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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

Harvard

Yakulov, TA, Todkar, AP, Slanchev, K, Wiegel, J, Bona, A, Groß, M, Scholz, A, Hess, I, Wurditsch, A, Grahammer, F, Huber, TB, Lecaudey, V, Bork, T, Hochrein, J, Boerries, M, Leenders, J, de Tullio, P, Jouret, F, Kramer-Zucker, A & Walz, G 2018, 'CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury', NAT COMMUN, Jg. 9, S. 3660. https://doi.org/10.1038/s41467-018-06094-4

APA

Yakulov, T. A., Todkar, A. P., Slanchev, K., Wiegel, J., Bona, A., Groß, M., Scholz, A., Hess, I., Wurditsch, A., Grahammer, F., Huber, T. B., Lecaudey, V., Bork, T., Hochrein, J., Boerries, M., Leenders, J., de Tullio, P., Jouret, F., Kramer-Zucker, A., & Walz, G. (2018). CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury. NAT COMMUN, 9, 3660. https://doi.org/10.1038/s41467-018-06094-4

Vancouver

Yakulov TA, Todkar AP, Slanchev K, Wiegel J, Bona A, Groß M et al. CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury. NAT COMMUN. 2018 Sep 10;9:3660. https://doi.org/10.1038/s41467-018-06094-4

Bibtex

@article{9907e2c9e5e54b94adf97d30b362d8e4,
title = "CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury",
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.",
keywords = "Animals, Animals, Genetically Modified, Cell Movement, Chemokine CXCL12, Energy Metabolism, Gene Deletion, Gene Expression Profiling, Gene Expression Regulation, Developmental, Glycolysis, Homeostasis, Kidney, Kidney Diseases, Male, Mice, Mice, Inbred C57BL, Proto-Oncogene Proteins, Signal Transduction, Tretinoin, Zebrafish, Zebrafish Proteins, Journal Article, Research Support, Non-U.S. Gov't",
author = "Yakulov, {Toma A} and Todkar, {Abhijeet P} and Krasimir Slanchev and Johannes Wiegel and Alexandra Bona and Martin Gro{\ss} and Alexander Scholz and Isabell Hess and Anne Wurditsch and Florian Grahammer and Huber, {Tobias B} and Virginie Lecaudey and Tillmann Bork and Jochen Hochrein and Melanie Boerries and Justine Leenders and {de Tullio}, Pascal and Fran{\c c}ois Jouret and Albrecht Kramer-Zucker and Gerd Walz",
year = "2018",
month = sep,
day = "10",
doi = "10.1038/s41467-018-06094-4",
language = "English",
volume = "9",
pages = "3660",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

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 -