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Article ; Online: Urinary titin is not an early biomarker of skeletal muscle atrophy induced by muscle denervation in mice.

Tanihata, Jun / Minamisawa, Susumu

2023 Volume 18, Issue 8, Page(s) e0289185

Abstract: Early detection of skeletal muscle atrophy is important to prevent further muscle weakness. However, there are few non-invasive biomarkers for skeletal muscle atrophy. Recent studies have reported that the N-terminal fragment (N-titin) of titin, a giant ... ...

Abstract	Early detection of skeletal muscle atrophy is important to prevent further muscle weakness. However, there are few non-invasive biomarkers for skeletal muscle atrophy. Recent studies have reported that the N-terminal fragment (N-titin) of titin, a giant sarcomeric protein, is detected in the urine of patients with muscle damage. In this study, we hypothesized that urinary N-titin would be a potential early biomarker of skeletal muscle atrophy in mice caused by sciatic nerve denervation. Male mice were randomly divided into control and denervation groups, and urinary N-titin levels were assessed daily for 9 days using an enzyme-linked immunosorbent assay system. Despite reduced titin protein levels in atrophic muscles 10 days after denervation, cleaved N-titin fragments were not increased in the urine of mice with denervation-induced muscle atrophy. Furthermore, we found no uptake of Evans blue dye from the extracellular space into the cytoplasm in atrophic muscles, suggesting that the sarcomeric membrane is intact in those muscles. The present results suggest that cleaved N-titin in the urine is not suitable as an early biomarker of skeletal muscle atrophy.
MeSH term(s)	Mice ; Male ; Animals ; Connectin/metabolism ; Muscle, Skeletal/metabolism ; Muscle Denervation ; Muscular Atrophy/pathology ; Biomarkers/metabolism ; Denervation/adverse effects ; Protein Kinases/metabolism
Chemical Substances	Connectin ; Biomarkers ; titin protein, mouse (EC 2.7.11.1) ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2023-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0289185
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Article ; Online: Elusive mechanisms responsible for pulmonary hypertension.

Fujimoto, Yoshitaka / Minamisawa, Susumu

The Journal of thoracic and cardiovascular surgery

2017 Volume 155, Issue 1, Page(s) 282

MeSH term(s)	Animals ; Heart Diseases ; Hypertension ; Hypertension, Pulmonary ; Pulmonary Artery ; Rats
Language	English
Publishing date	2017-12-11
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	3104-5
ISSN	1097-685X ; 0022-5223
ISSN (online)	1097-685X
ISSN	0022-5223
DOI	10.1016/j.jtcvs.2017.09.021
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Article: Urinary Titin Is Increased in Patients After Cardiac Surgery.

Tanihata, Jun / Nishioka, Naritomo / Inoue, Takahiro / Bando, Ko / Minamisawa, Susumu

Frontiers in cardiovascular medicine

2019 Volume 6, Page(s) 7

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2019-02-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2019.00007
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Article ; Online: Standard-dose gentamicin does not increase risk of patent ductus arteriosus.

Kishibuchi, Ayana / Akaike, Toru / Minamisawa, Susumu

Pediatrics and neonatology

2019 Volume 61, Issue 1, Page(s) 45–50

Abstract: Background: Rates of patent ductus arteriosus (PDA) and infection are high in preterm infants. Preterm infants with infection are more likely to develop symptomatic PDA, a potentially fatal disease. Clinically, gentamicin is widely used for early-onset ... ...

Abstract	Background: Rates of patent ductus arteriosus (PDA) and infection are high in preterm infants. Preterm infants with infection are more likely to develop symptomatic PDA, a potentially fatal disease. Clinically, gentamicin is widely used for early-onset infection in neonates including preterm infants. A recent study demonstrated that standard-dose gentamicin itself, not infection, increased risk of PDA in mice, suggesting that gentamicin should be avoided in neonates with a risk of PDA. This claim has been insufficiently investigated in subsequent in-vivo experiments. We reevaluated the in-vivo effect of standard-dose gentamicin on patency of the rat ductus arteriosus (DA). Methods: 1) To evaluate the effect of gentamicin on DA patency duration, gentamicin was intraperitoneally injected immediately after birth. 2) To evaluate the effect of gentamicin on DA reopening, gentamicin was intraperitoneally injected 30 min after birth. In both scenarios, 30 min after gentamicin administration, rapid whole-body freezing was performed and the inner diameter of the DA was measured. Results: Standard-dose gentamicin (5 μg/g) did not prolong patency of the DA or increase the likelihood of DA reopening in rat neonates. High-dose gentamicin (100 μg/g), however, significantly prolonged patency of the DA and was associated with DA reopening in rat neonates, although the dilative effect did not reach statistical significance. Conclusion: Standard-dose gentamicin does not increase the risk of PDA in rat neonates. This study suggests that standard-dose gentamicin can be used to treat infection in neonates without increasing PDA morbidity.
MeSH term(s)	Animals ; Animals, Newborn ; Anti-Bacterial Agents/adverse effects ; Ductus Arteriosus, Patent/etiology ; Gentamicins/adverse effects ; Rats ; Rats, Wistar ; Risk
Chemical Substances	Anti-Bacterial Agents ; Gentamicins
Language	English
Publishing date	2019-06-05
Publishing country	Singapore
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2441816-X
ISSN	2212-1692 ; 1875-9572
ISSN (online)	2212-1692
ISSN	1875-9572
DOI	10.1016/j.pedneo.2019.05.011
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Article ; Online: Prostaglandin E

Sakuma, Toshiki / Akaike, Toru / Minamisawa, Susumu

Circulation journal : official journal of the Japanese Circulation Society

2018 Volume 83, Issue 1, Page(s) 209–216

Abstract: Background: Patent ductus arteriosus (PDA) is common in premature infants. Cyclooxygenase inhibitors such as indomethacin, which inhibit prostaglandin E: Conclusions: EP4 inhibition contracts rat DA with fewer side-effects. EP4 inhibition is a ... ...

Abstract	Background: Patent ductus arteriosus (PDA) is common in premature infants. Cyclooxygenase inhibitors such as indomethacin, which inhibit prostaglandin E Conclusions: EP4 inhibition contracts rat DA with fewer side-effects. EP4 inhibition is a promising alternative strategy to treat patients with PDA.
MeSH term(s)	Animals ; Benzamides/pharmacology ; Dinoprostone/metabolism ; Ductus Arteriosus/embryology ; Ductus Arteriosus/pathology ; Ductus Arteriosus, Patent/embryology ; Myocardial Contraction/drug effects ; Rats ; Rats, Wistar ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & inhibitors
Chemical Substances	(S)-4-(1-(5-chloro-2-(4-fluorophenyoxy) benzamido)ethyl) benzoic acid ; Benzamides ; Receptors, Prostaglandin E, EP4 Subtype ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2018-11-10
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2068090-9
ISSN	1347-4820 ; 1346-9843
ISSN (online)	1347-4820
ISSN	1346-9843
DOI	10.1253/circj.CJ-18-0761
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Article ; Online: Notch and retinoic acid signals regulate macrophage formation from endocardium downstream of Nkx2-5.

Liu, Norika / Kawahira, Naofumi / Nakashima, Yasuhiro / Nakano, Haruko / Iwase, Akiyasu / Uchijima, Yasunobu / Wang, Mei / Wu, Sean M / Minamisawa, Susumu / Kurihara, Hiroki / Nakano, Atsushi

Nature communications

2023 Volume 14, Issue 1, Page(s) 5398

Abstract: Hematopoietic progenitors are enriched in the endocardial cushion and contribute, in a Nkx2-5-dependent manner, to tissue macrophages required for the remodeling of cardiac valves and septa. However, little is known about the molecular mechanism of ... ...

Abstract	Hematopoietic progenitors are enriched in the endocardial cushion and contribute, in a Nkx2-5-dependent manner, to tissue macrophages required for the remodeling of cardiac valves and septa. However, little is known about the molecular mechanism of endocardial-hematopoietic transition. In the current study, we identified the regulatory network of endocardial hematopoiesis. Signal network analysis from scRNA-seq datasets revealed that genes in Notch and retinoic acid (RA) signaling are significantly downregulated in Nkx2-5-null endocardial cells. In vivo and ex vivo analyses validate that the Nkx2-5-Notch axis is essential for the generation of both hemogenic and cushion endocardial cells, and the suppression of RA signaling via Dhrs3 expression plays important roles in further differentiation into macrophages. Genetic ablation study revealed that these macrophages are essential in cardiac valve remodeling. In summary, the study demonstrates that the Nkx2-5/Notch/RA signaling plays a pivotal role in macrophage differentiation from hematopoietic progenitors.
MeSH term(s)	Endocardium ; Macrophages ; Histiocytes ; Cell Differentiation ; Tretinoin
Chemical Substances	Tretinoin (5688UTC01R)
Language	English
Publishing date	2023-09-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41039-6
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Article ; Online: Troponin T amino acid mutation (ΔK210) knock-in mice as a neonatal dilated cardiomyopathy model.

Tanihata, Jun / Fujii, Teruyuki / Baba, Shunsuke / Fujimoto, Yoshitaka / Morimoto, Sachio / Minamisawa, Susumu

Pediatric research

2020 Volume 89, Issue 4, Page(s) 846–857

Abstract: Background: Dilated cardiomyopathy (DCM) in children is often associated with poor morbidity and mortality and exhibits distinct pathological entities from those of adult DCM. Owing to the limited number of patients and the lack of a good animal model, ... ...

Abstract	Background: Dilated cardiomyopathy (DCM) in children is often associated with poor morbidity and mortality and exhibits distinct pathological entities from those of adult DCM. Owing to the limited number of patients and the lack of a good animal model, the molecular mechanisms underlying pediatric DCM remain poorly understood. The purpose of this study is to establish an animal model of neonatal DCM and identify early progression factors. Methods: Cardiac phenotypes and comprehensive gene expression profiles in homozygous ΔK210 knock-in (TNNT2 Results: Immediately after birth, the cardiac weight in TNNT2 Conclusions: TNNT2 Impact: TNNT2
MeSH term(s)	Animals ; Animals, Newborn ; Cardiomyopathy, Dilated/genetics ; Disease Models, Animal ; Down-Regulation ; Echocardiography ; Gene Expression Profiling ; Heart Ventricles/physiopathology ; Homozygote ; Mice ; Mice, Transgenic ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Prognosis ; Troponin T/genetics ; Up-Regulation
Chemical Substances	Troponin T
Language	English
Publishing date	2020-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/s41390-020-1016-1
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Zs.A 564: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Oxygenation decreases elastin secretion from rat ductus arteriosus smooth muscle cells.

Kawakami, Shoji / Minamisawa, Susumu

Pediatrics international : official journal of the Japan Pediatric Society

2015 Volume 57, Issue 4, Page(s) 541–545

Abstract: Background: The ductus arteriosus (DA), a fetal arterial connection between the main pulmonary artery and the descending aorta, normally closes immediately after birth. The oxygen concentration in the blood rises after birth, and in the DA this increase ...

Abstract	Background: The ductus arteriosus (DA), a fetal arterial connection between the main pulmonary artery and the descending aorta, normally closes immediately after birth. The oxygen concentration in the blood rises after birth, and in the DA this increase in oxygen concentration causes functional closure, which is induced by smooth muscle contraction. Previous studies have demonstrated that hypoxia and/or oxygenation affect vascular remodeling of various vessels. Therefore, we hypothesized that the rise in oxygen concentration would affect the vascular structure of the DA due to production of proteins secreted from DA smooth muscle cells (SMC). Methods and results: Liquid chromatography-tandem mass spectrometry was used to comprehensively investigate the secreted proteins in the supernatant of rat DA SMC harvested under hypoxic conditions (1% oxygen) or under normoxic conditions (21% oxygen). We found that the rise in oxygen concentration reduced the secretion of elastin from DA SMC. On reverse transcription-polymerase chain reaction, the expression of elastin mRNA was not significantly changed in DA SMC from hypoxic to normoxic conditions. Conclusions: Given that elastin forms internal elastic lamina and elastic fibers in the vascular muscle layers, and that a rise in oxygen concentration reduced the secretion of elastin, this suggests that the rise in blood oxygen concentration after birth reduces the secretion of elastin, and therefore may play a role in DA structural remodeling after birth.
MeSH term(s)	Animals ; Blotting, Western ; Cells, Cultured ; Disease Models, Animal ; Ductus Arteriosus/cytology ; Ductus Arteriosus/embryology ; Ductus Arteriosus/metabolism ; Elastin/biosynthesis ; Elastin/genetics ; Female ; Gas Chromatography-Mass Spectrometry ; Gene Expression Regulation, Developmental ; Hypoxia/genetics ; Hypoxia/metabolism ; Hypoxia/pathology ; Muscle, Smooth, Vascular/embryology ; Muscle, Smooth, Vascular/metabolism ; Oxygen/metabolism ; Oxygen Consumption/physiology ; Pregnancy ; Pregnancy, Animal ; RNA/genetics ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Vascular Remodeling/genetics
Chemical Substances	RNA (63231-63-0) ; Elastin (9007-58-3) ; Oxygen (S88TT14065)
Language	English
Publishing date	2015-08
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1470376-2
ISSN	1442-200X ; 1328-8067
ISSN (online)	1442-200X
ISSN	1328-8067
DOI	10.1111/ped.12684
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Zs.A 848: Show issues

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Article ; Online: Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1.

Kuga, Kazuhiro / Kusakari, Yoichiro / Uesugi, Ken / Semba, Kentaro / Urashima, Takashi / Akaike, Toru / Minamisawa, Susumu

PloS one

2020 Volume 15, Issue 4, Page(s) e0231905

Abstract: Myocardial fibrosis is often associated with cardiac hypertrophy; indeed, fibrosis is one of the most critical factors affecting prognosis. We aimed to identify the molecules involved in promoting fibrosis under hypertrophic stimuli. We previously ... ...

Abstract	Myocardial fibrosis is often associated with cardiac hypertrophy; indeed, fibrosis is one of the most critical factors affecting prognosis. We aimed to identify the molecules involved in promoting fibrosis under hypertrophic stimuli. We previously established a rat model of cardiac hypertrophy by pulmonary artery banding, in which approximately half of the animals developed fibrosis in the right ventricle. Here, we first comprehensively analyzed mRNA expression in the right ventricle with or without fibrosis in pulmonary artery banding model rats by DNA microarray analysis (GSE141650 at NCBI GEO). The expression levels of 19 genes were up-regulated more than 1.5-fold in fibrotic hearts compared with non-fibrotic hearts. Among them, fibrosis growth factor (FGF) 23 showed one of the biggest increases in expression. Real-time PCR analysis also revealed that, among the FGF receptor (FGFR) family, FGFR1 was highly expressed in fibrotic hearts. We then found that FGF23 was expressed predominantly in cardiomyocytes, while FGFR1 was predominantly expressed in fibroblasts in the rat ventricle. Next, we added FGF23 and transforming growth factor (TGF)-β1 (10-50 ng/mL of each) to isolated fibroblasts from normal adult rat ventricles and cultured them for three days. While FGF23 itself did not directly affect the expression levels of any fibrosis-related mRNAs, FGF23 enhanced the effect of TGF-β1 on increasing the expression levels of α-smooth muscle actin (α-SMA) mRNA. This increase in xx-SMA mRNA levels due to the combination of TGF-β1 and FGF23 was attenuated by the inhibition of FGFR1 or the knockdown of FGFR1 in fibroblasts. Thus, FGF23 synergistically promoted the activation of fibroblasts with TGF-β1, transforming fibroblasts into myofibroblasts via FGFR1. Thus, we identified FGF23 as a paracrine factor secreted from cardiomyocytes to promote cardiac fibrosis under conditions in which TGF-β1 is activated. FGF23 could be a possible target to prevent fibrosis following myocardial hypertrophy.
MeSH term(s)	Actins/genetics ; Actins/metabolism ; Animals ; Cells, Cultured ; Disease Models, Animal ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Fibroblast Growth Factors/pharmacology ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Fibrosis ; Heart Diseases/metabolism ; Heart Diseases/pathology ; Male ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Pyrroles/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor, Fibroblast Growth Factor, Type 1/antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 1/metabolism ; Transforming Growth Factor beta1/pharmacology ; Up-Regulation/drug effects
Chemical Substances	Actins ; Pyrroles ; SU 5402 ; Transforming Growth Factor beta1 ; smooth muscle actin, rat ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Fgfr1 protein, rat (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2020-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0231905
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Article ; Online: Pathology and molecular mechanisms of coarctation of the aorta and its association with the ductus arteriosus.

Yokoyama, Utako / Ichikawa, Yasuhiro / Minamisawa, Susumu / Ishikawa, Yoshihiro

The journal of physiological sciences : JPS

2016 Volume 67, Issue 2, Page(s) 259–270

Abstract: Coarctation of the aorta (CoA) is defined as a congenital stenosis of the thoracic aorta and is one of the most common congenital cardiovascular diseases. Despite successful surgical treatment for CoA, arterial abnormalities, including refractory ... ...

Abstract	Coarctation of the aorta (CoA) is defined as a congenital stenosis of the thoracic aorta and is one of the most common congenital cardiovascular diseases. Despite successful surgical treatment for CoA, arterial abnormalities, including refractory hypertension, aortic aneurysm, and proatherogenic phenotypic changes, frequently affect patients' quality of life. Emerging evidence from morphological and molecular biological investigations suggest that the area of CoA is characterized by phenotypic modulation of smooth muscle cells, intimal thickening, and impaired elastic fiber formation. These changes extend to the pre-and post-stenotic aorta and impair arterial elasticity. The aim of this review is to present current findings on the pathology and molecular mechanisms of vascular remodeling due to CoA. In particular, we will discuss the association between CoA and the ductus arteriosus since the most common site for the stenosis is in the proximity of the ductus arteriosus.
MeSH term(s)	Animals ; Aorta/pathology ; Aortic Coarctation/pathology ; Ductus Arteriosus/pathology ; Endothelium, Vascular/pathology ; Humans ; Muscle, Smooth, Vascular/pathology
Language	English
Publishing date	2016-12-20
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	2234472-X
ISSN	1880-6562 ; 1880-6546
ISSN (online)	1880-6562
ISSN	1880-6546
DOI	10.1007/s12576-016-0512-x
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