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Manipulation of autophagy: a novelly potential therapeutic strategy for retinal neovascularization.

Abstract The relationship between the role of VEGF and autophagy in the process of retinal angiogenesis is still unclear. In this study, we explored this issue by using the mouse retinal vascular endothelial cell (RVEC) as a model.
PMID
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Authors

Mayor MeshTerms
Keywords

Angiogenesis

Autophagy

Hypoxia

Retinal neovascularization

VEGF

Journal Title bmc ophthalmology
Publication Year Start




PMID- 29703256
OWN - NLM
STAT- MEDLINE
DCOM- 20180511
LR  - 20180511
IS  - 1471-2415 (Electronic)
IS  - 1471-2415 (Linking)
VI  - 18
IP  - 1
DP  - 2018 Apr 27
TI  - Manipulation of autophagy: a novelly potential therapeutic strategy for retinal
      neovascularization.
PG  - 110
LID - 10.1186/s12886-018-0774-6 [doi]
AB  - BACKGROUND: The relationship between the role of VEGF and autophagy in the
      process of retinal angiogenesis is still unclear. In this study, we explored this
      issue by using the mouse retinal vascular endothelial cell (RVEC) as a model.
      METHODS: RVECs were divided into the following groups: control, hypoxia (H),
      3-methyladenine (3-MA) + H, VEGF + H, 3-MA + VEGF+H, anti-VEGF antibody + H,
      3-MA+ anti-VEGF antibody + H. We then examined activation of autophagy by
      detecting formation of autophagosomes with transmission electron microscopy (TEM)
      and by counting the number of green fluorescent protein-positive (GFP+) puncta in
      RVECs. The turnover of microtubule associated protein 1 light chain 3 B (LC3B)
      and VEGF were examined by western blot. Cell migratory capacity was measured with
      wound healing assay and transwell assay. The capillary formation assay was
      performed to investigate the angiogenic capacity. RESULTS: Hypoxia led to an
      increased number of autophagosome and of the GFP+ puncta, an increased ratio of
      LC3B-II/I and enhanced migratory and capillary-formation capacities of RVECs.
      Pre-treatment with 3-MA attenuated activation of autophagy and abrogated the
      enhanced cell migration and capillary formation under hypoxia. Exposure to VEGF
      significantly increased migratory and capillary formation capacities of RVECs
      under hypoxia and 3-MA decreased VEGF-induced angiogenesis without its
      expression. Formation of autophagosome, the number of GFP+ puncta of RVECs and
      expression of LC3B-II/I were both elevated in cells treated with anti-VEGF
      antibody and these effects were partially inhibited by 3-MA pretreatment.
      CONCLUSION: Our present data may identify autophagic response as a novel target
      for enhancing the therapeutic efficacy of angiogenesis inhibitors.
FAU - Li, Rong
AU  - Li R
AD  - Department of Ophthalmology, the First Affiliated Hospital of Xi'an Medical
      University, Xi'an, Shaanxi, China. [email protected]
FAU - Tian, Jin
AU  - Tian J
AD  - Department of Ophthalmology, the Weinan Central Hospital, Weinan, Shaanxi, China.
FAU - Du, Junhui
AU  - Du J
AD  - Department of Ophthalmology, Xi'an Ninth Hospital Affiliated to Medical College
      of Xi'an Jiaotong University, Xi'an, Shaanxi, China. [email protected]
FAU - Zhao, Lei
AU  - Zhao L
AD  - Department of Molecular Physiology and Biophysics, Holden Comprehensive Cancer
      Center, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
FAU - Yao, Yang
AU  - Yao Y
AD  - Department of Central laboratory, The First Affiliated Hospital of Xi'an Medical 
      University, Xi'an, Shaanxi, China.
FAU - Yu, Zhaoxiang
AU  - Yu Z
AD  - Department of General surgery, The First Affiliated Hospital of Xi'an Medical
      University, Xi'an, Shaanxi, China.
FAU - Chang, Weiping
AU  - Chang W
AD  - Department of General surgery, The First Affiliated Hospital of Xi'an Medical
      University, Xi'an, Shaanxi, China.
FAU - Shi, Rui
AU  - Shi R
AD  - Department of Ophthalmology, Shaanxi Provincial People's Hospital, Xi'an,
      Shaanxi, China.
FAU - Li, Jing
AU  - Li J
AD  - Department of Ophthalmology, Shaanxi Provincial People's Hospital, Xi'an,
      Shaanxi, China.
LA  - eng
GR  - Grants 81500726/National Natural Science Foundation of China
PT  - Journal Article
DEP - 20180427
PL  - England
TA  - BMC Ophthalmol
JT  - BMC ophthalmology
JID - 100967802
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Vascular Endothelial Growth Factor A)
SB  - IM
MH  - Animals
MH  - Autophagosomes/pathology
MH  - Autophagy/*physiology
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Endothelial Cells/metabolism
MH  - Endothelium, Vascular/metabolism
MH  - Hypoxia/physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microscopy, Electron, Transmission
MH  - Microtubule-Associated Proteins/metabolism
MH  - Retinal Neovascularization/metabolism/*physiopathology
MH  - Vascular Endothelial Growth Factor A/metabolism
MH  - Wound Healing/physiology
PMC - PMC5924499
OTO - NOTNLM
OT  - Angiogenesis
OT  - Autophagy
OT  - Hypoxia
OT  - Retinal neovascularization
OT  - VEGF
EDAT- 2018/04/29 06:00
MHDA- 2018/05/12 06:00
CRDT- 2018/04/29 06:00
PHST- 2018/01/11 00:00 [received]
PHST- 2018/04/13 00:00 [accepted]
PHST- 2018/04/29 06:00 [entrez]
PHST- 2018/04/29 06:00 [pubmed]
PHST- 2018/05/12 06:00 [medline]
AID - 10.1186/s12886-018-0774-6 [doi]
AID - 10.1186/s12886-018-0774-6 [pii]
PST - epublish
SO  - BMC Ophthalmol. 2018 Apr 27;18(1):110. doi: 10.1186/s12886-018-0774-6.