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Your search keyword '"Takeyama, Michiyasu"' showing total 27 results
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27 results on '"Takeyama, Michiyasu"'

9. Human apolipoprotein B transgenic SHR/NDmcr-cp rats show exacerbated kidney dysfunction

Author

ASAHINA, Makoto, SHIMIZU, Fumi, OHTA, Masayuki, TAKEYAMA, Michiyasu, and TOZAWA, Ryuichi

Subjects
Male, Original, kidney dysfunction, SHR/NDmcr-cprats, Kidney Glomerulus, Hyperlipidemias, metabolic syndrome, Hyperinsulinism, apolipoprotein B, Animals, Humans, Obesity, Rats, Wistar, Inflammation, Sclerosis, dyslipidemia, nutritional and metabolic diseases, Lipid Metabolism, Disease Models, Animal, Oxidative Stress, Proteinuria, Apolipoprotein B-100, Hypertension, Disease Progression, Kidney Diseases, Rats, Transgenic
Abstract

Nephropathy frequently co-occurs with metabolic syndrome in humans. Metabolic syndrome is a cluster of metabolic diseases including obesity, diabetes, hypertension, and dyslipidemia, and some previous studies revealed that dyslipidemia contributes to the progression of kidney dysfunction. To establish a new nephropathy model with metabolic syndrome, we produced human apolipoprotein B (apoB) transgenic (Tg.) SHR/NDmcr-cp (SHR-cp/cp) rats, in which dyslipidemia is exacerbated more than in an established metabolic syndrome model, SHR-cp/cp rats. Human apoB Tg. SHR-cp/cp rats showed obesity, hyperinsulinemia, hypertension, and severe hyperlipidemia. They also exhibited exacerbated early-onset proteinuria, accompanied by increased kidney injury and increased oxidative and inflammatory markers. Histological analyses revealed the characteristic features of human apoB Tg. SHR-cp/cp rats including prominent glomerulosclerosis with lipid accumulation. Our newly established human apoB Tg. SHR-cp/cp rat could be a useful model for the nephropathy in metabolic syndrome and for understanding the interaction between dyslipidemia and renal dysfunction in metabolic syndrome.

Published
2015

11. Establishment of X-linked Alport syndrome model mice with a Col4a5R471X mutation

Author

Hashikami, Kentarou, Asahina, Makoto, Nozu, Kandai, Iijima, Kazumoto, Nagata, Michio, and Takeyama, Michiyasu

Abstract

Alport syndrome (AS) is an inherited disorder characterized by glomerular basement membrane (GBM) abnormality and development of chronic kidney disease at an early age. The cause of AS is a genetic mutation in type IV collagen, and more than 80% of patients have X-linked AS (XLAS) with mutation in COL4A5. Although the causal gene has been identified, mechanisms of progression have not been elucidated, and no effective treatment has been developed. In this study, we generated a Col4a5mutant mouse harboring a nonsense mutation (R471X) obtained from a patient with XLAS using clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated system. Col4a5mRNA and protein expressions were not observed in the kidneys of hemizygous R471X male mice. R471X mice showed proteinuria and hematuria. Pathology revealed progression of glomerulosclerosis and interstitial fibrosis by age. Electron microscopy identified irregular thickening in GBM accompanied by irregular lamination. These observations were consistent with the clinical and pathological features of patients with AS and other established models. In addition, our mice models develop end-stage renal disease at the median age of 28 weeks, much later compared to previous models much more consistent with clinical course of human XLAS. Our models have advantages for future experiments in regard with treatment for human XLAS.

Published
2019
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13. Generation of gene-targeted mice using embryonic stem cells derived from a transgenic mouse model of Alzheimer’s disease

Author

Yamamoto, Satoshi, primary, Ooshima, Yuki, additional, Nakata, Mitsugu, additional, Yano, Takashi, additional, Matsuoka, Kunio, additional, Watanabe, Sayuri, additional, Maeda, Ryouta, additional, Takahashi, Hideki, additional, Takeyama, Michiyasu, additional, Matsumoto, Yoshio, additional, and Hashimoto, Tadatoshi, additional

Published
2012
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17. ß‐Subunit of Escherichia coliF1‐ATPase

Author

Hsu, Shih-Yuan, Noumi, Takato, Takeyama, Michiyasu, Maeda, Masatomo, Ishibashi, Sadahiko, and Futai, Masamitsu

Abstract

A mutant strain KF87 of E. coliwith a defective ß‐subunit (Ala‐151 → Val) of F1‐ATPase was isolated. The mutation is within the conserved sequence (G‐X‐X‐X‐X‐G‐K‐T/S) of nucleotide‐binding proteins. The mutant F1‐ATPase had a much higher rate of uni‐site hydrolysis of ATP than the wild type, and about 6% of the wild‐type multi‐site activity. The mutant enzyme showed defective transmission of conformational change(s) between the ligand‐ and aurovertin‐binding sites.

Published
1987
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18. ß-Subunit of Escherichia coliF 1-ATPase

Author

Hsu, Shih-Yuan, Noumi, Takato, Takeyama, Michiyasu, Maeda, Masatomo, Ishibashi, Sadahiko, and Futai, Masamitsu

Abstract

A mutant strain KF87 of E. coliwith a defective ß-subunit (Ala-151 → Val) of F 1-ATPase was isolated. The mutation is within the conserved sequence (G-X-X-X-X-G-K-T/S) of nucleotide-binding proteins. The mutant F 1-ATPase had a much higher rate of uni-site hydrolysis of ATP than the wild type, and about 6% of the wild-type multi-site activity. The mutant enzyme showed defective transmission of conformational change(s) between the ligand- and aurovertin-binding sites.

Published
1987
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27. Establishment of X-linked Alport syndrome model mice with a Col4a5 R471X mutation.

Author

Hashikami K, Asahina M, Nozu K, Iijima K, Nagata M, and Takeyama M

Abstract

Alport syndrome (AS) is an inherited disorder characterized by glomerular basement membrane (GBM) abnormality and development of chronic kidney disease at an early age. The cause of AS is a genetic mutation in type IV collagen, and more than 80% of patients have X-linked AS (XLAS) with mutation in COL4A5 . Although the causal gene has been identified, mechanisms of progression have not been elucidated, and no effective treatment has been developed. In this study, we generated a Col4a5 mutant mouse harboring a nonsense mutation (R471X) obtained from a patient with XLAS using clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated system. Col4a5 mRNA and protein expressions were not observed in the kidneys of hemizygous R471X male mice. R471X mice showed proteinuria and hematuria. Pathology revealed progression of glomerulosclerosis and interstitial fibrosis by age. Electron microscopy identified irregular thickening in GBM accompanied by irregular lamination. These observations were consistent with the clinical and pathological features of patients with AS and other established models. In addition, our mice models develop end-stage renal disease at the median age of 28 weeks, much later compared to previous models much more consistent with clinical course of human XLAS. Our models have advantages for future experiments in regard with treatment for human XLAS.

Published
2018
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