Extracellular nucleotides from dying cells act as molecular signals to promote wound repair in renal tubular injury.

Extracellular nucleotides from dying cells act as molecular signals to promote wound repair in renal tubular injury. Am J Physiol Renal Physiol. 2014 Oct 29;:ajprenal.00196.2014 Authors: Nakagawa S, Omura T, Yonezawa A, Yano I, Nakagawa T, Matsubara K Abstract Acute kidney injury (AKI) often correlates with poor prognosis, and is followed by various severe unfavorable systemic outcomes. It is important to understand the pathophysiology of AKI for the development of novel therapeutic approaches towards promoting renal regeneration after injury. Recent studies have indicated that AKI-induced tubular cell death plays an active role in the onset of tissue regeneration; however, the mechanisms underlying renal tubular repair following injury have yet to be understood. In the present study, we explored molecules that might serve as "danger" signals in mediating tubular regeneration. Rodent kidneys systemically administered with the nephrotoxicant cisplatin (to induce AKI) exhibited massive cell proliferation. The proportion of proliferating cells in the total cell distribution was highest in the outer stripe of the outer medulla coincided with where the tubular damage was the most severe in this study. This finding suggests that soluble factors may have been released from the damaged cells to stimulate the proliferation of the neighboring tubular epithelial cells. In elucidating the mechanism of dying cells-to-surviving cells communication using norm...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research

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