Mitochondria transfer via tunneling nanotubes is an important mechanism by which CD133+ scattered tubular cells eliminate hypoxic tubular cell injury.

Abstract

Renal CD133\xa0+\xa0scattered tubular cells (STCs) have been regarded as progenitor-like cells in the kidney and participated in ischemic renal injury repair. However, the mechanism of this effect is not fully elucidated yet. The primary objective of this study was to investigate the hypothesis that the protective effect of CD133\xa0+\xa0STCs depends on the transfer of mitochondria to injured tubular cells in\xa0vitro. In this study, renal ischemic reperfusion injury (IRI) rat model was established with one side kidney ischemic for 45\u202fmin and animals were sacrificed at 48\u202fh after operation. Tubular cells were isolated and cultured in\xa0vitro, and then CD133\xa0+\xa0STCs were selected from the cultured cells. Then, CD133\xa0+\xa0STCs were co-cultured with CD133-tubular cells (TECs) to detect the tunneling nanotubes like structures, and the transfer of mitochondria from CD133\xa0+\xa0STCs to injured tubular cells were detected by fluorescent imaging and flow cytometry. Further, cellular protective effects of CD133\xa0+\xa0STCs were tested when cultured with TECs under hypoxic conditions. In results, renal CD133\xa0+\xa0STCs were scattered throughout the normal kidney and increased upon ischemic injury. Nanotube formations were commonly found between CD133\xa0+\xa0STCs and TECs, and the transfer of mitochondria was detected from CD133\xa0+\xa0STCs to TECs. Further, CD133\xa0+\xa0STCs exist significant anti-apoptosis and pro-proliferation effects for TECs under hypoxic culture conditions. Thus, this study was first described that renal CD133\xa0+\xa0STCs could transfer mitochondria to injured TECs in\xa0vitro for its protective effects, which revealed an important novel mechanism for renal repair after ischemic injury.