File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Renal expression of genes that promote interstitial inflammation and fibrosis in rats with protein-overload proteinuria

TitleRenal expression of genes that promote interstitial inflammation and fibrosis in rats with protein-overload proteinuria
Authors
Issue Date1995
Citation
Kidney International, 1995, v. 47, n. 6, p. 1546-1557 How to Cite?
AbstractRats with significant proteinuria induced by daily injections of bovine serum albumin develop interstitial inflammation and fibrosis. The present study was designed to investigate the molecular basis of interstitial monocyte (M∅) recruitment and early interstitial fibrosis. Groups of rats were sacrificed after one, two and three weeks. Despite an increase in interstitial M∅ at week 1, whole kidney mRNA levels were not elevated for monocyte chemoattractant protein-1 (MCP-1), osteopontin or vascular cell adhesion molecule-1 (VCAM-1). Only osteopontin mRNA levels were significantly elevated in the renal cortex at four days. At two and three weeks, MCP-1 and osteopontin mRNA levels were increased and the proteins showed distinct tubular patterns of distribution, By immunostaining increased expression of VCAM-1 and intercellular adhesion molecule-1 (ICAM-1) was restricted to their presence or the surface of the interstitial inflammatory cells. TGF-β1 mRNA levels were increased at weeks 1, 2 and 3 (2.1, 2.9, 3.6x); interstitial and occasional cortical tubular cells expressed TGF-β1 mRNA and protein. There was a progressive rise in the number of cortical interstitial fields with increased staining for collagen (col) 1 (18, 29, 44%), col III (39, 61, 63%), col IV (7, 13, 29%), laminin (4, 10, 30%), fibronectin (14, 28, 37%), tenascin (19, 22, 14%) and in total renal col measured biochemically (1.1, 1.4, 2.0x) at weeks 1, 2 and 3, respectively. Renal matrix protein mRNA levels were variable and not always predictive of fibrosis. Only col I and tenascin levels were increased at week 1; all matrix protein mRNA levels except col IV were increased at week 2; but only tenascin, laminin and col IV mRNA levels remained elevated at three weeks. Plasminogen activator inhibitor-1 (PAI-1) and tissue inhibitor of metalloproteinases (TIMP)-1 mRNA levels were significantly increased at two weeks. During the three weeks there was no change in urokinase, stromelysin or TIMP-3 mRNA levels. These results suggest that both increased matrix protein synthesis and altered matrix remodeling/degradation contribute to the final interstitial fibrogenic process in rats with protein-overload proteinuria. M∅, one of the sources of TGF-β1, infiltrate the interstitium by complex recruitment mechanisms which may depend in part on osteopontin, ICAM-1 and VCAM-1 expression.
Persistent Identifierhttp://hdl.handle.net/10722/205689
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorEddy, Allison Alan-
dc.contributor.authorGiachelli, Cecilia M.-
dc.contributor.authorMcCulloch, Lori-
dc.contributor.authorLiu, Elaine-
dc.date.accessioned2014-10-06T08:02:12Z-
dc.date.available2014-10-06T08:02:12Z-
dc.date.issued1995-
dc.identifier.citationKidney International, 1995, v. 47, n. 6, p. 1546-1557-
dc.identifier.issn0085-2538-
dc.identifier.urihttp://hdl.handle.net/10722/205689-
dc.description.abstractRats with significant proteinuria induced by daily injections of bovine serum albumin develop interstitial inflammation and fibrosis. The present study was designed to investigate the molecular basis of interstitial monocyte (M∅) recruitment and early interstitial fibrosis. Groups of rats were sacrificed after one, two and three weeks. Despite an increase in interstitial M∅ at week 1, whole kidney mRNA levels were not elevated for monocyte chemoattractant protein-1 (MCP-1), osteopontin or vascular cell adhesion molecule-1 (VCAM-1). Only osteopontin mRNA levels were significantly elevated in the renal cortex at four days. At two and three weeks, MCP-1 and osteopontin mRNA levels were increased and the proteins showed distinct tubular patterns of distribution, By immunostaining increased expression of VCAM-1 and intercellular adhesion molecule-1 (ICAM-1) was restricted to their presence or the surface of the interstitial inflammatory cells. TGF-β1 mRNA levels were increased at weeks 1, 2 and 3 (2.1, 2.9, 3.6x); interstitial and occasional cortical tubular cells expressed TGF-β1 mRNA and protein. There was a progressive rise in the number of cortical interstitial fields with increased staining for collagen (col) 1 (18, 29, 44%), col III (39, 61, 63%), col IV (7, 13, 29%), laminin (4, 10, 30%), fibronectin (14, 28, 37%), tenascin (19, 22, 14%) and in total renal col measured biochemically (1.1, 1.4, 2.0x) at weeks 1, 2 and 3, respectively. Renal matrix protein mRNA levels were variable and not always predictive of fibrosis. Only col I and tenascin levels were increased at week 1; all matrix protein mRNA levels except col IV were increased at week 2; but only tenascin, laminin and col IV mRNA levels remained elevated at three weeks. Plasminogen activator inhibitor-1 (PAI-1) and tissue inhibitor of metalloproteinases (TIMP)-1 mRNA levels were significantly increased at two weeks. During the three weeks there was no change in urokinase, stromelysin or TIMP-3 mRNA levels. These results suggest that both increased matrix protein synthesis and altered matrix remodeling/degradation contribute to the final interstitial fibrogenic process in rats with protein-overload proteinuria. M∅, one of the sources of TGF-β1, infiltrate the interstitium by complex recruitment mechanisms which may depend in part on osteopontin, ICAM-1 and VCAM-1 expression.-
dc.languageeng-
dc.relation.ispartofKidney International-
dc.titleRenal expression of genes that promote interstitial inflammation and fibrosis in rats with protein-overload proteinuria-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/ki.1995.218-
dc.identifier.pmid7643523-
dc.identifier.scopuseid_2-s2.0-0029064922-
dc.identifier.volume47-
dc.identifier.issue6-
dc.identifier.spage1546-
dc.identifier.epage1557-
dc.identifier.isiWOS:A1995QZ86800008-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats