Our results confirm that TIMP-1 is active in the early phase of the fibrotic process and we demonstrated that initially TIMP-1 mRNA is transcribed by very few ED1+ macrophages but mainly by other, presently unidentified, interstitial cells. During later stages of post-ligation, both TIMP-1 (transcribed among others by alpha-SMA+ myofibroblasts, ED1+ macrophages, and possibly neutrophils) and PAI-1 are involved in the progression of tubulointerstitial scarring.
Prevention of cellular infiltration by mAbs to LFA-1 and ICAM-1 has no effect on renal morphology, function, or regeneration following mercuric chloride-induced ARF in the rat. This result contrasts with the functional protection of the rat kidney to ischemia/reperfusion injury by virtue of an identical antibody treatment protocol. Resolving that controversy should bring better insight in fundamental processes underlying different types of ARF, and will be the subject of further study.
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