CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury

Toma A. Yakulov, Abhijeet P. Todkar, Krasimir Slanchev, Johannes Wiegel, Alexandra Bona, Martin Groß, Alexander Scholz, Isabell Hess, Anne Wurditsch, Florian Grahammer, Tobias B. Huber, Virginie Lecaudey, Tillmann Bork, Jochen Hochrein, Melanie Boerries, Justine Leenders, Pascal de Tullio, François Jouret, Albrecht Kramer-Zucker and Gerd Walz ()
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Toma A. Yakulov: University of Freiburg
Abhijeet P. Todkar: University of Freiburg
Krasimir Slanchev: University of Freiburg
Johannes Wiegel: University of Freiburg
Alexandra Bona: University of Freiburg
Martin Groß: University of Freiburg
Alexander Scholz: University of Freiburg
Isabell Hess: University of Freiburg
Anne Wurditsch: University of Freiburg
Florian Grahammer: University of Freiburg
Tobias B. Huber: University of Freiburg
Virginie Lecaudey: University of Freiburg
Tillmann Bork: University of Freiburg
Jochen Hochrein: University of Freiburg
Melanie Boerries: University of Freiburg
Justine Leenders: University of Liège
Pascal de Tullio: University of Liège
François Jouret: University of Liège Hospital
Albrecht Kramer-Zucker: University of Freiburg
Gerd Walz: University of Freiburg

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos. Gene expression profiles between these two developmental stages identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.

Date: 2018
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DOI: 10.1038/s41467-018-06094-4

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