Dokumenttyp	Journal Article
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-023-06459-8
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Novel mechanisms and therapeutic options in diabetic nephropathy.

Miyata, Toshio

Polskie Archiwum Medycyny Wewnetrznej

2009 Band 119, Heft 4, Seite(n) 261–264

Abstract: Despite multiple therapeutic options, the incidence of diabetic nephropathy remains worrisome. Time has therefore come to undertake a new approach based on some breakthrough not only in medical biology but also in structural biology, chemistry, ... ...

Abstract	Despite multiple therapeutic options, the incidence of diabetic nephropathy remains worrisome. Time has therefore come to undertake a new approach based on some breakthrough not only in medical biology but also in structural biology, chemistry, pharmacology and even computer science. Recent investigations have tried to translate several target molecules or factors identified by basic researches into clinical medicine, as delineated in this. Classical factors contributing to the pathology of diabetic nephropathy, e.g., hypertension, hyperglycemia, hyperinsulinemia, and hyperlipidemia, are now amenable to treatment. Current therapies however do not fully prevent its renal complications. Recent studies, mainly performed in experimental animals, have identified newer culprits in the pathogenesis, such as hypoxia, advanced glycation, oxidative stress, and other bioactive molecules. Animal experiments highlight the fact that renoprotection is not necessarily linked to hemodymanic (blood pressure) or metabolic (glycemic and lipid controls) alterations but appears rather associated with an improved hypoxia, oxidative stress, and/or advanced glycation. To assess the respective contribution of each of these mediators, small molecular weight compounds were designed to interfere with each factor or target molecule. It is indeed important to acquire tools to evaluate and confirm our hypotheses and to translate experimental results into clinical practice.
Mesh-Begriff(e)	Animals ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/physiopathology ; Diabetic Nephropathies/prevention & control ; Disease Models, Animal ; Humans ; Hypoxia/complications ; Hypoxia/physiopathology ; Kidney/blood supply ; Oxidative Stress ; Plasminogen Activator Inhibitor 1/therapeutic use ; Serpins/metabolism
Chemische Substanzen	Plasminogen Activator Inhibitor 1 ; SERPINB7 protein, human ; Serpins
Sprache	Englisch
Erscheinungsdatum	2009-04
Erscheinungsland	Poland
Dokumenttyp	Journal Article
ZDB-ID	123500-x
ISSN	1897-9483 ; 1897-9483 ; 0032-3772
ISSN (online)	1897-9483
ISSN	1897-9483 ; 0032-3772
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Plasminogen activator inhibitor-1 promotes immune evasion in tumors by facilitating the expression of programmed cell death-ligand 1.

Ibrahim, Abd Aziz / Fujimura, Taku / Uno, Tomoko / Terada, Tomoya / Hirano, Ken-Ichi / Hosokawa, Hiroyuki / Ohta, Akio / Miyata, Toshio / Ando, Kiyoshi / Yahata, Takashi

Frontiers in immunology

2024 Band 15, Seite(n) 1365894

Abstract: Background: Increased levels of plasminogen activator inhibitor-1 (PAI-1) in tumors have been found to correlate with poor clinical outcomes in patients with cancer. Although abundant data support the involvement of PAI-1 in cancer progression, whether ... ...

Abstract	Background: Increased levels of plasminogen activator inhibitor-1 (PAI-1) in tumors have been found to correlate with poor clinical outcomes in patients with cancer. Although abundant data support the involvement of PAI-1 in cancer progression, whether PAI-1 contributes to tumor immune surveillance remains unclear. The purposes of this study are to determine whether PAI-1 regulates the expression of immune checkpoint molecules to suppresses the immune response to cancer and demonstrate the potential of PAI-1 inhibition for cancer therapy. Methods: The effects of PAI-1 on the expression of the immune checkpoint molecule programmed cell death ligand 1 (PD-L1) were investigated in several human and murine tumor cell lines. In addition, we generated tumor-bearing mice and evaluated the effects of a PAI-1 inhibitor on tumor progression or on the tumor infiltration of cells involved in tumor immunity either alone or in combination with immune checkpoint inhibitors. Results: PAI-1 induces PD-L1 expression through the JAK/STAT signaling pathway in several types of tumor cells and surrounding cells. Blockade of PAI-1 impedes PD-L1 induction in tumor cells, significantly reducing the abundance of immunosuppressive cells at the tumor site and increasing cytotoxic T-cell infiltration, ultimately leading to tumor regression. The anti-tumor effect elicited by the PAI-1 inhibitor is abolished in immunodeficient mice, suggesting that PAI-1 blockade induces tumor regression by stimulating the immune system. Moreover, combining a PAI-1 inhibitor with an immune checkpoint inhibitor significantly increases tumor regression. Conclusions: PAI-1 protects tumors from immune surveillance by increasing PD-L1 expression; hence, therapeutic PAI-1 blockade may prove valuable in treating malignant tumors.
Mesh-Begriff(e)	Animals ; Humans ; B7-H1 Antigen/metabolism ; B7-H1 Antigen/genetics ; Mice ; Cell Line, Tumor ; Plasminogen Activator Inhibitor 1/metabolism ; Plasminogen Activator Inhibitor 1/genetics ; Tumor Escape ; Neoplasms/immunology ; Neoplasms/metabolism ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Signal Transduction ; Female ; Gene Expression Regulation, Neoplastic ; Tumor Microenvironment/immunology ; Immune Evasion ; Mice, Inbred C57BL
Chemische Substanzen	B7-H1 Antigen ; Plasminogen Activator Inhibitor 1 ; Immune Checkpoint Inhibitors ; SERPINE1 protein, human ; CD274 protein, human
Sprache	Englisch
Erscheinungsdatum	2024-05-08
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1365894
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Phase II, multicenter study of plasminogen activator inhibitor-1 inhibitor (TM5614) plus nivolumab for treating anti-PD-1 antibody-refractory malignant melanoma: TM5614-MM trial.

Fujimura, Taku / Yoshino, Koji / Kato, Hiroshi / Fukushima, Satoshi / Ishizuki, Shoichiro / Otsuka, Atsushi / Matsushita, Shigeto / Amagai, Ryo / Muto, Yusuke / Yamazaki, Emi / Kambayashi, Yumi / Yahata, Takashi / Miyata, Toshio / Fujisawa, Yasuhiro / Asano, Yoshihide

The British journal of dermatology

2024

Abstract: Background: Anti-programmed cell death 1 antibodies (anti-PD-1 Abs) are widely used for advanced melanoma, but the efficacy of an anti-PD-1 Abs is limited in the Asian population. There remains an unmet need to improve the therapeutic effects of anti-PD- ...

Abstract	Background: Anti-programmed cell death 1 antibodies (anti-PD-1 Abs) are widely used for advanced melanoma, but the efficacy of an anti-PD-1 Abs is limited in the Asian population. There remains an unmet need to improve the therapeutic effects of anti-PD-1 Abs treatment, particularly in melanoma patients who are refractory to anti-PD-1 Abs. The aim was to evaluate anti-PD-1 Abs treatment in combination with TM5614 (plasminogen activator inhibitor-1: PAI-1 inhibitor) in patients with unresectable melanoma. Methods: The TM5614-MM study was a multicentre, open-label, single-arm, phase 2 clinical trial to evaluate the efficacy and safety of nivolumab in combination with TM5614 in patients with advanced, unresectable malignant melanoma recruited at 7 Japanese institutes between 13 September 2021 and 31 March 2023. Patients with metastatic or unresectable melanoma previously treated with anti-PD-1 Abs were enrolled. Nivolumab 480 mg was administered intravenously every 4 weeks for 8 weeks, while TM5614 was administered orally at a dose of 120 mg (0-4 weeks) and 180 mg once daily (5-8 weeks). The primary endpoint was the overall response rate after 8 weeks of concomitant use of TM5614. Results: Thirty nine patients were enrolled, and 34 patients in the anti-PD-1 Abs-refractory cohort. The overall response rate at 8 weeks was 25.9% (95% CI: 12.9-44.9%; P = .027) in 27 anti-PD-1-Abs refractory patients by investigator assessment in the protocol per set cohort. Seven patients discontinued treatment due to progressive disease or adverse events. Treatment-related grade 3 or higher adverse events occurred in 3 of 39 patients (7.7%) in the intention-to-treat cohort. Conclusions: TM5614 in combination with nivolumab is well-tolerated and effective in anti-PD-1 Abs-refractory, unresectable melanoma. Trial registration: This trial was registered with Clinical Trial gov, jRCT2021210029.
Sprache	Englisch
Erscheinungsdatum	2024-06-04
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	80076-4
ISSN	1365-2133 ; 0007-0963
ISSN (online)	1365-2133
ISSN	0007-0963
DOI	10.1093/bjd/ljae231
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Structural Insight into the Two-Step Mechanism of PAI-1 Inhibition by Small Molecule TM5484.

Sillen, Machteld / Miyata, Toshio / Vaughan, Douglas E / Strelkov, Sergei V / Declerck, Paul J

International journal of molecular sciences

2021 Band 22, Heft 3

Abstract: Plasminogen activator inhibitor-1 (PAI-1), a key regulator of the fibrinolytic system, is the main physiological inhibitor of plasminogen activators. By interacting with matrix components, including vitronectin (Vn), PAI-1 plays a regulatory role in ... ...

Abstract	Plasminogen activator inhibitor-1 (PAI-1), a key regulator of the fibrinolytic system, is the main physiological inhibitor of plasminogen activators. By interacting with matrix components, including vitronectin (Vn), PAI-1 plays a regulatory role in tissue remodeling, cell migration, and intracellular signaling. Emerging evidence points to a role for PAI-1 in various pathological conditions, including cardiovascular diseases, cancer, and fibrosis. Targeting PAI-1 is therefore a promising therapeutic strategy in PAI-1-related pathologies. A class of small molecule inhibitors including TM5441 and TM5484, designed to bind the cleft in the central β-sheet A of PAI-1, showed to be potent PAI-1 inhibitors in vivo. However, their binding site has not yet been confirmed. Here, we report two X-ray crystallographic structures of PAI-1 in complex with TM5484. The structures revealed a binding site at the flexible joint region, which is distinct from the presumed binding site. Based on the structural analysis and biochemical data we propose a mechanism for the observed dose-dependent two-step mechanism of PAI-1 inhibition. By binding to the flexible joint region in PAI-1, TM5484 might restrict the structural flexibility of this region, thereby inducing a substrate form of PAI-1 followed by a conversion to an inert form.
Mesh-Begriff(e)	Binding Sites ; Catalytic Domain ; Crystallization ; Crystallography, X-Ray ; Dose-Response Relationship, Drug ; Humans ; Models, Molecular ; Plasminogen Activator Inhibitor 1/chemistry ; Plasminogen Activator Inhibitor 1/drug effects ; Protein Conformation ; Structure-Activity Relationship
Chemische Substanzen	Plasminogen Activator Inhibitor 1 ; SERPINE1 protein, human
Sprache	Englisch
Erscheinungsdatum	2021-02-02
Erscheinungsland	Switzerland
Dokumenttyp	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/ijms22031482
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Inhibition of PAI-1 Promotes Lipolysis and Enhances Weight Loss in Obese Mice.

Levine, Joshua A / Olivares, Shantel / Miyata, Toshio / Vaughan, Douglas E / Henkel, Anne S

Obesity (Silver Spring, Md.)

2021 Band 29, Heft 4, Seite(n) 713–720

Abstract: Objective: This study investigates the therapeutic potential of a small molecule inhibitor of plasminogen activator inhibitor-1 (PAI-1), TM5441, in reversing diet-induced obesity in mice.: Methods: Wild-type C57BL/6J mice were fed a high-fat high- ... ...

Abstract	Objective: This study investigates the therapeutic potential of a small molecule inhibitor of plasminogen activator inhibitor-1 (PAI-1), TM5441, in reversing diet-induced obesity in mice. Methods: Wild-type C57BL/6J mice were fed a high-fat high-sugar (HFHS) diet for 8 weeks to induce obesity. After the first 8 weeks, TM5441 was added to the diet for an additional 8 weeks. In order to determine the efficacy of PAI-1 inhibition in conjunction with dietary modification, mice were fed an HFHS diet for 8 weeks to induce obesity and were then switched to a low-fat diet with or without TM5441 for an additional 2 to 8 weeks. Results: Obese mice showed weight reduction and significant improvement in hepatic steatosis when TM5441 was added to the HFHS diet. Obese mice that were treated with TM5441 in conjunction with dietary modification showed enhanced weight loss and a more rapid reversal of hepatic steatosis compared with obese mice treated with dietary modification alone. The enhanced weight loss among mice treated with TM5441 was associated with increased adipose tissue expression of adipose triglyceride lipase, phosphorylated hormone-sensitive lipase, and phosphorylated perilipin-1 as well as induction of adipose tissue lipolysis. Conclusions: Pharmacologic PAI-1 inhibition stimulates adipose tissue lipolysis and enhances weight loss in obese mice.
Mesh-Begriff(e)	Animals ; Lipolysis/physiology ; Male ; Mice ; Mice, Obese ; Plasminogen Activator Inhibitor 1/therapeutic use ; Weight Loss/drug effects
Chemische Substanzen	Plasminogen Activator Inhibitor 1
Sprache	Englisch
Erscheinungsdatum	2021-02-16
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.23112
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: [Novel therapeutic approaches to diabetic nephropathy].

Miyata, Toshio

Nihon Jinzo Gakkai shi

2007 Band 49, Heft 5, Seite(n) 491–495

Mesh-Begriff(e)	Animals ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/etiology ; Drug Design ; Genome, Human ; Genomics ; Humans ; Hypoxia-Inducible Factor 1/physiology ; Plasminogen Activator Inhibitor 1/physiology ; Serpins/genetics ; Serpins/immunology ; Serpins/physiology
Chemische Substanzen	Hypoxia-Inducible Factor 1 ; Plasminogen Activator Inhibitor 1 ; SERPINB7 protein, human ; Serpins
Sprache	Japanisch
Erscheinungsdatum	2007
Erscheinungsland	Japan
Dokumenttyp	Journal Article ; Review
ZDB-ID	1195538-7
ISSN	0385-2385
ISSN	0385-2385
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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