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32 results on '"Yasuda-Yamahara, Mako"'

10. The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier

Author

Schell, Christoph, Rogg, Manuel, Suhm, Martina, Helmstädter, Martin, Sellung, Dominik, Yasuda-Yamahara, Mako, Kretz, Oliver, Küttner, Victoria, Suleiman, Hani, Kollipara, Laxmikanth, Zahedi, René P., Sickmann, Albert, Eimer, Stefan, Shaw, Andrey S., Kramer-Zucker, Albrecht, Hirano-Kobayashi, Mariko, Abe, Takaya, Aizawa, Shinichi, Grahammer, Florian, Hartleben, Björn, Dengjel, Jörn, and Huber, Tobias B.

Published
2017

12. Ketone bodies: A double‐edged sword for mammalian life span

Author

Tomita, Issei, primary, Tsuruta, Hiroaki, additional, Yasuda‐Yamahara, Mako, additional, Yamahara, Kosuke, additional, Kuwagata, Shogo, additional, Tanaka‐Sasaki, Yuki, additional, Chin‐Kanasaki, Masami, additional, Fujita, Yukihiro, additional, Nishi, Eiichiro, additional, Katagiri, Hideki, additional, Maegawa, Hiroshi, additional, and Kume, Shinji, additional

Published
2023
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13. Improvement in Decline Rate of Estimated Glomerular Filtration Rate after Febuxostat Treatment in a Fabry Disease Patient with Enzyme Replacement Therapy-resistant Proteinuria

Author

Kume, Shinji, primary, Yasuda-Yamahara, Mako, additional, Imamura-Uehara, Yoshimi, additional, Kuwagata, Shogo, additional, Yamahara, Kosuke, additional, Takeda, Naoko, additional, Chin-Kanasaki, Masami, additional, Kato, Koichi, additional, Ohno, Seiko, additional, Nakagawa, Yoshihisa, additional, and Maegawa, Hiroshi, additional

Published
2022
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18. SRGAP1 Controls Small Rho GTPases To Regulate Podocyte Foot Process Maintenance

Author

Rogg, Manuel, primary, Maier, Jasmin I., additional, Dotzauer, Robert, additional, Artelt, Nadine, additional, Kretz, Oliver, additional, Helmstädter, Martin, additional, Abed, Ahmed, additional, Sammarco, Alena, additional, Sigle, August, additional, Sellung, Dominik, additional, Dinse, Patrick, additional, Reiche, Karoline, additional, Yasuda-Yamahara, Mako, additional, Biniossek, Martin L., additional, Walz, Gerd, additional, Werner, Martin, additional, Endlich, Nicole, additional, Schilling, Oliver, additional, Huber, Tobias B., additional, and Schell, Christoph, additional

Published
2021
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19. SP430Potential role for ketone body metabolism in an SGLT2 inhibitor-mediated anti-albuminuric effect in type 2 diabetic db/db mice

Author

Kume, Shinji, primary, Tomita, Issei, additional, Yamahara, Kosuke, additional, Yasuda-Yamahara, Mako, additional, Takeda, Naoko, additional, Osawa, Norihisa, additional, Chin-Kanasaki, Masami, additional, Kaneko, Tatsuroh, additional, Pieper, Michael, additional, Araki, Shin-Ichi, additional, and Maegawa, Hiroshi, additional

Published
2019
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20. FO053ROLE OF KETONE BODY METABOLISM IN SGLT2 INHIBITOR-MEDIATED RENOPROTECTION IN HIGH FAT DIET-FED APOE-KNOCKOUT MICE

Author

Tomita, Issei, primary, Kume, Shinji, additional, Yamahara, Kosuke, additional, Yasuda-Yamahara, Mako, additional, Takeda, Naoko, additional, Osawa, Norihisa, additional, Chin-Kanasaki, Masami, additional, Kaneko, Tatsuroh, additional, Pieper, Michael, additional, Araki, Shin-Ichi, additional, and Maegawa, Hiroshi, additional

Published
2019
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21. Protein O-GlcNAcylation Is Essential for the Maintenance of Renal Energy Homeostasis and Function via Lipolysis during Fasting and Diabetes

Author

Sugahara, Sho, primary, Kume, Shinji, additional, Chin-Kanasaki, Masami, additional, Tomita, Issei, additional, Yasuda-Yamahara, Mako, additional, Yamahara, Kosuke, additional, Takeda, Naoko, additional, Osawa, Norihisa, additional, Yanagita, Motoko, additional, Araki, Shin-ichi, additional, and Maegawa, Hiroshi, additional

Published
2019
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22. Arp3 controls the podocyte architecture at the kidney filtration barrier

Author

Schell, Christoph, Sabass, Benedikt, Helmstaedter, Martin, Geist, Felix, Abed, Ahmed, Yasuda-Yamahara, Mako, Sigle, August, Maier, Jasmin I., Grahammer, Florian, Siegerist, Florian, Artelt, Nadine, Endlich, Nicole, Kerjaschki, Dontscho, Arnold, Hans-Henning, Dengjel, Jörn, Rogg, Manuel, Huber, Tobias B., Schell, Christoph, Sabass, Benedikt, Helmstaedter, Martin, Geist, Felix, Abed, Ahmed, Yasuda-Yamahara, Mako, Sigle, August, Maier, Jasmin I., Grahammer, Florian, Siegerist, Florian, Artelt, Nadine, Endlich, Nicole, Kerjaschki, Dontscho, Arnold, Hans-Henning, Dengjel, Jörn, Rogg, Manuel, and Huber, Tobias B.

Abstract

Podocytes, highly specialized epithelial cells, build the outer part of the kidney filtration barrier and withstand high mechanical forces through a complex network of cellular protrusions. Here, we show that Arp2/3-dependent actin polymerization controls actomyosin contractility and focal adhesion maturation of podocyte protrusions and thereby regulates formation, maintenance, and capacity to adapt to mechanical requirements of the filtration barrier. We find that N-WASP-Arp2/3 define the development of complex arborized podocyte protrusions in vitro and in vivo. Loss of dendritic actin networks results in a pronounced activation of the actomyosin cytoskeleton and the generation of over-maturated but less efficient adhesion, leading to detachment of podocytes. Our data provide a model to explain podocyte protrusion morphology and their mechanical stability based on a tripartite relationship between actin polymerization, contractility, and adhesion.

Published
2019

24. Role of dietary amino acid balance in diet restriction-mediated lifespan extension, renoprotection, and muscle weakness in aged mice

Author

Yoshida, Shohei, primary, Yamahara, Kosuke, additional, Kume, Shinji, additional, Koya, Daisuke, additional, Yasuda-Yamahara, Mako, additional, Takeda, Naoko, additional, Osawa, Norihisa, additional, Chin-Kanasaki, Masami, additional, Adachi, Yusuke, additional, Nagao, Kenji, additional, Maegawa, Hiroshi, additional, and Araki, Shin-ichi, additional

Published
2018
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28. Novel Therapeutic Role for Dipeptidyl Peptidase III in the Treatment of Hypertension.

Author

Xiaoling Pang, Akio Shimizu, Souichi Kurita, Zankov, Dimitar P., Keisuke Takeuchi, Mako Yasuda-Yamahara, Shinji Kume, Tetsuo Ishida, Hisakazu Ogita, Pang, Xiaoling, Shimizu, Akio, Kurita, Souichi, Takeuchi, Keisuke, Yasuda-Yamahara, Mako, Kume, Shinji, Ishida, Tetsuo, and Ogita, Hisakazu

Abstract

Dipeptidyl peptidase III (DPP III) cleaves dipeptide residues from the N terminus of polypeptides ranging from 3 to 10 amino acids in length and is implicated in pathophysiological processes through the breakdown of certain oligopeptides or their fragments. In this study, we newly identified the biochemical properties of DPP III for angiotensin II (Ang II), which consists of 8 amino acids. DPP III quickly and effectively digested Ang II with Km = 3.7×10(-6) mol/L. In the in vivo experiments, DPP III remarkably reduced blood pressure in Ang II-infused hypertensive mice without alteration of heart rate. DPP III did not affect hemodynamics in noradrenalin-induced hypertensive mice or normotensive mice, suggesting specificity for Ang II. When DPP III was intravenously injected every other day for 4 weeks after Ang II osmotic minipump implantation in mice, Ang II-induced cardiac fibrosis and hypertrophy were significantly attenuated. This DPP III effect was at least similar to that caused by an angiotensin receptor blocker candesartan. Furthermore, administration of DPP III dramatically reduced the increase in urine albumin excretion and kidney injury and inflammation markers caused by Ang II infusion. Both DPP III and candesartan administration showed slight additive inhibition in the albumin excretion. These results reveal a novel potential use of DPP III in the treatment of hypertension and its protective effects on hypertension-sensitive organs, such as the heart and kidneys. [ABSTRACT FROM AUTHOR]

Published
2016
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30. Arp3 controls the podocyte architecture at the kidney filtration barrier

Author

Schell, Christoph, Sabass, Benedikt, Helmstaedter, Martin, Geist, Felix, Abed, Ahmed, Yasuda-Yamahara, Mako, Sigle, August, Maier, Jasmin I., Grahammer, Florian, Siegerist, Florian, Artelt, Nadine, Endlich, Nicole, Kerjaschki, Dontscho, Arnold, Hans-Henning, Dengjel, Jörn, Rogg, Manuel, Huber, Tobias B., Schell, Christoph, Sabass, Benedikt, Helmstaedter, Martin, Geist, Felix, Abed, Ahmed, Yasuda-Yamahara, Mako, Sigle, August, Maier, Jasmin I., Grahammer, Florian, Siegerist, Florian, Artelt, Nadine, Endlich, Nicole, Kerjaschki, Dontscho, Arnold, Hans-Henning, Dengjel, Jörn, Rogg, Manuel, and Huber, Tobias B.

Abstract

Podocytes, highly specialized epithelial cells, build the outer part of the kidney filtration barrier and withstand high mechanical forces through a complex network of cellular protrusions. Here, we show that Arp2/3-dependent actin polymerization controls actomyosin contractility and focal adhesion maturation of podocyte protrusions and thereby regulates formation, maintenance, and capacity to adapt to mechanical requirements of the filtration barrier. We find that N-WASP-Arp2/3 define the development of complex arborized podocyte protrusions in vitro and in vivo. Loss of dendritic actin networks results in a pronounced activation of the actomyosin cytoskeleton and the generation of over-maturated but less efficient adhesion, leading to detachment of podocytes. Our data provide a model to explain podocyte protrusion morphology and their mechanical stability based on a tripartite relationship between actin polymerization, contractility, and adhesion.

31. The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier

Author

Schell, Christoph, Rogg, Manuel, Suhm, Martina, Helmstädter, Martin, Sellung, Dominik, Yasuda-Yamahara, Mako, Kretz, Oliver, Küttner, Victoria, Suleiman, Hani, Kollipara, Laxmikanth, Zahedi, René P., Sickmann, Albert, Eimer, Stefan, Shaw, Andrey S., Kramer-Zucker, Albrecht, Hirano-Kobayashi, Mariko, Abe, Takaya, Aizawa, Shinichi, Grahammer, Florian, Hartleben, Björn, Dengjel, Jörn, Huber, Tobias B., Schell, Christoph, Rogg, Manuel, Suhm, Martina, Helmstädter, Martin, Sellung, Dominik, Yasuda-Yamahara, Mako, Kretz, Oliver, Küttner, Victoria, Suleiman, Hani, Kollipara, Laxmikanth, Zahedi, René P., Sickmann, Albert, Eimer, Stefan, Shaw, Andrey S., Kramer-Zucker, Albrecht, Hirano-Kobayashi, Mariko, Abe, Takaya, Aizawa, Shinichi, Grahammer, Florian, Hartleben, Björn, Dengjel, Jörn, and Huber, Tobias B.

Abstract

Podocytes form the outer part of the glomerular filter, where they have to withstand enormous transcapillary filtration forces driving glomerular filtration. Detachment of podocytes from the glomerular basement membrane precedes most glomerular diseases. However, little is known about the regulation of podocyte adhesion in vivo. Thus, we systematically screened for podocyte-specific focal adhesome (FA) components, using genetic reporter models in combination with iTRAQ-based mass spectrometry. This approach led to the identification of FERM domain protein EPB41L5 as a highly enriched podocyte-specific FA component in vivo. Genetic deletion of Epb41l5 resulted in severe proteinuria, detachment of podocytes, and development of focal segmental glomerulosclerosis. Remarkably, by binding and recruiting the RhoGEF ARGHEF18 to the leading edge, EPB41L5 directly controls actomyosin contractility and subsequent maturation of focal adhesions, cell spreading, and migration. Furthermore, EPB41L5 controls matrix-dependent outside-in signaling by regulating the focal adhesome composition. Thus, by linking extracellular matrix sensing and signaling, focal adhesion maturation, and actomyosin activation EPB41L5 ensures the mechanical stability required for podocytes at the kidney filtration barrier. Finally, a diminution of EPB41L5-dependent signaling programs appears to be a common theme of podocyte disease, and therefore offers unexpected interventional therapeutic strategies to prevent podocyte loss and kidney disease progression.

32. Establishment of a novel mouse model of renal artery coiling-based chronic hypoperfusion-related kidney injury.

Author

Imamura-Uehara Y, Yasuda-Yamahara M, Kuwagata S, Yamahara K, Yoshibayashi M, Tanaka-Sasaki Y, Shimizu A, Ogita H, Chin-Kanasaki M, and Kume S

Abstract

Renal artery stenosis-induced chronic renal ischemia is an important cause of renal dysfunction, especially in older adults, and its incidence is currently increasing. To elucidate the mechanisms underlying chronic renal hypoperfusion-induced kidney damage, we developed a novel mouse model of renal artery coiling-based chronic hypoperfusion-related kidney injury. This model exhibits decreased renal blood flow and function, atrophy, and parenchymal injury in the coiled kidney, along with compensatory hypertrophy in the non-coiled kidney, without chronic hypertension. The availability of this mouse model, which can develop renal ischemia without genetic modification, will enhance kidney disease research by serving as a new tool to investigate the effects of acquired factors (e.g., obesity and aging) and genetic factors on renal artery stenosis-related renal parenchymal damage., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Shinji Kume reports financial support was provided by Nippon Boehringer Ingelheim Co Ltd. Shinji Kume reports financial support was provided by 10.13039/501100001691Japan Society for the Promotion of Science. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Published
2023
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