 |
||||
| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
| CURRENT ISSUE | ARCHIVES | JASN Express | ONLINE SUBMISSION | |
|
||||
| 2007 JASN IMPACT FACTOR 7.111 | HOME AUTHOR INFO EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP | |||
| CURRENT ISSUE | ARCHIVES | JASN Express | ONLINE SUBMISSION | |
*
Department of Nephrology, University of Heidelberg, Heidelberg,
Germany
Department of Pathology, University of Heidelberg, Heidelberg,
Germany
Department of Nephrology, University of Hannover, Hannover,
Germany.
Correspondence to Dr. Jürgen Wagner, Department of Nephrology, University Hospital, University of Heidelberg, Bergheimerstrasse 56a, D-69115 Heidelberg, Germany. Phone: +49 6221 91120; Fax: +49 6221 16 24 76; E-mail: juergen_wagner{at}med.uni-heidelberg.de
Abstract. In the reaction of kidneys to injury, cytokine-driven proliferation plays an important role and precedes the development of glomerulosclerosis. There is great interest in agents that may interfere with such proliferation. Therefore, a rat model of mesangioproliferative glomerulonephritis (induced by anti-Thy1.1) was studied, and the effects of all-trans-retinoic acid (all-trans-RA) and isotretinoin, powerful antiproliferative and anti-inflammatory substances, on glomerular damage and cell proliferation were examined. Vehicle-injected control rats were compared with rats treated with daily subcutaneous injections of 10 mg/kg body wt all-trans-RA or 40 mg/kg body wt isotretinoin (n = 9 to 11 per group), using either a pretreatment (days -2 through 8) or posttreatment (days +3 through +8) protocol, i.e., starting before or after the induction of anti-Thy1.1 nephritis, respectively. All-trans-RA prevented the BP increase evoked by anti-Thy1.1 (anti-Thy1.1/vehicle, 112.2 ± 4.8 mmHg; anti-Thy1.1/RA, 87.5 ± 2.5 mmHg; P < 0.001). Treatment with all-trans-RA or isotretinoin produced a 70% decrease in the urinary albumin excretion rate (P < 0.02). Periodic acid-Schiff staining of saline-perfused kidneys (day 8) revealed significantly fewer glomerular cells in RA-treated nephritic rats (anti-Thy1.1/vehicle, 97 ± 3.1 cells/glomerulus; anti-Thy1.1/RA, 80 ± 4.4; P < 0.02; control/vehicle, 69 ± 1.2). No difference was observed between all-trans-RA and isotretinoin treatment. The capillary occlusion scores were significantly lower for the anti-Thy1.1/RA-treated group (1.9 ± 0.1) than for the anti-Thy1.1/vehicle-treated group (2.9 ± 0.5, P < 0.001). In the anti-Thy1.1/vehicle-treated group, 11.9 ± 1.1 glomerular cells were proliferating cell nuclear antigen-positive; however, in the anti-Thy1.1/RA-treated group, only 5.3 ± 0.8 cells were proliferating cell nuclear antigen-positive (P < 0.002; control, 2.2 ± 0.2). Glomerular mitoses were reduced by 67% in the anti-Thy1.1/RA-treated group, compared with the anti-Thy1.1/control group (P < 0.002). Glomerular staining for platelet-derived growth factor B-chain was significantly reduced in anti-Thy1.1-treated nephritic rats in the presence of isotretinoin or all-trans-RA, compared with the vehicle-treated group (P < 0.001). It is concluded that all-trans-RA limits glomerular proliferation, glomerular lesions, and albuminuria in an established model of renal damage. The findings point to retinoids as potential novel modulators of glomerular injury.
This article has been cited by other articles:
 |
|
 |
|
  T.-C. Lu, Z. Wang, X. Feng, P. Chuang, W. Fang, Y. Chen, S. Neves, A. Maayan, H. Xiong, Y. Liu, et al. Retinoic Acid Utilizes CREB and USF1 in a Transcriptional Feed-Forward Loop in Order To Stimulate MKP1 Expression in Human Immunodeficiency Virus-Infected Podocytes Mol. Cell. Biol., September 15, 2008; 28(18): 5785 - 5794. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Zhang, H. Meng, Z.-H. Li, Z. Shu, X. Ma, and B.-X. Zhang Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells Am J Physiol Renal Physiol, March 1, 2007; 292(3): F1054 - F1064. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. C. He, T.-C. Lu, M. Fleet, M. Sunamoto, M. Husain, W. Fang, S. Neves, Y. Chen, S. Shankland, R. Iyengar, et al. Retinoic Acid Inhibits HIV-1-Induced Podocyte Proliferation through the cAMP Pathway J. Am. Soc. Nephrol., January 1, 2007; 18(1): 93 - 102. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Xing, J. Ding, Q. Fan, and N. Guan Diversities of Podocyte Molecular Changes Induced by Different Antiproteinuria Drugs. Experimental Biology and Medicine, May 1, 2006; 231(5): 585 - 593. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Wen, Y. Li, K. Hu, C. Dai, and Y. Liu Hepatocyte Growth Factor Receptor Signaling Mediates the Anti-Fibrotic Action of 9-cis-Retinoic Acid in Glomerular Mesangial Cells Am. J. Pathol., October 1, 2005; 167(4): 947 - 957. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Yamauchi, A. Ishibashi, K. Shikata, N. Tokuhara, K.-i. Seino, S. Kobayashi, and M. Nagai Effect of E6060 [4-{5-[7-Fluoro-4-(trifluoromethyl)benzo[b]furan-2-yl]-1H-2-pyrrolyl}benzoic Acid], a Novel Subtype-Selective Retinoid, on Lupus-Like Nephritis in Female (NZBxNZW)F1 Mice J. Pharmacol. Exp. Ther., March 1, 2005; 312(3): 938 - 944. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Perez, M. Ramirez-Ramos, C. Calleja, D. Martin, M. C. Namorado, G. Sierra, M. E. Ramirez-Ramos, R. Paniagua, Y. Sanchez, L. Arreola, et al. Beneficial effect of retinoic acid on the outcome of experimental acute renal failure Nephrol. Dial. Transplant., October 1, 2004; 19(10): 2464 - 2471. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Liebler, B. Uberschar, H. Kubert, S. Brems, A. Schnitger, M. Tsukada, C. C. Zouboulis, E. Ritz, and J. Wagner The renal retinoid system: time-dependent activation in experimental glomerulonephritis Am J Physiol Renal Physiol, March 1, 2004; 286(3): F458 - F465. [Abstract] [Full Text]
|
|
|
|
 |
|
 K. Kinoshita, B.-S. Yoo, Y. Nozaki, M. Sugiyama, S. Ikoma, M. Ohno, M. Funauchi, and A. Kanamaru Retinoic Acid Reduces Autoimmune Renal Injury and Increases Survival in NZB/W F1 Mice J. Immunol., June 1, 2003; 170(11): 5793 - 5798. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Suzuki, T. Ito, E. Imai, M. Yamato, H. Iwatani, H. Kawachi, and M. Hori Retinoids Regulate the Repairing Process of the Podocytes in Puromycin Aminonucleoside-induced Nephrotic Rats J. Am. Soc. Nephrol., April 1, 2003; 14(4): 981 - 991. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. MORATH, C. DECHOW, I. LEHRKE, V. HAXSEN, R. WALDHERR, J. FLOEGE, E. RITZ, and J. WAGNER Effects of Retinoids on the TGF-{beta} System and Extracellular Matrix in Experimental Glomerulonephritis J. Am. Soc. Nephrol., November 1, 2001; 12(11): 2300 - 2309. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. LUCIO-CAZANA, K. NAKAYAMA, Q. XU, T. KONTA, V. MORENO-MANZANO, A. FURUSU, and M. KITAMURA Suppression of Constitutive but Not IL-1{beta}-Inducible Expression of Monocyte Chemoattractant Protein-1 in Mesangial Cells by Retinoic Acids: Intervention in the Activator Protein-1 Pathway J. Am. Soc. Nephrol., April 1, 2001; 12(4): 688 - 694. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Haxsen, S. Adam-Stitah, E. Ritz, and J. Wagner Retinoids Inhibit the Actions of Angiotensin II on Vascular Smooth Muscle Cells Circ. Res., March 30, 2001; 88(6): 637 - 644. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Wagner Potential role of retinoids in the therapy of renal disease Nephrol. Dial. Transplant., March 1, 2001; 16(3): 441 - 444. [Full Text] [PDF]
|
|
|
|
|
|
I. Lehrke, M. Schaier, K. Schade, C. Morath, R. Waldherr, E. Ritz, and J. Wagner Retinoid receptor-specific agonists alleviate experimental glomerulonephritis Am J Physiol Renal Physiol, April 1, 2002; 282(4): F741 - F751. [Abstract] [Full Text] [PDF]
|
|
|
HOME
CURRENT ISSUE
ARCHIVES
JASN Express
ONLINE SUBMISSION
AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP |
Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673
