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

Renal CD133 + scattered 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 + STCs depends on the transfer of mitochondria to injured tubular cells in vitro. In this study, renal ischemic reperfusion injury (IRI) rat model was established with one side kidney ischemic for 45 min and animals were sacrificed at 48 h after operation. Tubular cells were isolated and cultured in vitro, and then CD133 + STCs were selected from the cultured cells. Then, CD133 + STCs were co-cultured with CD133-tubular cells (TECs) to detect the tunneling nanotubes like structures, and the transfer of mitochondria from CD133 + STCs to injured tubular cells were detected by fluorescent imaging and flow cytometry. Further, cellular protective effects of CD133 + STCs were tested when cultured with TECs under hypoxic conditions. In results, renal CD133 + STCs were scattered throughout the normal kidney and increased upon ischemic injury. Nanotube formations were commonly found between CD133 + STCs and TECs, and the transfer of mitochondria was detected from CD133 + STCs to TECs. Further, CD133 + STCs exist significant anti-apoptosis and pro-proliferation effects for TECs under hypoxic culture conditions. Thus, this study was first described that renal CD133 + STCs could transfer mitochondria to injured TECs in vitro for its protective effects, which revealed an important novel mechanism for renal repair after ischemic injury.