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1. Relaxin down-regulates renal fibroblast function and promotes matrix remodelling in vitro

Author

Tim D. Hewitson, Laura J. Parry, Kristen J. Kelynack, Gavin J. Becker, Rosemary Masterson, Ian A. Darby, Ross A. D. Bathgate, and Marina Martic

Subjects
Male, medicine.medical_specialty, Kidney Cortex, Cell Culture Techniques, Down-Regulation, Biology, Immediate early protein, Immediate-Early Proteins, Rats, Sprague-Dawley, Fibrosis, Internal medicine, medicine, Animals, RNA, Messenger, Fibroblast, Relaxin, Transplantation, Kidney, urogenital system, Connective Tissue Growth Factor, Fibroblasts, medicine.disease, Extracellular Matrix, Rats, CTGF, Endocrinology, medicine.anatomical_structure, Nephrology, Collagenase, Intercellular Signaling Peptides and Proteins, Procollagen, hormones, hormone substitutes, and hormone antagonists, medicine.drug, Transforming growth factor
Abstract

Background. Renal fibroblasts are important effector cells in tubulointerstitial fibrosis, with experimental antifibrotic strategies focusing on the functional downregulation of these cells. Several experimental models of fibrosis have provided evidence for the effectiveness of the polypeptide hormone relaxin as a potential antifibrotic agent. This study was conducted to further elucidate the antifibrotic mechanisms of relaxin on renal fibroblasts in vitro. Methods. Rat cortical fibroblasts were obtained from outgrowth culture of renal tissue isolated from kidneys 3 days post-unilateral ureteric obstruction and constituted 100% of cells studied. A relaxin radio-receptor assay was used to establish binding of relaxin to renal fibroblasts in vitro. Functional studies then examined the effects of H2 relaxin (0, 1, 10 and 100 ng/ml) on fibroblast kinetics, expression of alpha-smooth muscle actin (-SMA), total collagen synthesis, collagenase production and collagen-I lattice contraction. CTGF mRNA expression was also measured by northern analysis. Results. H2 relaxin bound with high affinity to rat renal fibroblasts, but receptor numbers were low. Consistent with its previously reported bimodal effect, transforming growth factor (TGF-1) reduced fibroblast proliferation, an effect abrogated by H2 relaxin. Fibroblasts exposed to H2 relaxin (100 ng/ml) for 24 h demonstrated decreased immunostaining for -SMA and reduced -SMA protein expression compared with controls. There was a trend for a relaxin-mediated reduction in total collagen synthesis and 1(I) mRNA expression with large dose-related increases in collagenase protein expression being observed. TGF-1-stimulated collagen-I lattice contraction was significantly inhibited following co-incubation with 100 ng/ml relaxin. Incremental doses of H2 relaxin had no significant effect on CTGF mRNA expression. Conclusions. The findings of this study suggest that the antifibrotic effects of relaxin involve down-regulation of fibroblast activity, increase in collagenase synthesis and restructuring of collagen-I lattices, which are consistent with its known physiological role of matrix remodelling. Although there appears to be an interaction between TGF-1 and H2 relaxin, this does not appear to involve a reduction in CTGF mRNA expression.

Published
2004

2. Parathyroid Hormone Has a Prosclerotic Effect on Vascular Smooth Muscle Cells

Author

Marina Martic, Melanie G. Tait, Kristen J. Kelynack, Vlado Perkovic, Gavin J. Becker, and Tim D. Hewitson

Subjects
medicine.medical_specialty, Contraction (grammar), Vascular smooth muscle, Cell division, Arteriosclerosis, Parathyroid hormone, In Vitro Techniques, Muscle, Smooth, Vascular, Pathogenesis, Fibrosis, Internal medicine, medicine, Humans, In patient, skin and connective tissue diseases, Aorta, Cells, Cultured, Uremia, Accelerated atherosclerosis, business.industry, General Medicine, medicine.disease, Peptide Fragments, Extracellular Matrix, Endocrinology, Parathyroid Hormone, Nephrology, sense organs, Cardiology and Cardiovascular Medicine, business, Cell Division, hormones, hormone substitutes, and hormone antagonists
Abstract

Although accelerated atherosclerosis and arteriosclerosis are common in patients with renal failure, the pathogenesis of these changes is poorly understood. Parathyroid hormone (PTH) levels are elevated in renal failure, and have been linked to uraemic vascular changes in some studies. We examined the in vitro effects of increasing doses of the 1–34 fragment of PTH on human aortic vascular smooth muscle cells (VSMCs). Factors examined were: (1) collagen production using tritiated hydroxyproline incorporation and transcription of procollagen α1(I) mRNA; (2) change in the surface area of collagen I lattices; (3) mRNA transcription of the collagen binding protein β1 integrin; (4) proliferation using tritiated thymidine incorporation, and (5) methyl tetrazolium salt conversion to estimate live cell number after 5 days’ exposure to PTH. PTH at a concentration of 200 pmol/l increased total collagen synthesis (188 ± 25% of control, p < 0.01) as well as transcription of procollagen α1(I) mRNA (136 ± 11% of control, p < 0.005). PTH also increased reorganisation of collagen I lattices (surface area 47 ± 8% of well for control vs. 35.7 ± 2.5 and 34.3 ± 3.0% for PTH 100 and 200 pmol/l, respectively, p = 0.02) and upregulated β1 integrin mRNA expression (160 ± 20% of control at PTH concentration of 200 pmol/l, p < 0.05). PTH had no effect on VSMC proliferation or number at doses up to 200 pmol/l. In conclusion, PTH increases production and reorganisation of collagen by VSMCs in vitro. It is possible that more aggressive control of hyperparathyroidism in patients with renal failure may help to reduce the burden of cardiovascular disease in this patient population.

Published
2003

3. Subject Index Vol. 91, 2002

Author

Hiroyuki Sasamura, Olaf Hergesell, K. Tabei, Osamu Hotta, Norio Sunagawa, Ioannis Tzanakis, Emanuela Rizzioli, Mingcai Qiu, Paul F. Laflam, Gian Marco Ghiggeri, Yasufumi Kyuden, D. Ljubanovic, M.J. Nubé, W.E.M. Schouten, Carla Carasi, Joachim Lundahl, Mariko Miyazaki, Isao Ishikawa, Yasuhiko Ueda, Kazuhiko Funabiki, Michael Nomikos, Tatsuo Kobayashi, Maria Magalhães, Manabu Asano, Takayuki Fujita, Shaul M. Shasha, Revital Shurtz-Swirski, Susana Sampaio, H. Furuya, Kefaia El-Sayed Mohamed, Mitsuhiro Satoh, A. Bihorac, Ç. Özener, Renza Cristofani, Ikue Mori-Kudo, U. Assogba, Satoshi Ogata, A.J. van Houte, Shifra Sela, Hidetake Kurihara, Maria Rita Metelli, Kayoko Nomura, Giovanni Montini, Atsushi Satomura, S. Krizanac, Rodo O. von Vigier, Morito Endo, Jürgen Floege, Lara Alonso da Silva, Yasuharu Nomura, Satoko Honda, Manuel Pestana, Hassan Abd-El-Hady Ahmed, Omar da Rosa Santos, P. Cacoub, Toshihiro Shinosaki, Ikuko Miyai, Y. Asano, Yoshiharu Nishitani, Yoshio Taguma, Chien-Liang Chen, Chizuru Ishiguro, P. Xavier, Gianluca Caridi, Marina Martic, Jean-Pierre Guignard, Maura Zanolari Calderari, Akira Saito, Hua-Chang Fang, F. A. W. Kemperman, Huiqi Qu, Atsushi Yamauchi, Hisaya Tada, Gavin J. Becker, Koji Harada, Mohamed Abel-Kader Sobh, Galal Mohamed Amer, Luisa Murer, P A Conz, Hiroyuki Ohi, Ali Moshfegh, Armando A. Mendes, Osama Gheith, Daisuke Suzuki, Fatma Elhusseini, Ciro Tetta, Eugênio Pacelle Queiroz Madeira, Yoshinobu Fuke, Takashi Uzu, Kang-Ju Chou, Savvas Kazoulis, Manuel Palacín, Ioannis Christoulakis, P. Hausfater, G. Kantarcı, Hideyuki Kurioka, Ivano Moschèn, Stefan H. Jacobson, Graziella Zacchello, Satoshi Horikoshi, Atsushi Tsuchida, Ryoko Shimizu-Hirota, Petros Hatzilias, Alberto Bettinelli, Tim D. Hewitson, Raymond T. Krediet, J.C. Piette, Jacek Borawski, S. Tokay, Takafumi Ito, Mutsuo Taiji, Ronit Geron, Makoto Watanabe, M. Schoorl, Carlo Catalano, Pia Thylén, Péter Tóth-Heyn, Ching-Bun Chen, Rajiv Kumar, Shigemi Chiba, Stefan Bröer, Takao Saruta, Mahmoud El-Baz, Yuji Fujita, E. Akoğlu, Roberto Palla, Michał Myśliwiec, Toshiki Inokuchi, Yasuhiko Tomino, Yasuhiro Akai, E. Kusano, Yukiteru Asakimori, Maria Norpoth, Shih-Yuan Hung, Yee-Hsuan Chiou, Kristen J. Kelynack, Hideo Shiiki, Alberto A.E. Bertelli, Mari Kuroda, Yoshihiko Taniguchi, Kazumasa Hamano, Massimiliano Migliori, Steven McTaggart, P. Lebon, Toshio Miyata, Vincenzo Panichi, Gunilla Halldén, Soichi Haraguchi, Mario G. Bianchetti, Po-Tsang Lee, M.P.C. Grooteman, Hideaki Nakaya, Ken Takahara, Fabio Fabbian, Yutaka Yaguchi, Florian Lang, Anna Maria Bianchi, Birgit Kallinowski, Mitchell L. Halperin, M. Inoue, Mizuo Mifune, Masayuki Iwano, Masafumi Yamato, Stefano De Pietro, Hiroshi Noguchi, Koji Kuboki, Hsiao-Min Chung, Hideto Sakai, Tomokazu Nagano, Iwan Setiawan, Surinder Cheema-Dhadli, Nobuoki Kohno, Shan Lin, M. Vrkljan, Isao Shirato, Noriaki Yorioka, Adriana MacIntyre Innocenzi, Marcella Normanno, José Gerardo Oliveira, Matsuhiko Hayashi, Y. Ando, Lambertus Arisz, Krystyna Pawlak, Galina Shapiro, Ikuo Horigome, Takashi Furuta, Y. Akai, Batya Kristal, João Ramos, Mahmoud Wageh Rasem, Alexandra Albers, Sarantos Xirakis, Sérgio Fernando Ferreira Santos, Takao Kawamura, Martin Zeier, Hiroo Noshiro, Manuela Della Vella, Daniele Taccola, Isao Ohsawa, K. Galesic, Mie Ko, Sana Sayed Gazarin, Eduardo H. Garin, Guilherme Santoro-Lopes, Mutsuko Hidaka, Luca Giovannini, and Giulietta Sbragia

Subjects
Index (economics), business.industry, Statistics, Medicine, Subject (documents), business
Published
2002

4. Contents Vol. 91, 2002

Author

Steven McTaggart, Hisaya Tada, D. Ljubanovic, Gunilla Halldén, M.J. Nubé, Marina Martic, Yasufumi Kyuden, Luisa Murer, Vincenzo Panichi, W.E.M. Schouten, Eugênio Pacelle Queiroz Madeira, Mariko Miyazaki, Yasuhiko Ueda, Hidetake Kurihara, Maria Norpoth, Guilherme Santoro-Lopes, Mutsuko Hidaka, Galal Mohamed Amer, Ali Moshfegh, Carlo Catalano, Chien-Liang Chen, Stefano De Pietro, Koji Kuboki, Ryoko Shimizu-Hirota, P. Hausfater, Susana Sampaio, Yoshinobu Fuke, Manuel Palacín, Luca Giovannini, Savvas Kazoulis, Satoshi Ogata, A.J. van Houte, Ikuo Horigome, Graziella Zacchello, Alberto Bettinelli, Batya Kristal, Tim D. Hewitson, Isao Shirato, Noriaki Yorioka, Makoto Watanabe, Renza Cristofani, Sérgio Fernando Ferreira Santos, Takao Kawamura, Y. Akai, S. Krizanac, Jacek Borawski, Maura Zanolari Calderari, Nobuoki Kohno, Marcella Normanno, Giulietta Sbragia, Iwan Setiawan, U. Assogba, Mitsuhiro Satoh, Mutsuo Taiji, Y. Asano, Mahmoud El-Baz, Daisuke Suzuki, Gavin J. Becker, Akira Saito, Giovanni Montini, Stefan Bröer, Yuji Fujita, Revital Shurtz-Swirski, Paul F. Laflam, P A Conz, Ching-Bun Chen, Ioannis Christoulakis, Toshihiro Shinosaki, Takafumi Ito, Takashi Uzu, Yasuhiro Akai, Kang-Ju Chou, G. Kantarcı, Shan Lin, Atsushi Tsuchida, Hideo Shiiki, Mari Kuroda, Atsushi Satomura, Huiqi Qu, Soichi Haraguchi, Michał Myśliwiec, Masayuki Iwano, Masafumi Yamato, M. Vrkljan, Petros Hatzilias, Yoshihiko Taniguchi, Atsushi Yamauchi, Emanuela Rizzioli, Mingcai Qiu, Mohamed Abel-Kader Sobh, Sana Sayed Gazarin, Shigemi Chiba, M. Schoorl, E. Kusano, Yukiteru Asakimori, Anna Maria Bianchi, Birgit Kallinowski, Mario G. Bianchetti, Armando A. Mendes, Yutaka Yaguchi, Isao Ishikawa, Manuel Pestana, Pia Thylén, M. Inoue, Shifra Sela, Po-Tsang Lee, Massimiliano Migliori, Jean-Pierre Guignard, Olaf Hergesell, P. Lebon, Hideto Sakai, Yee-Hsuan Chiou, Kristen J. Kelynack, Alberto A.E. Bertelli, Osamu Hotta, Shaul M. Shasha, Tomokazu Nagano, Lambertus Arisz, Martin Zeier, H. Furuya, Kefaia El-Sayed Mohamed, A. Bihorac, Ç. Özener, Lara Alonso da Silva, Hiroshi Noguchi, Toshio Miyata, Takao Saruta, E. Akoğlu, Stefan H. Jacobson, Krystyna Pawlak, Ivano Moschèn, Maria Rita Metelli, Hsiao-Min Chung, Takashi Furuta, Adriana MacIntyre Innocenzi, Yoshiharu Nishitani, Kazumasa Hamano, Manabu Asano, Mizuo Mifune, Kayoko Nomura, Tatsuo Kobayashi, Gian Marco Ghiggeri, João Ramos, Mahmoud Wageh Rasem, José Gerardo Oliveira, Hassan Abd-El-Hady Ahmed, Hiroyuki Ohi, S. Tokay, Matsuhiko Hayashi, Osama Gheith, Carla Carasi, P. Xavier, Ikue Mori-Kudo, Hiroo Noshiro, Kazuhiko Funabiki, Michael Nomikos, Chizuru Ishiguro, Ikuko Miyai, Maria Magalhães, Péter Tóth-Heyn, Satoko Honda, Manuela Della Vella, Daniele Taccola, Gianluca Caridi, Yasuharu Nomura, Hideyuki Kurioka, Joachim Lundahl, P. Cacoub, Y. Ando, Ronit Geron, Toshiki Inokuchi, Eduardo H. Garin, Galina Shapiro, Roberto Palla, Shih-Yuan Hung, Yasuhiko Tomino, Ciro Tetta, Surinder Cheema-Dhadli, Alexandra Albers, Sarantos Xirakis, Florian Lang, Mitchell L. Halperin, Hideaki Nakaya, Ken Takahara, Fabio Fabbian, Jürgen Floege, Yoshio Taguma, Koji Harada, Hua-Chang Fang, F. A. W. Kemperman, Satoshi Horikoshi, Rodo O. von Vigier, Morito Endo, Omar da Rosa Santos, Norio Sunagawa, M.P.C. Grooteman, Fatma Elhusseini, Takayuki Fujita, Raymond T. Krediet, J.C. Piette, Rajiv Kumar, Hiroyuki Sasamura, K. Tabei, Ioannis Tzanakis, K. Galesic, Mie Ko, and Isao Ohsawa

Subjects
Traditional medicine, business.industry, Medicine, business
Published
2002

5. Relaxin down-regulates renal fibroblast function and promotes matrix remodelling in vitro.

Author

Rosemary Masterson, Tim D. Hewitson, Kristen Kelynack, Marina Martic, Laura Parry, Ross Bathgate, Ian Darby, and Gavin Becker

Subjects
RELAXIN, FIBROBLASTS, CORPUS luteum, SEX hormones
Abstract

Background. Renal fibroblasts are important effector cells in tubulointerstitial fibrosis, with experimental antifibrotic strategies focusing on the functional down-regulation of these cells. Several experimental models of fibrosis have provided evidence for the effectiveness of the polypeptide hormone relaxin as a potential antifibrotic agent. This study was conducted to further elucidate the antifibrotic mechanisms of relaxin on renal fibroblasts in vitro.Methods. Rat cortical fibroblasts were obtained from outgrowth culture of renal tissue isolated from kidneys 3 days post-unilateral ureteric obstruction and constituted 100% of cells studied. A relaxin radio-receptor assay was used to establish binding of relaxin to renal fibroblasts in vitro. Functional studies then examined the effects of H2 relaxin (0, 1, 10 and 100?ng/ml) on fibroblast kinetics, expression of alpha-smooth muscle actin (a-SMA), total collagen synthesis, collagenase production and collagen-I lattice contraction. CTGF mRNA expression was also measured by northern analysis.Results. H2 relaxin bound with high affinity to rat renal fibroblasts, but receptor numbers were low. Consistent with its previously reported bimodal effect, transforming growth factor (TGF-1) reduced fibroblast proliferation, an effect abrogated by H2 relaxin. Fibroblasts exposed to H2 relaxin (100?ng/ml) for 24?h demonstrated decreased immunostaining for a-SMA and reduced a-SMA protein expression compared with controls. There was a trend for a relaxin-mediated reduction in total collagen synthesis and a1(I) mRNA expression with large dose-related increases in collagenase protein expression being observed. TGF-1-stimulated collagen-I lattice contraction was significantly inhibited following co-incubation with 100?ng/ml relaxin. Incremental doses of H2 relaxin had no significant effect on CTGF mRNA expression.Conclusions. The findings of this study suggest that the antifibrotic effects of relaxin involve down-regulation of fibroblast activity, increase in collagenase synthesis and restructuring of collagen-I lattices, which are consistent with its known physiological role of matrix remodelling. Although there appears to be an interaction between TGF-1 and H2 relaxin, this does not appear to involve a reduction in CTGF mRNA expression. [ABSTRACT FROM AUTHOR]

Published
2004
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