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Article: 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 Volume 35, Page(s) 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
Language	English
Publishing date	2023-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821908-9
ISSN	2214-4269
ISSN	2214-4269
DOI	10.1016/j.ymgmr.2023.100970
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Article ; Online: [Drug discovery and development in academia].

Miyata, Toshio

Rinsho shinkeigaku = Clinical neurology

2012 Volume 51, Issue 11, Page(s) 1084

MeSH term(s)	Drug Discovery ; Universities
Language	Japanese
Publishing date	2012-01-03
Publishing country	Japan
Document type	Journal Article
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
DOI	10.5692/clinicalneurol.51.1084
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Article ; 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 Volume 14, Issue 2, Page(s) 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 term(s)	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
Chemical Substances	Plasminogen Activator Inhibitor 1 ; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase (EC 1.14.15.18) ; RNA, Messenger
Language	English
Publishing date	2023-12-25
Publishing country	England
Document type	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
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Article ; 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 Volume 240, Issue 12, Page(s) 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 term(s)	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
Chemical Substances	Amyloid beta-Peptides ; Plasminogen Activator Inhibitor 1 ; Amyloid beta-Protein Precursor ; Presenilin-1
Language	English
Publishing date	2023-09-12
Publishing country	Germany
Document type	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
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Article: Novel mechanisms and therapeutic options in diabetic nephropathy.

Miyata, Toshio

Polskie Archiwum Medycyny Wewnetrznej

2009 Volume 119, Issue 4, Page(s) 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 term(s)	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
Chemical Substances	Plasminogen Activator Inhibitor 1 ; SERPINB7 protein, human ; Serpins
Language	English
Publishing date	2009-04
Publishing country	Poland
Document type	Journal Article
ZDB-ID	123500-x
ISSN	1897-9483 ; 1897-9483 ; 0032-3772
ISSN (online)	1897-9483
ISSN	1897-9483 ; 0032-3772
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Article ; 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 Volume 22, Issue 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 term(s)	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
Chemical Substances	Plasminogen Activator Inhibitor 1 ; SERPINE1 protein, human
Language	English
Publishing date	2021-02-02
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/ijms22031482
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Article ; 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 Volume 29, Issue 4, Page(s) 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 term(s)	Animals ; Lipolysis/physiology ; Male ; Mice ; Mice, Obese ; Plasminogen Activator Inhibitor 1/therapeutic use ; Weight Loss/drug effects
Chemical Substances	Plasminogen Activator Inhibitor 1
Language	English
Publishing date	2021-02-16
Publishing country	United States
Document type	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
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Article: [Novel therapeutic approaches to diabetic nephropathy].

Miyata, Toshio

Nihon Jinzo Gakkai shi

2007 Volume 49, Issue 5, Page(s) 491–495

MeSH term(s)	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
Chemical Substances	Hypoxia-Inducible Factor 1 ; Plasminogen Activator Inhibitor 1 ; SERPINB7 protein, human ; Serpins
Language	Japanese
Publishing date	2007
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	1195538-7
ISSN	0385-2385
ISSN	0385-2385
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Article: Plasminogen activator inhibitor type-1 is a negative regulator of hematopoietic regeneration in the adipocyte-rich bone marrow microenvironment

Harada, Kaito / Yahata, Takashi / Onizuka, Makoto / Ibrahim, Abd Aziz / Kikkawa, Eri / Miyata, Toshio / Ando, Kiyoshi

Biochemical and biophysical research communications. 2021 June 11, v. 557

2021

Abstract: Bone marrow adipocytes (BMAs) have recently been recognized as a niche component with a suppressive function. Obese individuals with abundant BMAs exhibit impaired hematopoietic regeneration after hematopoietic stem cell transplantation (HSCT). We ... ...

Abstract	Bone marrow adipocytes (BMAs) have recently been recognized as a niche component with a suppressive function. Obese individuals with abundant BMAs exhibit impaired hematopoietic regeneration after hematopoietic stem cell transplantation (HSCT). We hypothesized that plasminogen activator inhibitor type-1 (PAI-1), an adipokine that regulates the fibrinolytic system, contributes to impaired hematopoiesis in bone marrow (BM) microenvironment with abundant BMAs. We demonstrated that BMAs differentiated in vitro could secrete PAI-1 and were positive for PAI-1 in vivo. In addition, the abundance of BMAs was associated with high levels of PAI-1 expression. The BMA-rich microenvironment exhibited impaired hematopoietic regeneration after HSCT when compared with a BMA-less microenvironment. The impaired hematopoietic regeneration in BMA-rich microenvironment was significantly alleviated by PAI-1 knockout or PAI-1 inhibitor treatment. Obese mice with abundant BMAs, compared with normal-weight mice, exhibited higher bone marrow PAI-1 concentrations, increased fibrinolytic system suppression, and lower stem cell factor (SCF) concentrations after HSCT. PAI-1 inhibitor administration significantly activated the fibrinolytic system in obese mice, contributing to the higher SCF concentration. Moreover, PAI-1 inhibitor treatment significantly alleviated the impaired hematopoietic regeneration in obese mice both after 5-fluorouracil injection and HSCT. These results indicate that PAI-1 hinders hematopoietic regeneration in BMA-rich microenvironments. The blockade of PAI-1 activity could be a novel therapeutic means of facilitating hematopoietic reconstitution in BMA-rich patients.
Keywords	adipocytes ; adipokines ; bone marrow ; cell transplantation ; fluorouracil ; hematopoiesis ; hematopoietic stem cells ; plasminogen activator inhibitors ; research ; stem cell factor
Language	English
Dates of publication	2021-0611
Size	p. 180-186.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.04.017
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Article ; Online: Deep molecular response in patients with chronic phase chronic myeloid leukemia treated with the plasminogen activator inhibitor-1 inhibitor TM5614 combined with a tyrosine kinase inhibitor.

Takahashi, Naoto / Kameoka, Yoshihiro / Onizuka, Makoto / Onishi, Yasushi / Takahashi, Fumiaki / Dan, Takashi / Miyata, Toshio / Ando, Kiyoshi / Harigae, Hideo

Cancer medicine

2022 Volume 12, Issue 4, Page(s) 4250–4258

Abstract: Background: We recently showed that pharmacological inhibition of plasminogen activator inhibitor-1 (PAI-1) activity, based on TM5614, increases cell motility and induces the detachment of hematopoietic stem cells from their niches. In this TM5614 phase ...

Abstract	Background: We recently showed that pharmacological inhibition of plasminogen activator inhibitor-1 (PAI-1) activity, based on TM5614, increases cell motility and induces the detachment of hematopoietic stem cells from their niches. In this TM5614 phase II clinical trial, we investigated whether the combination of a PAI-1 inhibitor and tyrosine kinase inhibitors (TKIs) would induce a deep molecular response (DMR) in patients affected by chronic myeloid leukemia (CML) by quantifying BCR-ABL1 transcripts. Methods: Patients with chronic phase CML treated with a stable daily dose of TKIs for at least 1 year and yielding a major molecular response (MMR) but not achieving MR Results: Thirty-three patients were enrolled in the study. The median age was 59.0 years and 58% were male. No Sokal high-risk patients were enrolled in this trial. The median TKI treatment duration was 4.8 years. At the start of this study, seven patients and 26 patients received imatinib and second-generation TKIs, respectively. The cumulative MR Conclusion: TM5614 combined with TKI was well tolerated and induced MR
MeSH term(s)	Humans ; Male ; Middle Aged ; Female ; Tyrosine Kinase Inhibitors ; Fusion Proteins, bcr-abl/genetics ; Plasminogen Activator Inhibitor 1/genetics ; Protein Kinase Inhibitors/adverse effects ; Leukemia, Myeloid, Chronic-Phase/drug therapy ; Leukemia, Myeloid, Chronic-Phase/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics
Chemical Substances	Tyrosine Kinase Inhibitors ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Plasminogen Activator Inhibitor 1 ; Protein Kinase Inhibitors
Language	English
Publishing date	2022-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2659751-2
ISSN	2045-7634 ; 2045-7634
ISSN (online)	2045-7634
ISSN	2045-7634
DOI	10.1002/cam4.5292
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