ArticleFrontiers in endocrinology2020
Role of Moesin Phosphorylation in Retinal Pericyte Migration and Detachment Induced by Advanced Glycation Endproducts.
Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 22 citations in OpenAlex.
- Increased CD44 Expression in Endothelial Cells Induced by Advanced Glycation End Products Leads to Insufficient Maturation of Angiogenesis.Journal of cellular and molecular medicine · 2026Article
- Pericyte-derived extracellular vesicles improve vascular barrier function in sepsis via the Angpt1/PI3K/AKT pathway and pericyte recruitment: an in vivo and in vitro study.Stem cell research & therapy · 2025Article
- CD44, ACAN, PLVAP, and HBEGF Emerged as Potential Biomarkers in Diabetic Retinopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Radixin: Roles in the Nervous System and Beyond.Biomedicines · 2024Review
- Microvascular destabilization and intricated network of the cytokines in diabetic retinopathy: from the perspective of cellular and molecular components.Cell & bioscience · 2024Review
- Contraction of human brain vascular pericytes in response to islet amyloid polypeptide is reversed by pramlintide.Molecular brain · 2023Article
- SENP6-Mediated deSUMOylation of VEGFR2 Enhances Its Cell Membrane Transport in Angiogenesis.International journal of molecular sciences · 2023Article
- Diabetic retinopathy: Involved cells, biomarkers, and treatments.Frontiers in pharmacology · 2022Review
- Single-cell RNA sequencing reveals the Müller subtypes and inner blood-retinal barrier regulatory network in early diabetic retinopathy.Frontiers in molecular neuroscience · 2022Article
- Article
- Identification of potential ferroptosis-related biomarkers and a pharmacological compound in diabetic retinopathy based on machine learning and molecular docking.Frontiers in endocrinology · 2022Article
- Hyperglycemia-induced effects on glycocalyx components in the retina.Experimental eye research · 2021Article
- Progress of the study of pericytes and their potential research value in adenomyosis.Science progressReview
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proliferative diabetic retinopathy (PDR) involves persistent, uncontrolled formation of premature blood vessels with reduced number of pericytes. Our previous work showed that advanced glycation endproducts (AGEs) induced angiogenesis in human umbilical vein endothelial cells, mouse retina, and aortic ring, which was associated with moesin phosphorylation. Here we investigated whether moesin phosphorylation may contribute to pericyte detachment and the development of PDR. Primary retinal microvascular pericytes (RMPs) were isolated, purified from weanling rats, and identified by cellular markers α-SMA, PDGFR-β, NG2, and desmin using immunofluorescence microscopy. Effects of AGE-BSA on proliferation and migration of RMPs were examined using CCK-8, wound healing, and transwell assays. Effects on moesin phosphorylation were examined using western blotting. The RMP response to AGE-BSA was also examined when cells expressed the non-phosphorylatable Thr558Ala mutant or phospho-mimicking Thr558Asp mutant of moesin or were treated with ROCK inhibitor Y27632. Colocalization and interaction between CD44, phospho-moesin, and F-actin were observed. Experiments with cultured primary RMPs showed that AGE-BSA inhibited the proliferation, enhanced the migration, and increased moesin phosphorylation in a dose- and time-dependent manner. AGE-BSA also triggered the rearrangement of F-actin and promoted the interaction of CD44 with phospho-moesin in RMPs. These effects were abrogated in cells expressing the non-phosphorylatable moesin mutant and the application of ROCK inhibitor Y27632 attenuated AGE-induced alteration in cultured RMPs by abolishing the phosphorylation of moesin. However, those AGE-induced pathological process occurred in RMPs expressed the phospho-mimicking moesin without AGE-BSA treatment. It is concluded that AGEs could activate ROCK to mediate moesin phosphorylation at Thr558, and resulting phospho-moesin interacts with CD44 to form CD44 cluster, which might stimulate the migration of RMPs and subsequent RMP detachment in microvessel. This pathway may provide new drug targets against immature neovessel formation in PDR.
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