| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
From the Medical Research Service,* Audie Murphy Memorial Veterans Administration Hospital, South Texas Veterans Health Care System, San Antonio; and the Department of Medicine, Division of Nephrology, The University of Texas Health Science Center, San Antonio, Texas
To determine whether previous renal injury accelerates the progression of glomerulosclerosis and interstitial fibrosis, we examined the effect of treating rats with angiotensin II after Habu venom injury. After initiating disease, we examined the origin of interstitial myofibroblasts by locating 
-smooth muscle actin (-SMA)-positive and Na+,K+-ATPase-positive cells relative to interstitial space, tubular epithelial cells, the tubular basement membrane (TBM), and vascular structures. Tubular epithelial-mesenchymal transition was also assessed by examining TBM integrity and by using Texas Red (TR)-dextran in intravital tracking experiments. The staining of -SMA-positive myofibroblasts dramatically increased in peritubular interstitial spaces 48 hours after Habu venom plus angiotensin II, particularly in and around perivascular and periglomerular regions, while tubular epithelial cells were -SMA-negative. Na+,K+-ATPase-positive and TR-dextran-labeled cells were restricted to the tubular epithelium and excluded from the interstitium. By 7 and 14 days, expanded interstitial space contained only -SMA-positive myofibroblasts without TR-dextran endocytic particles. Epithelium of atrophic tubules containing TR-dextran remained confined by surrounding interstitium and myofibroblasts. These studies indicate that early expansion of -SMA-positive cells in the interstitium and loss of tubular area occur via encroachment of interstitial myofibroblasts from perivascular into atrophic tubular spaces rather than via epithelial-mesenchymal transition and migration of tubular cells through the TBM into the interstitium.
This article has been cited by other articles:
 |
|
 |
|
  C. D. Bondi, N. Manickam, D. Y. Lee, K. Block, Y. Gorin, H. E. Abboud, and J. L. Barnes NAD(P)H Oxidase Mediates TGF-{beta}1-Induced Activation of Kidney Myofibroblasts J. Am. Soc. Nephrol., January 1, 2010; 21(1): 93 - 102. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. T. Cook The Origin of Renal Fibroblasts and Progression of Kidney Disease Am. J. Pathol., January 1, 2010; 176(1): 22 - 24. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. D. Humphreys, S.-L. Lin, A. Kobayashi, T. E. Hudson, B. T. Nowlin, J. V. Bonventre, M. T. Valerius, A. P. McMahon, and J. S. Duffield Fate Tracing Reveals the Pericyte and Not Epithelial Origin of Myofibroblasts in Kidney Fibrosis Am. J. Pathol., January 1, 2010; 176(1): 85 - 97. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Grgic, E. Kiss, B. P. Kaistha, C. Busch, M. Kloss, J. Sautter, A. Muller, A. Kaistha, C. Schmidt, G. Raman, et al. Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels PNAS, August 25, 2009; 106(34): 14518 - 14523. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. A. Eid, Y. Gorin, B. M. Fagg, R. Maalouf, J. L. Barnes, K. Block, and H. E. Abboud Mechanisms of Podocyte Injury in Diabetes: Role of Cytochrome P450 and NADPH Oxidases Diabetes, May 1, 2009; 58(5): 1201 - 1211. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Strutz How Many Different Roads May a Cell Walk down in Order to Become a Fibroblast? J. Am. Soc. Nephrol., December 1, 2008; 19(12): 2246 - 2248. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Murphy, R. Summer, and A. Fine Stem Cells in Airway Smooth Muscle: State of the Art Proceedings of the ATS, January 1, 2008; 5(1): 11 - 14. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Sataranatarajan, M. M. Mariappan, M. J. Lee, D. Feliers, G. G. Choudhury, J. L. Barnes, and B. S. Kasinath Regulation of Elongation Phase of mRNA Translation in Diabetic Nephropathy: Amelioration by Rapamycin Am. J. Pathol., December 1, 2007; 171(6): 1733 - 1742. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Sato, K. Harada, S. Ozaki, S. Furubo, K. Kizawa, T. Sanzen, M. Yasoshima, H. Ikeda, M. Sasaki, and Y. Nakanuma Cholangiocytes with Mesenchymal Features Contribute to Progressive Hepatic Fibrosis of the Polycystic Kidney Rat Am. J. Pathol., December 1, 2007; 171(6): 1859 - 1871. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Ideura, K. Hiromura, N. Hiramatsu, T. Shigehara, S. Takeuchi, M. Tomioka, T. Sakairi, S. Yamashita, A. Maeshima, Y. Kaneko, et al. Angiotensin II provokes podocyte injury in murine model of HIV-associated nephropathy Am J Physiol Renal Physiol, October 1, 2007; 293(4): F1214 - F1221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. O'Riordan, N. Mendelev, S. Patschan, D. Patschan, J. Eskander, L. Cohen-Gould, P. Chander, and M. S. Goligorsky Chronic NOS inhibition actuates endothelial-mesenchymal transformation Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H285 - H294. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Strutz and G. A. Muller Renal fibrosis and the origin of the renal fibroblast Nephrol. Dial. Transplant., December 1, 2006; 21(12): 3368 - 3370. [Full Text] [PDF]
|
|
|
|
|
|
F. Strutz and M. Zeisberg Renal Fibroblasts and Myofibroblasts in Chronic Kidney Disease J. Am. Soc. Nephrol., November 1, 2006; 17(11): 2992 - 2998. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
