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1. The Renin-Angiotensin-Aldosterone System in Metabolic Diseases and Other Pathologies

Author

Ortiz, Rudy M, Satou, Ryousuke, Zhuo, Jia L, and Nishiyama, Akira

Subjects
Biochemistry and Cell Biology, Biological Sciences, Medicinal and Biomolecular Chemistry, Chemical Sciences, Microbiology, Hypertension, Humans, Renin-Angiotensin System, Metabolic Diseases, Aldosterone, Renin, Angiotensin II, Other Chemical Sciences, Genetics, Other Biological Sciences, Chemical Physics, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

It has been our pleasure to have been able to develop two special issues within the International Journal of Molecular Sciences: (1) Renin-Angiotensin-Aldosterone System in Pathologies and (2) Renin-Angiotensin-Aldosterone System in Metabolism & Disease [...].

Published
2023

2. Passive antibody transfer from pregnant women to their fetus are maximized after SARS-CoV-2 vaccination irrespective of prior infection

Author

Lauritsen, Cody J., Trinh, Ivy V., Desai, Srushti P., Clancey, Erin, Murrell, Amelie E., Rambaran, Saraswatie, Chandra, Sruti, Elliott, Debra H., Smira, Ashley R., Mo, Zhiyin, Stone, Addison E., Agbodji, Ayitevi, Dugas, Courtney M., Satou, Ryousuke, Pridjian, Gabriella, Longo, Sherri, Ley, Sylvia H., Robinson, James E., Norton, Elizabeth B., Piedimonte, Giovanni, and Gunn, Bronwyn M.

Published
2024
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6. Passive antibody transfer from pregnant women to their fetus are maximized after SARS-CoV-2 vaccination irrespective of prior infection.

Author

Lauritsen, Cody J., primary, Trinh, Ivy V., additional, Desai, Srushti P., additional, Clancey, Erin, additional, Murrell, Amelie E., additional, Rambaran, Saraswatie, additional, Chandra, Sruti, additional, Elliott, Debra H., additional, Smira, Ashley R., additional, Mo, Zhiyin, additional, Stone, Addison E., additional, Agbodji, Ayitevi, additional, Dugas, Courtney M., additional, Satou, Ryousuke, additional, Pridjian, Gabriella, additional, Longo, Sherri, additional, Ley, Sylvia H., additional, Robinson, James E., additional, Norton, Elizabeth B., additional, Piedimonte, Giovanni, additional, and Gunn, Bronwyn M., additional

Published
2023
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24. Tumor necrosis factor-[alpha] suppresses angiotensinogen expression through formation of a p50/p50 homodimer in human renal proximal tubular cells

Author

Satou, Ryousuke, Miyata, Kayoko, Katsurada, Akemi, Navar, L. Gabriel, and Kobori, Hiroyuki

Subjects
Tumor necrosis factor -- Properties, Enzyme-linked immunosorbent assay -- Methods, Angiotensin -- Dosage and administration, Microtubules -- Properties, Biological sciences
Abstract

Angiotensinogen (AGT) expression in renal proximal tubular cells (RPTCs) and intrarenal tumor necrosis factor-[alpha] (TNF-[alpha]) levels are increased in hypertension and renal diseases However, the contribution of TNF-[alpha] to AGT expression in RPTCs has not been established. Therefore, the objective of the present study was to determine influence of TNF-[alpha] on AGT expression in RPTCs. Human kidney-2 (HK-2) cells, immortalized human RPTCs, were treated with several concentrations of TNF-[alpha] up to 24 h. AGT mRNA and protein expression were evaluated by RT-PCR and ELISA, respectively. Activation of nuclear factor-[kappa]B (NF-[kappa]B) by TNF-[alpha] was evaluated by Western blot analysis, immunocytochemistry, and electrophoretic mobility shift assay (EMSA). TNF-[alpha] suppressed AGT mRNA expression in a dose- and time-dependent manner. Maximum AGT mRNA reduction was caused by 40 ng/ml of TNF-[alpha] (0.52 [+ or -] 0.09, ratio to control, at 24 h) and at 24 h (0.66 [+ or -] 0.05, ratio to control, by 10 ng/ml TNF-[alpha]). TNF-[alpha] reduced AGT protein accumulation in the medium between 8 and 24 h (0.62 [+ or -] 0.13 by 40 ng/ml TNF-[alpha], ratio to control). TNF-[alpha] activated and induced translocalization of p50 and p65, which are NF-[kappa]B subunits. Elevated formation of p50/p65 and p50/p50 dimers by TNF-[alpha] were observed by EMSA and supershift assay. Gene silencing of p50, but not p65, attenuated the effect of TNF-[alpha] on reduction of AGT expression in RPTCs. These results indicate that TNF-[alpha] suppresses AGT expression through p50/p50 homodimer formation in human RPTCs, suggesting a possible counteracting mechanism that limits excessive intrarenal AGT production. nuclear factor-[kappa]B; human kidney-2 doi: 10.1152/ajpcell.00078.2010.

Published
2010

25. Intrarenal mouse renin-angiotensin system during ANG II-induced hypertension and ACE inhibition

Author

Gonzalez-Villalobos, Romer A., Satou, Ryousuke, Ohashi, Naro, Semprun-Prieto, Laura C., Katsurada, Akemi, Kim, Catherine, Upchurch, G.M., Prieto, Minolfa C., Kobori, Hiroyuki, and Navar, L. Gabriel

Subjects
Renin-angiotensin system -- Physiological aspects, Renin-angiotensin system -- Genetic aspects, Renin-angiotensin system -- Research, Hypertension -- Risk factors, Hypertension -- Drug therapy, Hypertension -- Research, ACE inhibitors -- Health aspects, Biological sciences
Abstract

Am J Physiol Renal Physiol 298: F150-F157, 2010. First published October 21, 2009; doi:10.1152/ajprenal.00477.2009.--Angiotensin-converting enzyme (ACE) inhibition (ACEi) ameliorates the development of hypertension and the intrarenal ANG II augmentation in ANG II-infused mice. To determine if these effects are associated with changes in the mouse intrarenal renin-angiotensin system, the expression of angiotensinogen (AGT), renin, ACE, angiotensin type 1 receptor ([AT.sub.1]R) mRNA (by quanitative RT-PCR) and protein [by Western blot (WB) and/or immunohistochemistry (IHC)] were analyzed. C57BL/6J male mice (9-12 wk old) were distributed as controls (n = 10), ANG II infused (ANG II = 8,400 ng x [kg.sup.-1] x [min.sup.-1] for 12 days), ACEi only (ACEi = 10, lisinopril, 100 mg/1), and ANG II infused + ACEi (ANG II + ACEi = 11). When compared with controls (1.00), AGT protein (by WB) was increased by ANG II (1.29 [+ or -] 0.13, P < 0.05), and this was not prevented by ACEi (ACEi + ANG II, 1.31 [+ or -] 0.14, P < 0.05). ACE protein (by WB) was increased by ANG II (1.21 [+ or -] 0.08, P < 0.05), and it was reduced by ACEi alone (0.88 [+ or -] 0.07, P < 0.05) or in combination with ANG II (0.80 [+ or -] 0.07, P < 0.05). [AT.sub.1]R protein (by WB) was increased by ANG II (1.27 [+ or -] 0.06, P < 0.05) and ACEi (1.17 [+ or -] 0.06, P < 0.05) but not ANG II + ACEi [1.15 [+ or -] 0.06, not significant (NS)]. Tubular renin protein (semiquantified by IHC) was increased by ANG II (1.49 [+ or -] 0.23, P < 0.05) and ACEi (1.57 [+ or -] 0.15, P < 0.05), but not ANG II + ACEi (1.10 [+ or -] 0.15, NS). No significant changes were observed in AGT, ACE, or [AT.sub.1]R mRNA. In summary, reduced responses of intrarenal tubular renin, ACE, and the [AT.sub.1]R protein to the stimulatory effects of chronic ANG II infusions, in the presence of ACEi, are associated with the effects of this treatment to ameliorate augmentations in blood pressure and intrarenal ANG II content during ANG II-induced hypertension. angiotensin-converting enzyme; angiotensinogen; renin; lisinopril

Published
2010

26. Intrarenal angiotensin II and angiotensinogen augmentation in chronic angiotensin II-infused mice

Author

Gonzalez-Villalobos, Romer A., Seth, Dale M., Satou, Ryousuke, Horton, Heather, Ohashi, Naro, Miyata, Kayoko, Katsurada, Akemi, Tran, Duy V., Kobori, Hiroyuki, and Navar, L.G.

Subjects
Angiotensin -- Properties, Biotelemetry -- Methods, Renal hypertension -- Development and progression, Renal hypertension -- Diagnosis, Physiological research, Biological sciences
Abstract

The objectives of this study were to determine the effects of chronic angiotensin II (ANG II) infusions on ANG II content and angiotensinogen expression in the mouse kidney and the role of the angiotensin II type 1 receptor ([AT.sub.1]R) in mediating these changes. C57BL/6J male mice were subjected to ANG II infusions at doses of 400 or 1,000 ng x [kg.sup.-1] x [min.sup.-1] either alone or with an [AT.sub.1]R blocker (olmesartan; 3 mg x [kg.sup.-1] x [min.sup.-1]) for 12 days. Systolic and mean arterial pressures were determined by tail-cuff plethysmography and radiotelemetry. On day 13, blood and kidneys were collected for ANG II determinations by radioimmunoanalysis and intrarenal angiotensinogen expression studies by quantitative RT-PCR, Western blotting, and immunohistochemistry. ANG II infusions at the low dose elicited progressive increases in systolic blood pressure (135 [+ or -] 2.5 mmHg). In contrast, the high dose induced a rapid increase (152 [+ or -] 2.5, P < 0.05 vs. controls, 109 [+ or -] 2.8). Renal ANG II content was increased by ANG II infusions at the low dose (1,203 [+ or -] 253 fmol/g) and the high dose (1,258 [+ or -] 173) vs. controls (499 [+ or -] 40, P < 0.05). Kidney angiotensinogen mRNA and protein were increased only by the low dose to 1.13 [+ or -] 0.02 and 1.26 [+ or -] 0.10, respectively, over controls (1.00, P < 0.05). These effects were not observed in mice infused at the high dose and those receiving olmesartan. The results indicate that chronic ANG II infusions augment mouse intrarenal ANG II content with [AT.sub.1]R-dependent uptake occurring at both doses, but only the low dose of infusion, which elicited a slow progressive response, causes an [AT.sub.1]R-dependent increase in intrarenal angiotensinogen expression. telemetry; mouse kidney; hypertension

Published
2008

27. Costimulation with angiotensin II and interleukin 6 augments angiotensinogen expression in cultured human renal proximal tubular cells

Author

Satou, Ryousuke, Gonzalez-Villalobos, Romer A., Miyata, Kayoko, Ohashi, Naro, Katsurada, Akemi, Navar, L. Gabriel, and Kobori, Hiroyuki

Subjects
Kidney diseases -- Risk factors, Kidney diseases -- Genetic aspects, Kidney diseases -- Care and treatment, Kidney diseases -- Research, Angiotensin -- Physiological aspects, Angiotensin -- Research, Gene expression -- Physiological aspects, Gene expression -- Research, Biological sciences
Abstract

Augmented intrarenal ANG II stimulates 1L-6, which contributes to renal injury. The expression of intrarenal angiotensinogen (AGT) is enhanced by increased intrarenal ANG II in human renin/human AGT double transgenic mice. ANG II also augments AGT expression in hepatocytes and cardiac myocytes. However, the mechanisms underlying AGT augmentation by ANG II and the contribution of IL-6 to this system are poorly understood. This study was performed in human renal proximal tubular epithelial cells (HRPTECs) to test the hypothesis that IL-6 contributes to the upregulation of AGT expression by ANG II. Human kidney-2 (HK-2) cells, immortalized HRPTECs, were incubated with [10.sup.-7] M ANG II and/or 10 ng/ml IL-6 for up to 24 h. AGT mRNA and protein expressions were measured by real-time RT-PCR and ELISA, respectively. The activities of NF-[kappa]B and STAT3 were evaluated by Western blotting and EMSA. Stimulation with either ANG II or IL-6 did not significantly alter AGT mRNA or protein expression. In contrast, costimulation with ANG II and IL-6 significantly increased AGT mRNA and protein expressions (1.26 [+ or -] 0.10 and 1.16 [+ or -] 0.13 over control, respectively). Olmesartan, an ANG II type 1 receptor blocker, and an IL-6 receptor antibody individually inhibited this synergistic effect. NF-[kappa]B was also activated by costimulation with ANG II and 1L-6. Phosphorylation and activity of STAT3 were increased by stimulation with IL-6 alone and by costimulation. The present study indicates that IL-6 plays an important role in ANG II-mediated augmentation of AGT expression in human renal proximal tubular cells. angiotensinogen; kidney; renin-angiotensin system; cytokines

Published
2008

28. Determination of plasma and urinary angiotensinogen levels in rodents by newly developed ELISA

Author

Kobori, Hiroyuki, Katsurada, Akemi, Miyata, Kayoko, Ohashi, Naro, Satou, Ryousuke, Saito, Toshie, Hagiwara, Yoshiaki, Miyashita, Kazuya, and Navar, L. Gabriel

Subjects
Enzyme-linked immunosorbent assay -- Methods, Blood plasma -- Properties, Renin-angiotensin system -- Properties, Urine -- Properties, Biological sciences
Abstract

We recently reported that urinary excretion rates of angiotensinogen provide a specific index of the intrarenal renin-angiotensin system status in angiotensin II-dependent hypertensive rats. Angiotensinogen concentrations in mouse plasma are thought to be much lower than those in rat plasma; however, detailed information is deficient due to lack of direct quantitative measurements of rodent angiotensinogen. To elucidate this issue, we have developed a quantitative method for measurement of rodent angiotensinogen using a sandwich-type ELISA. The standard curve for mouse and rat angiotensinogen exhibited a high linearity at 0.16-10 and 0.08-5 ng/ml, respectively, with correlation coefficients >0.99. While plasma angiotensinogen concentrations of male high serum IgA (HIGA) mice (IgA nephritis model animals, 1,308 [+ or -] 47 ng/ml; n = 10) were lower than those of control BALB/c mice (1,620 [+ or -] 384; n = 12), urinary angiotensinogen concentrations of HIGA mice (14.6 [+ or -] 1.5 ng/ml; n = 34) were higher than those of BALB/c mice (4.6 [+ or -] 0.1; n = 2). In a similar manner, while plasma angiotensinogen concentrations of Zucker diabetic fatty (ZDF) obese rats (type 2 diabetic model animals, 1,789 [+ or -] 50 ng/ml; n = 5) were lower than those of control ZDF lean rats (2,296 [+ or -] 47; n = 5), urinary angiotensinogen concentrations of ZDF obese rats (88.2 [+ or -] 11.4 ng/ml; n = 15) were higher than those of ZDF lean rats (31.3 [+ or -] 1.9; n = 15). These data indicate that plasma and urinary angiotensinogen concentrations are less in mice than rats. However, these data suggest that urinary angiotensinogen levels are different from plasma angiotensinogen levels in rodents. The development of rodent angiotensinogen ELISA allows quantitative comparisons in mouse and rat angiotensinogen levels in models of hypertension and cardiovascular and kidney diseases. enzyme-linked immunosorbent assay; renin-angiotensin system; plasma; urine; mouse; rat

Published
2008

29. Novel sandwich ELISA for human angiotensinogen

Author

Katsurada, Akemi, Hagiwara, Yoshiaki, Miyashita, Kazuya, Satou, Ryousuke, Miyata, Kayoko, Ohashi, Naro, Navar, Gabriel, and Kobori, Hiroyuki

Subjects
Enzyme-linked immunosorbent assay -- Methods, Angiotensin -- Properties, Blood plasma -- Composition, Urine -- Composition, Biological sciences
Abstract

We recently reported that urinary excretion rates of angiotensinogen ([U.sub.AGT]) provide a specific index of intrarenal renin-angiotensin (ANG) system (RAS) status in ANG If-dependent hypertensive rats. When this is shown to be applicable to human subjects, a diagnostic test to identify those hypertensive patients most likely to respond to an RAS blockade could provide useful information to allow a mechanistic rationale for selection of an optimized approach to treatment of hypertensive patients. However, simple and accurate methods to measure human angiotensinogen (hAGT) are unavailable. For future studies of human subjects, we developed antibodies and a sensitive and specific quantification system for hAGT using a sandwich ELISA. We raised two antibodies against hAGT: a mouse monoclonal antibody and a rabbit polyclonal antibody. The standard curve of this ELISA exhibited a high linearity (0.31-20 ng/ml). The correlation coefficient was >0.99. Plasma angiotensinogen concentrations of healthy volunteers ranged from 28 to 71 [micro]g/ml (n = 10). The ratio of [U.sub.AGT] to urinary creatinine concentration ranged from 5.0 to 30 [micro]g/g (n = 7). Intra- and interassay coefficients of variation ranged from 4.4 to 5.5% and from 4.3 to 7.0%, respectively. This ELISA system had no cross-reactivity with major proteins in proteinuric urine samples, such as human albumin, immunoglobulin, or transferrin. Moreover, the cross-reactivity of the system with angiotensin peptides was also negligible. This hAGT ELISA will be a useful tool to investigate the relationship of [U.sub.AGT] and reactivity to antihypertensive drugs in hypertensive patients. renin-angiotensin system; plasma; urine

Published
2007

30. Kidney-specific enhancement of ANG II stimulates endogenous intrarenal angiotensinogen in gene-targeted mice

Author

Kobori, Hiroyuki, Ozawa, Yuri, Satou, Ryousuke, Katsurada, Akemi, Miyata, Kayoko, Ohashi, Naro, Hase, Naoki, Suzaki, Yuki, Sigmund, Curt D., and Navar, L. Gabriel

Subjects
Renal hypertension -- Physiological aspects, Angiotensin -- Influence, Genetically modified mice -- Diseases, Kidneys -- Properties, Biological sciences
Abstract

This study was performed in transgenic mice to test the hypothesis that the selective intrarenal overproduction of ANG II increases intrarenal mouse (m) angiotensinogen (AGT) expression. We used the following three groups: 1) single transgenic mice (group A, n = 14) expressing human (h) AGT only in the kidney, 2) double-transgenic mice (group D, n = 13) expressing human renin systemically in addition to hAGT only in the kidney, and 3) wild-type (group W, n = 12) mice. Exogenous hAGT protein is inactive in group A because endogenous mouse renin cannot cleave hAGT to ANG I because of a high species specificity. All mice were monitored from 12 to 18 wk of age. Systolic blood pressure progressively increased from 116 [+ or -] 5 mmHg (12 wk) to 140 [+ or -] 7 (18 wk) in group D. This increase was not observed in groups A or W. Intrarenal hAGT levels were similar in groups A and D; however, hAGT was not detectable in kidneys of group W. Kidney ANG II levels were increased in group D (216 [+ or -] 43 fmol/g) compared with groups A (117 [+ or -] 16) and W (118 [+ or -] 17). However, plasma ANG II concentrations were similar among the three groups. Endogenous renal mAGT mRNA was increased significantly in group D (1.46 [+ or -] 0.19, ratio) compared with groupsA (0.97 [+ or -]0.12) and W (1.00 [+ or -] 0.08). Endogenous renal mAGT protein was also significantly increased in group D compared with groups A and W. Interstitial collagen-positive area, interstitial macrophage/monocyte infiltration, and afferent arteriolar wall thickness were increased significantly in group D compared with groups A and W. These data indicate for the first time that the selective stimulation of intrarenal production of ANG II from hAGT augments endogenous intrarenal mAGT mRNA and protein expression. hypertension; transgenic mouse; angiotensin II; renal injury

Published
2007

33. Renin–Angiotensin System

Author

Prieto, Minolfa C., primary, Gonzalez, Alexis A, additional, Satou, Ryousuke, additional, Kobori, Hiroyuki, additional, and Navar, L. Gabriel, additional

Published
2013
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34. Contributors

Author

Aalen, Reidunn B., primary, Abdel-Wahab, Yasser H.A., additional, Adams, Michael E., additional, Adan, Roger A.H., additional, Ahima, Rexford S., additional, Ahmed, Naima, additional, Al-Massadi, Omar, additional, Altstein, Miriam, additional, Anouar, Youssef, additional, Anselmi, Laura, additional, Ansorge, Siegfried, additional, Antcheva, Nikolinka, additional, Antonova-Koch, Yevgeniya, additional, Appel, Jon R., additional, Arik, Anam J., additional, Arter, Alison L., additional, Arvan, Peter, additional, Ashkenazi, Avraham, additional, Baas, P.W., additional, Bado, André, additional, Baird, Andrew, additional, Baiula, Monica, additional, Bakaletz, Lauren O., additional, Bakken, Earl E., additional, Balaskó, Márta, additional, Baldwin, Graham S., additional, Banks, William A., additional, Barra, Donatella, additional, Barson, Jessica R., additional, Basille, Magali, additional, Bauer, Natalie N., additional, Bedini, Andrea, additional, Beeton, Christine, additional, Begley, David J., additional, Beinfeld, Margery C., additional, Bendena, William G., additional, Benoit, Stephen C., additional, Bentov, Itay, additional, Bern, Howard, additional, Bierbaum, Gabriele, additional, Billington, Charles J., additional, Blasiak, Anna, additional, Block, Norman L., additional, Bloom, Stephen. R., additional, Bonney, Iwona, additional, Bowie, John H., additional, Boyd, Sunny K., additional, Brain, Susan D., additional, Brede, Dag A., additional, Broeck, Jozef Vanden, additional, Brown, Kelly L., additional, Brown, Mark R., additional, Bugni, James M., additional, Bundgaard, Jens R., additional, Burel, Delphine, additional, Butenko, Melinka A., additional, Call, Melissa J., additional, Calò, Girolamo, additional, Campbell, Duncan John, additional, Carlsson, Anna, additional, Carr, Daniel B., additional, Carraway, Robert E., additional, Carreira, Marcos C., additional, Casanueva, Felipe F., additional, Cassella, Sarah N., additional, Casson, Stuart A., additional, Castaño, Justo P., additional, Cebrat, Marek, additional, Chappe, Valerie, additional, Chatenet, David, additional, Chen, Keqiang, additional, Chen, Chen, additional, Chen, Longchuan, additional, Chen, Duan, additional, Cheng, Carrie Y.Y., additional, Cho, Sung Ki, additional, Chow, Billy K.C., additional, Christopoulos, Arthur, additional, Chu, Shijian, additional, Clarke, Iain J., additional, Coast, Geoffrey M., additional, Compere, Vincent, additional, Concepcion, Gisela P., additional, Cone, Roger D., additional, Conlon, J. Michael, additional, Cornélissen, Germaine, additional, Courel, Maité, additional, Couture, Réjean, additional, Cramer, W.A., additional, Croft, Nathan P., additional, Crujeiras, Ana B., additional, Cuttitta, Frank, additional, Cynis, Holger, additional, D’Acquisto, F., additional, Davis, Jon F., additional, Davis, Thomas P., additional, de La Serre, Claire Barbier, additional, de Lartigue, Guillaume, additional, de Lecea, Luis, additional, de Oliveira Santos, Marcelo, additional, De Waard, Michel, additional, Bolette Hartmann, Carolyn F. Deacon, additional, Delestre, Charlène, additional, Delgado, Mario, additional, Demuth, Hans-Ulrich, additional, Deng, Xiaoming, additional, Dharmawardhana, Palitha, additional, Di Cosmo, Anna, additional, Dias, Simoni Campos, additional, Dickerson, Jonathan W., additional, Diep, Dzung B., additional, Dircksen, H., additional, Dischinger, Jasmin, additional, do Rego, Jean-Claude, additional, Dobner, Paul R., additional, Dockray, Graham J., additional, Dores, Robert M., additional, Ducroc, Robert, additional, Dudek, Nadine L., additional, Dumont, Yvan, additional, Duraffourd, Celine, additional, Duterte-Boucher, Dominique, additional, Eberlé, Alex N., additional, Egleton, Richard D., additional, Eipper, Betty A., additional, Engel, Jorg B., additional, Englander, Ella W., additional, Epelbaum, Jacques, additional, Erlanson-Albertsson, Charlotte, additional, Evangelista, S., additional, Fagan, Karen A., additional, Farber, Joshua M., additional, Farkasfalvi, Klára, additional, Fekete, Csaba, additional, Flatt, Peter R., additional, Flower, R.J., additional, Forssmann, Wolf-Georg, additional, Fournier, Alain, additional, Foy, Kevin Chu, additional, Franco, Octávio Luiz, additional, Frenkel, Dan, additional, Fricker, Lloyd D., additional, de la Fuente-Núñez, César, additional, Fukuda, Hiroo, additional, Gäde, Gerd, additional, Galas, Ludovic, additional, Gallagher, Patricia E., additional, Gandolfo, Pierrick, additional, Garcia-Espinosa, Maria A., additional, García-Sanmartín, Josune, additional, Geary, Nori, additional, Geng, Hua, additional, Germano, Patrizia M., additional, Goetze, Jens P., additional, Gonzalez, Alexis A., additional, Gonzalez, Ana, additional, Gosnell, Blake A., additional, Goto, Katsutoshi, additional, Gourcerol, Guillaume, additional, Gozes, I., additional, Gracia-Navarro, Francisco, additional, Grayson, Bernadette E., additional, Greeley, George H., additional, Greenwald-Yarnell, Megan, additional, Gressens, Pierre, additional, Grider, John R., additional, Grünewald, Jan, additional, Guerreiro, Juliano R., additional, Guerrini, Remo, additional, Guida, Filomena, additional, Guilhaudis, Laure, additional, Guilmeau, Sandra, additional, Gundlach, Andrew L., additional, Gutkowska, Jolanta, additional, Hackbarth, Clifton, additional, Haim Ohana, Y., additional, Halberg, Franz, additional, Hallberg, Mathias, additional, Hamidi, Sayyed A., additional, Han, Song, additional, Han, Ji-Sheng, additional, Hancock, Robert E.W., additional, Haque, Samer-ul, additional, Hara-Nishimura, Ikuko, additional, Hariton, Aliza, additional, Hartsock, Wendy J., additional, Harvey, Alan L., additional, Hasunuma, Itaru, additional, Henning, Robert J., additional, Heppner, Kristy M., additional, Hertweck, Kate L., additional, Herzog, Herbert, additional, Higashiyama, Tetsuya, additional, Hinuma, Shuji, additional, Hippenstiel, Stefan, additional, Hirakawa, Yuki, additional, Hirose, Shuichi, additional, Hirsch, Jochen R., additional, Hocke, Andreas C., additional, Hodges, Robert S., additional, Hoffmann, Werner, additional, Hökfelt, Tomas, additional, Holst, Jens Juul, additional, Holzer, Peter, additional, Horodyski, Frank M., additional, Hosoda, Hiroshi, additional, Hou, Xiaowen, additional, Huffaker, Alisa, additional, Iijima, Norio, additional, Ikeuchi, Momoko, additional, Imperial, Julita S., additional, Improta, Giovanna, additional, Inui, Akio, additional, Irwin, Nigel, additional, Ishii, Munehiro, additional, Iturrioz, Xavier, additional, Ivanisevic, Ljubica, additional, Iwao, Hiroshi, additional, Iwata, Takeo, additional, Izumi, Yasukatsu, additional, Izumiyama, Hajime, additional, Jankowski, Marek, additional, Janssen, Tom, additional, Jégou, Sylvie, additional, Jensen, Robert T., additional, Jethwa, Preeti H., additional, Johannessen, Helene, additional, Johanson, Conrad, additional, Judkowski, Valeria, additional, Kaczmarek, Przemyslaw, additional, Kageyama, Haruaki, additional, Kakimoto, Tatsuo, additional, Kang, Ki Sung, additional, Kangawa, Kenji, additional, Kastin, Abba J., additional, Kato, Johji, additional, Kaumaya, Pravin T.P., additional, Keep, Richard F., additional, Kem, William R., additional, Khomenko, Tetyana, additional, Kikuyama, Sakae, additional, Kim, Young-Joon, additional, Kimura, Sadao, additional, King, Ross, additional, Kiptoo, Paul, additional, Kishimoto, Ichiro, additional, Kitamura, Kazuo, additional, Kluczyk, Alicja, additional, Kobori, Hiroyuki, additional, Kodama, Yosuke, additional, Kojima, Masayasu, additional, Kondo, Yuki, additional, Körner, Meike, additional, Kosson, Piotr, additional, Kotz, Catherine M., additional, Krishnan, Bhavani, additional, Kulseng, Bård, additional, Kumpf, Robert, additional, Laburthe, Marc, additional, Lacaille, Hélène, additional, Ladenheim, Ellen E., additional, Ladram, Ali, additional, Laksitorini, Marlyn D., additional, Lambert, David G., additional, Lange, Angela B., additional, Langhans, Wolfgang, additional, Larauche, Muriel, additional, Larhammar, Dan, additional, Larráyoz, Ignacio M., additional, Lattanzi, Roberta, additional, Lechan, Ronald M., additional, Lefranc, Benjamin, additional, Leibowitz, Sarah F., additional, Lelièvre, Vincent, additional, Leprince, Jérôme, additional, Levine, Allen S., additional, Li, Qun, additional, Lifshitz, Veronica, additional, Lihrmann, Isabelle, additional, Chi-Jen Lin, James, additional, Lindberg, Iris, additional, Lindsey, Keith, additional, Lipkowski, Andrzej W., additional, Liron, T., additional, Liu, Junli, additional, Liu, Ying, additional, Liu, Min, additional, Llorens-Cortes, Catherine, additional, Loizidou, Marilena, additional, Lopez, C., additional, Lovejoy, David A., additional, Luca, Vincenzo, additional, Lutz, Thomas A., additional, Ma, Sherie, additional, Mains, Richard E., additional, Malagon, Maria M., additional, Malendowicz, Ludwik K., additional, Wan, Jennifer Man-Fan, additional, Mangoni, Maria Luisa, additional, Manigrasso, Michaele B, additional, Marahiel, Mohamed A., additional, Marco, Heather G., additional, Maric-Bilkan, Christine, additional, Marks, Nikki J., additional, Martin, Roland, additional, Martinez, Vicente, additional, Martínez, Alfredo, additional, Martinez-Fuentes, Antonio J., additional, Masler, Edward P., additional, Matsubayashi, Yoshikatsu, additional, Mattu, Harman S., additional, Maule, Aaron G., additional, McLaughlin, Patricia J., additional, McMurtry, Ivan F., additional, Meelkop, Ellen, additional, Mehdi, Saher, additional, Melchiorri, Pietro, additional, Millar, R.P., additional, Miller, Laurence J., additional, Miller, Miles, additional, Million, Mulugeta, additional, Minamino, Naoto, additional, Mittelman, M., additional, Miyauchi, Takashi, additional, Miyazato, Mikiya, additional, Mizoguchi, Hirokazu, additional, Mohme, Malte, additional, Montero-Hadjadje, Maité, additional, Moody, Terry W., additional, Mookherjee, Neeloffer, additional, Moran, Timothy H., additional, Morganstern, Irene, 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Published
2013
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45. Data_Supplements_Penrose – Supplemental material for STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells

Author

Penrose, Harrison M, Katsurada, Akemi, Miyata, Kayoko, Urushihara, Maki, and Satou, Ryousuke

Subjects
FOS: Clinical medicine, Cardiology, 110306 Endocrinology
Abstract

Supplemental material, Data_Supplements_Penrose for STAT1 regulates interferon-γ-induced angiotensinogen and MCP-1 expression in a bidirectional manner in primary cultured mesangial cells by Harrison M Penrose, Akemi Katsurada, Kayoko Miyata, Maki Urushihara and Ryousuke Satou in Journal of the Renin-Angiotensin-Aldosterone System

Published
2020
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47. Angiotensin II biphasically regulates cell differentiation in human iPSC-derived kidney organoids.

Author

Yanofsky, Stacy M., Dugas, Courtney M., Katsurada, Akemi, Jiao Liu, Saifudeen, Zubaida, El-Dahr, Samir S., and Satou, Ryousuke

Subjects
ANGIOTENSIN II, CELL differentiation, PROXIMAL kidney tubules, ORGANOIDS, KIDNEY tubules
Abstract

Human kidney organoid technology holds promise for novel kidney disease treatment strategies and utility in pharmacological and basic science. Given the crucial roles of the intrarenal renin-angiotensin system (RAS) and angiotensin II (ANG II) in the progression of kidney development and injury, we investigated the expression of RAS components and effects of ANG II on cell differentiation in human kidney organoids. Human induced pluripotent stem cell-derived kidney organoids were induced using a modified 18-day Takasato protocol. Gene expression analysis by digital PCR and immunostaining demonstrated the formation of renal compartments and expression of RAS components. The ANG II type 1 receptor (AT1R) was strongly expressed in the early phase of organoid development (around day 0), whereas ANG II type 2 receptor (AT2R) expression levels peaked on day 5. Thus, the organoids were treated with 100 nM ANG II in the early phase on days 0-5 (ANG II-E) or during the middle phase on days 5-10 (ANG II-M). ANG II-E was observed to decrease levels of marker genes for renal tubules and proximal tubules, and the downregulation of renal tubules was inhibited by an AT1R antagonist. In contrast, ANG II-M increased levels of markers for podocytes, the ureteric tip, and the nephrogenic mesenchyme, and an AT2R blocker attenuated the ANG II-M-induced augmentation of podocyte formation. These findings demonstrate RAS expression and ANG II exertion of biphasic effects on cell differentiation through distinct mediatory roles of AT1R and AT2R, providing a novel strategy to establish and further characterize the developmental potential of human induced pluripotent stem cell-derived kidney organoids. [ABSTRACT FROM AUTHOR]

Published
2021
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