PMID- 35816041
OWN - NLM
STAT- MEDLINE
DCOM- 20220713
LR  - 20220822
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Print)
IS  - 0146-0404 (Linking)
VI  - 63
IP  - 8
DP  - 2022 Jul 8
TI  - Interleukin-19 Promotes Retinal Neovascularization in a Mouse Model of 
      Oxygen-Induced Retinopathy.
PG  - 9
LID - 10.1167/iovs.63.8.9 [doi]
LID - 9
AB  - PURPOSE: Retinal neovascularization is a major cause of blindness. This study 
      aimed to investigate the effects of IL-19 and the underlying mechanisms in a 
      mouse model of oxygen-induced retinopathy (OIR). METHODS: C57BL/6J wild-type mice 
      and IL-19 knockout (KO) mice were used to establish an OIR mouse model. Bone 
      marrow-derived macrophages (BMDMs) with or without recombinant IL-19 (rIL-19) 
      stimulation were injected intravitreally. Reverse transcription-quantitative 
      polymerase chain reaction was used to determine the mRNA expressions. ELISA and 
      western blotting were performed to assess the protein levels. Immunofluorescence 
      staining was applied to assess retinal neovascularization. Human retinal 
      endothelial cells (HRECs) stimulated with rIL-19 were cultured to evaluate the 
      effects on cell proliferation and migration. RESULTS: The level of IL-19 was 
      significantly elevated at postnatal day 17 in OIR retinas. Both the avascular 
      areas and pathological neovascular tufts were significantly increased in 
      rIL-19-treated OIR retinas and suppressed in IL-19 KO retinas. IL-19 KO mice 
      suppressed expression of ARG1, VEGFA, and pSTAT3. Moreover, BMDMs stimulated by 
      rIL-19 enhanced that expression and suppressed the expression of inducible nitric 
      oxide synthase (iNOS). The proliferation and migration of HRECs were 
      significantly augmented by rIL-19. In addition, intravitreal injection of BMDMs 
      stimulated by rIL-19 enhanced retinal neovascularization. CONCLUSIONS: These 
      findings suggest that IL-19 enhances pathological neovascularization through a 
      direct effect on microvascular endothelial cells and the promotion of M2 
      macrophage polarization. The inhibition of IL-19 may be a potential treatment for 
      retinal neovascularization.
FAU - Zou, Jingling
AU  - Zou J
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Tan, Wei
AU  - Tan W
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Li, Bingyan
AU  - Li B
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Wang, Zicong
AU  - Wang Z
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Li, Yun
AU  - Li Y
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Zeng, Jun
AU  - Zeng J
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Jiang, Bing
AU  - Jiang B
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
FAU - Yoshida, Shigeo
AU  - Yoshida S
AD  - Department of Ophthalmology, Kurume University School of Medicine, Kurume, Japan.
FAU - Zhou, Yedi
AU  - Zhou Y
AD  - Department of Ophthalmology, The Second Xiangya Hospital of Central South 
      University, Changsha, China.
AD  - Hunan Clinical Research Center of Ophthalmic Disease, Changsha, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Interleukins)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - S88TT14065 (Oxygen)
SB  - IM
EIN - Invest Ophthalmol Vis Sci. 2022 Aug 2;63(9):23. PMID: 35994253
MH  - Animals
MH  - Animals, Newborn
MH  - Disease Models, Animal
MH  - Endothelial Cells/metabolism
MH  - Humans
MH  - Interleukins/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Oxygen/metabolism/toxicity
MH  - *Retinal Diseases/metabolism
MH  - *Retinal Neovascularization/metabolism
MH  - Vascular Endothelial Growth Factor A/metabolism
PMC - PMC9284469
COIS- Disclosure: J. Zou, None; W. Tan, None; B. Li, None; Z. Wang, None; Y. Li, None; 
      J. Zeng, None; B. Jiang, None; S. Yoshida, None; Y. Zhou, None
EDAT- 2022/07/12 06:00
MHDA- 2022/07/14 06:00
PMCR- 2022/07/11
CRDT- 2022/07/11 09:33
PHST- 2022/07/11 09:33 [entrez]
PHST- 2022/07/12 06:00 [pubmed]
PHST- 2022/07/14 06:00 [medline]
PHST- 2022/07/11 00:00 [pmc-release]
AID - 2783460 [pii]
AID - IOVS-22-34810 [pii]
AID - 10.1167/iovs.63.8.9 [doi]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 2022 Jul 8;63(8):9. doi: 10.1167/iovs.63.8.9.