ArticleDrug design, development and therapy2015
The mechanism of CCN1-enhanced retinal neovascularization in oxygen-induced retinopathy through PI3K/Akt-VEGF signaling pathway.
Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- Integrinβ-1 in disorders and cancers: molecular mechanisms and therapeutic targets.Cell communication and signaling : CCS · 2024Review
- USP14 Regulates ATF2/PIK3CD Axis to Promote Microvascular Endothelial Cell Proliferation, Migration, and Angiogenesis in Diabetic Retinopathy.Biochemical genetics · 2023Article
- Splint-free line drawing model: An innovative method for excisional wound models.International wound journal · 2023Article
- CCN1 secreted by human adipose-derived stem cells enhances wound healing and promotes angiogenesis through activating the AKT signalling pathway.International wound journal · 2023Article
- Propranolol ameliorates retinopathy of prematurity in mice by downregulating HIF-1α via the PI3K/Akt/ERK pathway.Pediatric research · 2023Article
- Changes and related factors of blood CCN1 levels in diabetic patients.Frontiers in endocrinology · 2023Article
- Review
- LncRNAFrontiers in medicine · 2022Article
- Effects of long non-coding RNA myocardial infarction-associated transcript on retinal neovascularization in a newborn mouse model of oxygen-induced retinopathy.Neural regeneration research · 2021Article
- VEGF Production Is Regulated by the AKT/ERK1/2 Signaling Pathway and Controls the Proliferation ofFrontiers in cellular and infection microbiology · 2020Article
- β‑elemene inhibits oxygen‑induced retinal neovascularization via promoting miR‑27a and reducing VEGF expression.Molecular medicine reports · 2019Article
- Functional Vascular Tissue Engineering Inspired by Matricellular Proteins.Frontiers in cardiovascular medicine · 2019Review
- Article
- Advanced glycation end products promote VEGF expression and thus choroidal neovascularization via Cyr61-PI3K/AKT signaling pathway.Scientific reports · 2017Article
- HMGB1 siRNA can reduce damage to retinal cells induced by high glucose in vitro and in vivo.Drug design, development and therapy · 2017Article
- Effects of microRNA-29a on retinopathy of prematurity by targeting AGT in a mouse model.American journal of translational research · 2017Article
- Inositol Hexaphosphate and Inositol Inhibit Colorectal Cancer Metastasis to the Liver in BALB/c Mice.Nutrients · 2016Article
- Matrix metalloproteinase-9 and vascular endothelial growth factor expression change in experimental retinal neovascularization.International journal of ophthalmology · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCCN1 (also called Cyr 61) is an extracellular matrix signaling molecule that has been implicated in neovascularization through its interactions with several endothelial integrin receptors. The roles of vascular endothelial growth factor (VEGF) in angiogenesis are well described. The aim of this study was to investigate the signal transduction mechanism of CCN1-PI3K/Akt-VEGF in retinopathy of prematurity (ROP), and the effects of CCN1 knockdown on ROP.
methodsThe oxygen-induced retinopathy (OIR) model was established in C57BL/6J mice exposed to a high concentration of oxygen. Retinas were obtained from the normoxia, OIR, OIR control (treated with scramble siRNA) and OIR treated (with CCN1 siRNA) groups. Retinal neovascularization (RNV) was qualitatively analyzed with ADPase staining and quantitatively analyzed by counting neovascular endothelial cell nuclei at postnatal day 17 when RNV reached a peak. mRNA level and protein expression of CCN1, p-Akt, and VEGF were measured by real-time PCR and Western blotting, and located with immunohistochemistry.
resultsCCN1 depletion resulted in less neovascularization clock hour scores in the number of preretinal neovascular cells compared with the OIR treated group (1.28±0.83 versus 4.80±0.82; and 7.12±2.50 versus 23.25±2.35, respectively, both P<0.05). Furthermore, CCN1, p-Akt and VEGF mRNA, and protein were significantly expressed in the retina of the OIR and OIR control groups. Intravitreal injection of CCN1 siRNA significantly reduced PI3K/Akt-VEGF pathway expression of the OIR mouse model (all P<0.05). CCN1 siRNA significantly enhanced the avascular area and avascular diameter of OIR model (P<0.05). CCN1 siRNA decreased the levels of IL-1β, IL-6, and TNF-α significantly compared to the OIR group (P<0.05).
conclusionThese results suggest that CCN1 plays an important role in RNV via the PI3K/Akt-VEGF signaling pathway. CCN1 may be a potential target for the prevention and treatment of ROP.
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