Inhibition of tubular cell proliferation by neutralizing endogenous HGF leads to renal hypoxia and bone marrow-derived cell engraftment in acute renal failure

摘要

To reverse the S3 tubular injuries, there is an intrarenal repair system by remnant nephrons: surviving tubular epithelial cells are divided to propagate daughter cells, and the defective areas of S3 tubules can be sheeted with newly generated epithelial cells (50). In addition to the local repair system, recent studies have shown that bone marrow-derived cells (BMDC) contribute, more or less, to reconstruction of S3 tubules for reversing ARF (i.e., extrarenal system) (6, 26, 38). Since rapid recovery from morphological damages inhibits further hypoxia and dysfunction (24, 42, 44), it is important to elucidate the mechanism whereby damaged tubular S3 segments are repaired at the cellular and ligand levels. Nevertheless, molecular regulation of the balance between resident epithelial cell proliferation and BMDC recruitment has yet to be addressed.