PMID- 35577071
OWN - NLM
STAT- MEDLINE
DCOM- 20220614
LR  - 20220630
IS  - 1096-0384 (Electronic)
IS  - 0003-9861 (Linking)
VI  - 725
DP  - 2022 Aug 15
TI  - Protective effect of pentraxin 3 on pathological retinal angiogenesis in an in 
      vitro model of diabetic retinopathy.
PG  - 109283
LID - S0003-9861(22)00167-9 [pii]
LID - 10.1016/j.abb.2022.109283 [doi]
AB  - BACKGROUND: Diabetic retinopathy (DR) is the most common retinal microvascular 
      disease caused by diabetes. Previous studies indicated that Pentraxin 3 (PTX3), 
      an acute phase reactant, was closely related to the development of DR. But the 
      exact effect of PTX3 in diabetic retinopathy needs more investigations. METHODS: 
      Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) analysis 
      and western blot (WB) were used to detect the expression of PTX3 in vitro. The 
      Ki67 immunofluorescent staining, scratch-wound migration assay, and tube 
      formation experiments were performed to detect the effect of PTX3 knockdown and 
      overexpression on the fibroblast growth factor (FGF)-induced proliferation, 
      migration and tube-forming ability of human retinal microvascular endothelial 
      cells (HRMECs). The phosphorylation levels of extracellular regulated protein 
      kinases (ERK) and fibroblast growth factor receptor (FGFR) in HRMECs were 
      detected by WB. RESULTS: In vitro, the mRNA and protein expressions of PTX3 in 
      the high-concentration glucose condition group were upregulated compared with the 
      normal group (p < 0.05). The proliferation, migration and tube-forming abilities 
      of HRMECs exposed to high-concentration glucose were enhanced (p < 0.01, 
      p < 0.01, p < 0.05 respectively), and the phosphorylation of FGFR and ERK1/2 were 
      increased (p < 0.01, p < 0.05 respectively) compared with the normal condition 
      group. Compared with the high glucose condition group, the proliferation, 
      migration and tube-forming abilities of HRMECs in the high glucose + PTX3 siRNA 
      condition group were further strengthened (p < 0.001, p < 0.0001, p < 0.05 
      respectively), and the phosphorylation of FGFR and ERK1/2 were increased 
      (p < 0.001, p < 0.01 respectively).
 Compared with the high glucose condition 
      group, the proliferation, migration and tube-forming abilities of HRMECs in the 
      high glucose + PTX3 overexpression condition group were compromised (p < 0.001, 
      p < 0.05, p < 0.01 respectively), and the phosphorylation of FGFR and ERK1/2 were 
      inhibited (p < 0.001, p < 0.0001 respectively). Neither the scramble siRNA 
      condition group nor the blank plasmid condition group showed significant 
      difference on the proliferation, migration and tube-forming abilities of HRMECs 
      compared with the high glucose condition group (p > 0.05). CONCLUSIONS: The 
      upregulated expression of PTX3 may play a protective role on pathological 
      angiogenesis in DR. PTX3 may serve as a new target for the treatment of DR.
CI  - Copyright (c) 2022 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Jiang, Yan
AU  - Jiang Y
AD  - Department of Ophthalmology, Shibei Hospital, Jing'an District, Shanghai, 200040, 
      China.
FAU - Xing, Xindan
AU  - Xing X
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
FAU - Niu, Tian
AU  - Niu T
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
FAU - Wang, Hanying
AU  - Wang H
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
FAU - Wang, Chingyi
AU  - Wang C
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
FAU - Shi, Xin
AU  - Shi X
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
FAU - Liu, Kun
AU  - Liu K
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. 
      Electronic address: drliukun@sjtu.edu.cn.
FAU - Su, Li
AU  - Su L
AD  - Department of Ophthalmology, Shanghai General Hospital, National Clinical 
      Research Center for Eye Diseases, Shanghai Key Laboratory of Ocular Fundus 
      Diseases, Shanghai Engineering Center for Visual Science and Photomedicine, 
      Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, 
      Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China. 
      Electronic address: sujilin615@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220513
PL  - United States
TA  - Arch Biochem Biophys
JT  - Archives of biochemistry and biophysics
JID - 0372430
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Serum Amyloid P-Component)
RN  - 148591-49-5 (PTX3 protein)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - *C-Reactive Protein/biosynthesis/genetics
MH  - Cell Proliferation
MH  - Diabetes Mellitus/metabolism/pathology
MH  - *Diabetic Retinopathy/metabolism/pathology
MH  - Endothelial Cells/metabolism
MH  - Glucose/metabolism/pharmacology
MH  - Humans
MH  - *MicroRNAs/genetics/metabolism
MH  - Neovascularization, Pathologic/metabolism/pathology
MH  - RNA, Messenger/genetics/metabolism
MH  - RNA, Small Interfering/genetics/metabolism
MH  - *Serum Amyloid P-Component/biosynthesis/genetics
MH  - Up-Regulation
OTO - NOTNLM
OT  - Angiogenesis
OT  - Diabetic retinopathy
OT  - Pentraxin 3
EDAT- 2022/05/17 06:00
MHDA- 2022/06/15 06:00
CRDT- 2022/05/16 19:32
PHST- 2021/11/06 00:00 [received]
PHST- 2022/05/10 00:00 [revised]
PHST- 2022/05/10 00:00 [accepted]
PHST- 2022/05/17 06:00 [pubmed]
PHST- 2022/06/15 06:00 [medline]
PHST- 2022/05/16 19:32 [entrez]
AID - S0003-9861(22)00167-9 [pii]
AID - 10.1016/j.abb.2022.109283 [doi]
PST - ppublish
SO  - Arch Biochem Biophys. 2022 Aug 15;725:109283. doi: 10.1016/j.abb.2022.109283. 
      Epub 2022 May 13.