ArticleCardiovascular diabetology2012
RhoA/ROCK-dependent moesin phosphorylation regulates AGE-induced endothelial cellular response.
Article in Cardiovascular diabetology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- ROCK inhibitor fasudil attenuated high glucose-induced MCP-1 and VCAM-1 expression and monocyte-endothelial cell adhesion.Cardiovascular diabetology · 2012Trial
- Moesin is an αCellular and molecular life sciences : CMLS · 2026Article
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Serum moesin is associated with cognitive impairment and glucose fluctuations in patients with type 2 diabetes.Diabetology & metabolic syndrome · 2025Article
- Quantitative Proteomic Analysis Reveals Different Functional Subtypes amongJournal of proteome research · 2025Article
- Edema and lymphatic clearance: molecular mechanisms and ongoing challenges.Clinical science (London, England : 1979) · 2023Review
- Small Vessel Disease: Ancient Description, Novel Biomarkers.International journal of molecular sciences · 2022Review
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- Homocysteine in Neurology: A Possible Contributing Factor to Small Vessel Disease.International journal of molecular sciences · 2021Review
- Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?International journal of molecular sciences · 2020Review
- Role of Moesin Phosphorylation in Retinal Pericyte Migration and Detachment Induced by Advanced Glycation Endproducts.Frontiers in endocrinology · 2020Article
- Involvement of moesin phosphorylation in ischemia/reperfusion induced inner blood-retinal barrier dysfunction.International journal of ophthalmology · 2020Article
- Article
- Small GTPases and Their Role in Vascular Disease.International journal of molecular sciences · 2019Review
- Anti-inflammatory Mechanism of Geniposide: Inhibiting the Hyperpermeability of Fibroblast-Like Synoviocytes via the RhoA/p38MAPK/NF-κB/F-Actin Signal Pathway.Frontiers in pharmacology · 2018Article
- A functional siRNA screen identifies RhoGTPase-associated genes involved in thrombin-induced endothelial permeability.PloS one · 2018Article
- Bushen Huoxue Attenuates Diabetes-Induced Cognitive Impairment by Improvement of Cerebral Microcirculation: Involvement of RhoA/ROCK/moesin and Src Signaling Pathways.Frontiers in physiology · 2018Article
- [RhoA/Rho-kinase contributes to chronic pain following thoracotomy by up-regulating glutaminase 1 expression in rat spinal dorsal cord].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- The role of actin depolymerizing factor in advanced glycation endproducts-induced impairment in mouse brain microvascular endothelial cells.Molecular and cellular biochemistry · 2017Article
- Loss of cortactin causes endothelial barrier dysfunction via disturbed adrenomedullin secretion and actomyosin contractility.Scientific reports · 2016Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of advanced glycation end products (AGEs) in the development of diabetes, especially diabetic complications, has been emphasized in many reports. Accumulation of AGEs in the vasculature triggers a series of morphological and functional changes in endothelial cells (ECs) and induces an increase of endothelial permeability. This study was to investigate the involvement of RhoA/ROCK-dependent moesin phosphorylation in endothelial abnormalities induced by AGEs.
methodsUsing human dermal microvascular endothelial cells (HMVECs), the effects of human serum albumin modified-AGEs (AGE-HSA) on the endothelium were assessed by measuring monolayer permeability and staining of F-actin in HMVECs. Activations of RhoA and ROCK were determined by a luminescence-based assay and immunoblotting. Transfection of recombinant adenovirus that was dominant negative for RhoA (RhoA N19) was done to down-regulate RhoA expression, while adenovirus with constitutively activated RhoA (RhoA L63) was transfected to cause overexpression of RhoA in HMVECs. H-1152 was employed to specifically block activation of ROCK. Co-immunoprecipitation was used to further confirm the interaction of ROCK and its downstream target moesin. To identify AGE/ROCK-induced phosphorylation site in moesin, two mutants pcDNA3/HA-moesinT(558A) and pcDNA3/HA-moesinT(558D) were applied in endothelial cells.
resultsThe results showed that AGE-HSA increased the permeability of HMVEC monolayer and triggered the formation of F-actin-positive stress fibers. AGE-HSA enhanced RhoA activity as well as phosphorylation of ROCK in a time- and dose-dependent manner. Down-regulation of RhoA expression with RhoA N19 transfection abolished these AGE-induced changes, while transfection of RhoA L63 reproduced the AGE-evoked changes. H-1152 attenuated the AGE-induced alteration in monolayer permeability and cytoskeleton. The results also confirmed the AGE-induced direct interaction of ROCK and moesin. Thr558 was further identified as the phosphorylating site of moesin in AGE-evoked endothelial responses.
conclusionThese results confirm the involvement of RhoA/ROCK pathway and subsequent moesin Thr558 phosphorylation in AGE-mediated endothelial dysfunction.
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