PMID- 30495987
OWN - NLM
STAT- MEDLINE
DCOM- 20190513
LR  - 20200226
IS  - 1530-6860 (Electronic)
IS  - 0892-6638 (Linking)
VI  - 32
IP  - 12
DP  - 2018 Dec
TI  - Elevating ATP-binding cassette transporter G1 improves re-endothelialization 
      function of endothelial progenitor cells via Lyn/Akt/eNOS in diabetic mice.
PG  - 6525-6536
LID - 10.1096/fj.201800248RR [doi]
AB  - Endothelial progenitor cell (EPC) dysfunction contributes to diabetes-induced 
      delay in endothelium repair after vessel injury, prominently associated with 
      diabetic cardiovascular complications such as neointima formation. ATP-binding 
      cassette transporter G1 (ABCG1) promotes cholesterol efflux to HDL, which may 
      favorably affect EPC function. However, whether ABCG1 improves EPC function, 
      especially in diabetes, remains unknown. Here we investigated the role of ABCG1 
      in EPCs by using Tie2-mediated ABCG1 transgenic (Tie2- ABCG1(Tg)) mice. Mice were 
      injected with streptozotocin to induce diabetes mellitus. As compared with 
      wild-type (WT) mice, in Tie2- ABCG1(Tg) mice, diabetes-impaired EPC migration and 
      tube formation were reversed. In vitro gain-of-function and loss-of-function 
      studies further revealed that ABCG1-overexpressing EPCs showed increased 
      migration and tube formation and differentiation via the Lck/Yes-related novel 
      protein tyrosine kinase /Akt/endothelial NO synthase pathway by enhancing 
      cellular cholesterol efflux. Finally, type 1 and type 2 diabetic mouse models 
      with arterial injury were intravenously injected with labeled EPCs from WT or 
      Tie2- ABCG1(Tg) mice. Re-endothelialization in diabetic mice was improved to a 
      greater extent by injection of ABCG1-overexpressing than WT EPCs. Our study 
      demonstrated that ABCG1 in EPCs improved repair after vascular injury in diabetes 
      by increasing EPC function such as migration, tube formation and differentiation, 
      and subsequent re-endothelialization. ABCG1 might be a promising therapeutic 
      target for diabetes-associated vascular diseases.-Shi, Y., Lv, X., Liu, Y., Li, 
      B., Liu, M., Yan, M., Liu, Y., Li, Q., Zhang, X., He, S., Zhu, M., He, J., Zhu, 
      Y., Zhu, Y., Ai, D. Elevating ATP-binding cassette transporter G1 improves 
      re-endothelialization function of endothelial progenitor cells via Lyn/Akt/eNOS 
      in diabetic mice.
FAU - Shi, Ying
AU  - Shi Y
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
AD  - Tianjin Institute of Cardiovascular Disease, Tianjin Chest Hospital, Tianjin, 
      China.
FAU - Lv, Xue
AU  - Lv X
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Liu, Yanan
AU  - Liu Y
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Li, Bochuan
AU  - Li B
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Liu, Mingming
AU  - Liu M
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Yan, Meng
AU  - Yan M
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Liu, Yajin
AU  - Liu Y
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Li, Qi
AU  - Li Q
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Zhang, Xuejiao
AU  - Zhang X
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - He, Shuang
AU  - He S
AD  - Tianjin Key Laboratory of Modern Chinese Medicine, Tianjin University of 
      Traditional Chinese Medicine, Tianjin, China.
FAU - Zhu, Mason
AU  - Zhu M
AD  - Department of Molecular Biology, University of California, San Diego, La Jolla, 
      California, USA.
FAU - He, Jinlong
AU  - He J
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Zhu, Yan
AU  - Zhu Y
AD  - Tianjin Key Laboratory of Modern Chinese Medicine, Tianjin University of 
      Traditional Chinese Medicine, Tianjin, China.
FAU - Zhu, Yi
AU  - Zhu Y
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
FAU - Ai, Ding
AU  - Ai D
AD  - Tianjin Key Laboratory of Metabolic Diseases, Department of Physiology and 
      Pathophysiology, Tianjin Medical University, Tianjin, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American Societies for 
      Experimental Biology
JID - 8804484
RN  - 0 (ABCG1 protein, mouse)
RN  - 0 (ATP Binding Cassette Transporter, Subfamily G, Member 1)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, mouse)
RN  - EC 2.7.10.2 (lyn protein-tyrosine kinase)
RN  - EC 2.7.10.2 (src-Family Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily G, Member 1/*metabolism
MH  - Animals
MH  - Cardiovascular Diseases/metabolism
MH  - Cell Differentiation/physiology
MH  - Cell Movement/physiology
MH  - Diabetes Complications/metabolism
MH  - Diabetes Mellitus, Experimental
MH  - Endothelial Progenitor Cells/*metabolism
MH  - Endothelium/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Neointima/metabolism
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase Type III/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Signal Transduction/physiology
MH  - src-Family Kinases/*metabolism
OTO - NOTNLM
OT  - cholesterol efflux
OT  - high glucose
OT  - vascular repair
OT  - vasculogenesis
EDAT- 2018/11/30 06:00
MHDA- 2019/05/14 06:00
CRDT- 2018/11/30 06:00
PHST- 2018/11/30 06:00 [entrez]
PHST- 2018/11/30 06:00 [pubmed]
PHST- 2019/05/14 06:00 [medline]
AID - 10.1096/fj.201800248RR [doi]
PST - ppublish
SO  - FASEB J. 2018 Dec;32(12):6525-6536. doi: 10.1096/fj.201800248RR.