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PAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction.

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dc.contributor.authorOda, T-
dc.contributor.authorJung, YO-
dc.contributor.authorKim, HS-
dc.contributor.authorCai, X-
dc.contributor.authorLópez-Guisa, JM-
dc.contributor.authorIkeda, Y-
dc.contributor.authorEddy, AA-
dc.date.accessioned2011-08-19T07:02:49Z-
dc.date.available2011-08-19T07:02:49Z-
dc.date.issued2001-
dc.identifier.issn0085-2538-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3835-
dc.description.abstractBACKGROUND: Progressive renal disease is characterized by the induction of plasminogen activator inhibitor-1 (PAI-1), suggesting that impaired activity of the renal plasmin cascade may play a role in renal fibrosis.



METHODS: To test this hypothesis, the severity of renal fibrosis caused by unilateral ureteral obstruction (UUO) was compared in PAI-1 wild-type (+/+) and PAI-1 deficient (-/-) mice. The extent of interstitial inflammation and fibrosis, renal plasminogen activator and plasmin activity, and renal expression of profibrotic genes was evaluated after 3, 7, and 14 days of UUO.



RESULTS: Renal PAI-1 mRNA levels increased 8- to 16-fold in the +/+ mice after UUO surgery, and PAI-1 protein was detected in kidney homogenates. Interstitial fibrosis was significantly attenuated in -/- mice compared with +/+ mice at day 7 and day 14, based on the interstitial area stained with picrosirius red and total kidney collagen content. However, neither the mean renal plasminogen activator nor plasmin activities were increased in -/- mice compared with +/+ mice. The number of interstitial macrophages were significantly lower in the -/- mice three and seven days after UUO; interstitial myofibroblasts were significantly fewer at three days. At the same time points, this altered interstitial cellularity was associated with a significant reduction in renal mRNA levels for transforming growth factor-beta and procollagens alpha 1(I) and alpha 1(III).



CONCLUSIONS: These studies establish an important fibrogenic role for PAI-1 in the renal fibrogenic response. The results demonstrate that one important fibrosis-promoting function of PAI-1 is its role in the recruitment of fibrosis-inducing cells, including myofibroblasts and macrophages.
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dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHChemotaxis, Leukocyte-
dc.subject.MESHFibrinolysin-
dc.subject.MESHFibroblasts-
dc.subject.MESHFibrosis-
dc.subject.MESHKidney-
dc.subject.MESHMacrophages-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMice, Knockout-
dc.subject.MESHNephritis, Interstitial-
dc.subject.MESHPlasminogen Activator Inhibitor 1-
dc.subject.MESHPlasminogen Activators-
dc.subject.MESHUreteral Obstruction-
dc.titlePAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction.-
dc.typeArticle-
dc.identifier.pmid11473641-
dc.contributor.affiliatedAuthor김, 흥수-
dc.type.localJournal Papers-
dc.identifier.doi10.1046/j.1523-1755.2001.030002587.x-
dc.citation.titleKidney international-
dc.citation.volume60-
dc.citation.number2-
dc.citation.date2001-
dc.citation.startPage587-
dc.citation.endPage596-
dc.identifier.bibliographicCitationKidney international, 60(2). : 587-596, 2001-
dc.identifier.eissn1523-1755-
dc.relation.journalidJ000852538-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Nephrology
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