ArticleCells2023
Bone Morphogenetic Protein-4 Impairs Retinal Endothelial Cell Barrier, a Potential Role in Diabetic Retinopathy.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Network Pharmacology and Experimental Validation Elucidate the Anti-Angiogenic Mechanism of Silibinin.Chemistry & biodiversity · 2026Article
- Ythdf2 loss in microglia aggravates ischemic retinopathy by increasing microglia activation and microvascular anomalies.Journal of advanced research · 2026Article
- Targeting endoplasmic reticulum stress and YAP/TAZ-SMAD1/5 signaling to ameliorate endothelial dysfunction in diabetes.Acta pharmacologica Sinica · 2026Article
- Silencing SLC31A1 attenuates high glucose plus copper-induced cuproptosis-like signaling, oxidative stress, and barrier dysfunction in human retinal microvascular endothelial cells.International journal of ophthalmology · 2026Article
- Bone morphogenetic proteins (BMPs) at the forefront of ocular diseases and therapeutics.Eye and vision (London, England) · 2025Review
- Development of targeted drugs for diabetic retinopathy using Mendelian randomized pharmacogenomics.Frontiers in endocrinology · 2025Article
- Microvascular destabilization and intricated network of the cytokines in diabetic retinopathy: from the perspective of cellular and molecular components.Cell & bioscience · 2024Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Bone Morphogenetic Protein 4 (BMP4) is a secreted growth factor of the Transforming Growth Factor beta (TGFβ) superfamily. The goal of this study was to test whether BMP4 contributes to the pathogenesis of diabetic retinopathy (DR). Immunofluorescence of BMP4 and the vascular marker isolectin-B4 was conducted on retinal sections of diabetic and non-diabetic human and experimental mice. We used Akita mice as a model for type-1 diabetes. Proteins were extracted from the retina of postmortem human eyes and 6-month diabetic Akita mice and age-matched control. BMP4 levels were measured by Western blot (WB). Human retinal endothelial cells (HRECs) were used as an in vitro model. HRECs were treated with BMP4 (50 ng/mL) for 48 h. The levels of phospho-smad 1/5/9 and phospho-p38 were measured by WB. BMP4-treated and control HRECs were also immunostained with anti-Zo-1. We also used electric cell-substrate impedance sensing (ECIS) to calculate the transcellular electrical resistance (TER) under BMP4 treatment in the presence and absence of noggin (200 ng/mL), LDN193189 (200 nM), LDN212854 (200 nM) or inhibitors of vascular endothelial growth factor receptor 2 (VEGFR2; SU5416, 10 μM), p38 (SB202190, 10 μM), ERK (U0126, 10 μM) and ER stress (Phenylbutyric acid or PBA, 30 μmol/L). The impact of BMP4 on matrix metalloproteinases (MMP2 and MMP9) was also evaluated using specific ELISA kits. Immunofluorescence of human and mouse eyes showed increased BMP4 immunoreactivity, mainly localized in the retinal vessels of diabetic humans and mice compared to the control. Western blots of retinal proteins showed a significant increase in BMP4 expression in diabetic humans and mice compared to the control groups (
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Registered trials
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