CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury
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CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury. / Yakulov, Toma A; Todkar, Abhijeet P; Slanchev, Krasimir; Wiegel, Johannes; Bona, Alexandra; Groß, Martin; Scholz, Alexander; Hess, Isabell; Wurditsch, Anne; Grahammer, Florian; Huber, Tobias B; Lecaudey, Virginie; Bork, Tillmann; Hochrein, Jochen; Boerries, Melanie; Leenders, Justine; de Tullio, Pascal; Jouret, François; Kramer-Zucker, Albrecht; Walz, Gerd.
in: NAT COMMUN, Jahrgang 9, 10.09.2018, S. 3660.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury
AU - Yakulov, Toma A
AU - Todkar, Abhijeet P
AU - Slanchev, Krasimir
AU - Wiegel, Johannes
AU - Bona, Alexandra
AU - Groß, Martin
AU - Scholz, Alexander
AU - Hess, Isabell
AU - Wurditsch, Anne
AU - Grahammer, Florian
AU - Huber, Tobias B
AU - Lecaudey, Virginie
AU - Bork, Tillmann
AU - Hochrein, Jochen
AU - Boerries, Melanie
AU - Leenders, Justine
AU - de Tullio, Pascal
AU - Jouret, François
AU - Kramer-Zucker, Albrecht
AU - Walz, Gerd
PY - 2018/9/10
Y1 - 2018/9/10
N2 - 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.
AB - 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.
KW - Animals
KW - Animals, Genetically Modified
KW - Cell Movement
KW - Chemokine CXCL12
KW - Energy Metabolism
KW - Gene Deletion
KW - Gene Expression Profiling
KW - Gene Expression Regulation, Developmental
KW - Glycolysis
KW - Homeostasis
KW - Kidney
KW - Kidney Diseases
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Proto-Oncogene Proteins
KW - Signal Transduction
KW - Tretinoin
KW - Zebrafish
KW - Zebrafish Proteins
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1038/s41467-018-06094-4
DO - 10.1038/s41467-018-06094-4
M3 - SCORING: Journal article
C2 - 30202007
VL - 9
SP - 3660
JO - NAT COMMUN
JF - NAT COMMUN
SN - 2041-1723
ER -