| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Surgery, Beth Israel Deaconess Medical Center, Boston 02215; Departments of 2 Surgery and 3 Medicine, Harvard Medical School, Boston 02115; 4 Medical Services, Massachusetts General Hospital, Charlestown 02129; and 5 Division of Health Sciences and Technology, Harvard Medical School-Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Using an in vivo rat model of unilateral renal ischemia, we previously showed that the expression and distribution of fibronectin (FN), a major glycoprotein of plasma and the extracellular matrix, dramatically changes in response to ischemia-reperfusion. In the distal nephron in particular, FN accumulates in tubular lumens, where it may contribute to obstruction. In the present study, we examine whether the tubular FN is the plasma or cellular form, each of which is produced by alternative splicing of a single gene transcript. We demonstrate that FN in tubular lumens does not contain the extra type III A (EIIIA) and/or the extra type III B (EIIIB) region, both of which are unique to cellular FN. It does, however, contain the V95 region, which in the rat is a component of FNs in both plasma and the extracellular matrix. Expression of FN containing EIIIA increases dramatically in the renal interstitium after ischemic injury and continues to be produced at high levels 6 wk later. V95-containing FN also increases in the interstitial space, albeit more slowly and at lower levels than FN containing EIIIA; it also persists 6 wk later. FN containing the EIIIB region is not expressed in the injured kidney. The presence of V95 but not the EIIIA or EIIIB regions of FN in tubular lumens identifies the origin of FN in this location as the plasma; tubular FN is ultimately voided in the urine. The data indicate that both plasma and cellular FNs containing the V95 and/or EIIIA regions may contribute to the pathogenesis of acute renal failure and to the repair of the injured kidney.
alternative splicing; extracellular matrix; renal injury; regeneration; acute renal failure
This article has been cited by other articles:
|
|
 |
|
  K. R. Spurgeon, D. L. Donohoe, and D. P. Basile Transforming growth factor-{beta} in acute renal failure: receptor expression, effects on proliferation, cellularity, and vascularization after recovery from injury Am J Physiol Renal Physiol, March 1, 2005; 288(3): F568 - F577. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. V. Bonventre Dedifferentiation and Proliferation of Surviving Epithelial Cells in Acute Renal Failure J. Am. Soc. Nephrol., June 1, 2003; 14(90001): S55 - 61. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Zuk and K. S. Matlin Induction of a laminin isoform and alpha 3beta 1-integrin in renal ischemic injury and repair in vivo Am J Physiol Renal Physiol, November 1, 2002; 283(5): F971 - F984. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
