TY - JOUR
T1 - Quiescent Endothelial Cells Upregulate Fatty Acid β-Oxidation for Vasculoprotection via Redox Homeostasis
AU - Kalucka, Joanna
AU - Bierhansl, Laura
AU - Conchinha, Nadine Vasconcelos
AU - Missiaen, Rindert
AU - Elia, Ilaria
AU - Brüning, Ulrike
AU - Scheinok, Samantha
AU - Treps, Lucas
AU - Cantelmo, Anna Rita
AU - Dubois, Charlotte
AU - de Zeeuw, Pauline
AU - Goveia, Jermaine
AU - Zecchin, Annalisa
AU - Taverna, Federico
AU - Morales-Rodriguez, Francisco
AU - Brajic, Aleksandra
AU - Conradi, Lena Christin
AU - Schoors, Sandra
AU - Harjes, Ulrike
AU - Vriens, Kim
AU - Pilz, Gregor Alexander
AU - Chen, Rongyuan
AU - Cubbon, Richard
AU - Thienpont, Bernard
AU - Cruys, Bert
AU - Wong, Brian W.
AU - Ghesquière, Bart
AU - Dewerchin, Mieke
AU - De Bock, Katrien
AU - Sagaert, Xavier
AU - Jessberger, Sebastian
AU - Jones, Elizabeth A.V.
AU - Gallez, Bernard
AU - Lambrechts, Diether
AU - Mazzone, Massimiliano
AU - Eelen, Guy
AU - Li, Xuri
AU - Fendt, Sarah Maria
AU - Carmeliet, Peter
N1 - Funding Information:
We thank R. Adams for providing Cdh5(PAC)-CreERT2 mice, S. Christen for help with GC-MS data interpretation, P. Levêque for help with EPR experiments and data interpretation, and the lab members for their assistance, feedback, and discussion. J.K., R.M., N.V.C., J.G., P.d.Z., F.M.-R., C.D., and U.H. are supported by the Research Foundation Flanders (FWO); L.B. by a Leopoldina Postdoc Scholarship; L.T. by a Marie Curie-IEF Fellowship; and L.-C.C. by Fritz Thyssen Stiftung. The work of R.C. is supported by a British Heart Foundation Intermediate Clinical Fellowship (FS/12/80/29821); S.J. is supported by Swiss National Science Foundation (BSCGI0_157859), Switzerland; S.-M.F. is supported by Marie Curie CIG, grants from the Research Foundation Flanders (FWO-Vlaanderen), Belgium; P.C. is supported by the VIB TechWatch program, a Federal Government Belgium grant (IUAP7/03), long-term structural Methusalem funding by the Flemish Government, grants from the Research Foundation Flanders (FWO-Vlaanderen), grants from Foundation against Cancer (2012-175 and 2016-078), and ERC Advanced Research grant (EU-ERC743074). X.L. is supported by the State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center at the Sun Yat-Sen University and by the National Natural Science Foundation of China (81330021, 81670855).
Funding Information:
We thank R. Adams for providing Cdh5(PAC)-Cre ERT2 mice, S. Christen for help with GC-MS data interpretation, P. Levêque for help with EPR experiments and data interpretation, and the lab members for their assistance, feedback, and discussion. J.K., R.M., N.V.C., J.G., P.d.Z., F.M.-R., C.D., and U.H. are supported by the Research Foundation Flanders (FWO); L.B. by a Leopoldina Postdoc Scholarship; L.T. by a Marie Curie-IEF Fellowship; and L.-C.C. by Fritz Thyssen Stiftung. The work of R.C. is supported by a British Heart Foundation Intermediate Clinical Fellowship ( FS/12/80/29821 ); S.J. is supported by Swiss National Science Foundation (BSCGI0_157859), Switzerland; S.-M.F. is supported by Marie Curie CIG , grants from the Research Foundation Flanders (FWO-Vlaanderen), Belgium; P.C. is supported by the VIB TechWatch program, a Federal Government Belgium grant ( IUAP7/03 ), long-term structural Methusalem funding by the Flemish Government , grants from the Research Foundation Flanders (FWO-Vlaanderen), grants from Foundation against Cancer ( 2012-175 and 2016-078 ), and ERC Advanced Research grant ( EU-ERC743074 ). X.L. is supported by the State Key Laboratory of Ophthalmology , Zhongshan Ophthalmic Center at the Sun Yat-Sen University and by the National Natural Science Foundation of China ( 81330021 , 81670855 ).
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2018/12/4
Y1 - 2018/12/4
N2 - Kalucka et al. show that fatty acid β-oxidation in quiescent endothelial cells (QECs) is indispensable to maintain redox balance and prevent EC dysfunction. In contrast to proliferating ECs (PECs), QECs reprogram their metabolism to increase regeneration of NAPDH, which is then used by vasculoprotective (NADPH-consuming) enzymes for redox homeostasis.
AB - Kalucka et al. show that fatty acid β-oxidation in quiescent endothelial cells (QECs) is indispensable to maintain redox balance and prevent EC dysfunction. In contrast to proliferating ECs (PECs), QECs reprogram their metabolism to increase regeneration of NAPDH, which is then used by vasculoprotective (NADPH-consuming) enzymes for redox homeostasis.
KW - CPT1A
KW - angiogenesis
KW - endothelial cell dysfunction
KW - endothelial cells
KW - fatty acid β-oxidation
KW - metabolism
KW - quiescence
KW - redox homeostasis
UR - http://www.scopus.com/inward/record.url?scp=85059335593&partnerID=8YFLogxK
U2 - 10.1016/j.cmet.2018.07.016
DO - 10.1016/j.cmet.2018.07.016
M3 - Article
C2 - 30146488
AN - SCOPUS:85059335593
SN - 1550-4131
VL - 28
SP - 881-894.e13
JO - Cell metabolism
JF - Cell metabolism
IS - 6
ER -