ArticleArteriosclerosis, thrombosis, and vascular biology2013
Diabetes causes bone marrow endothelial barrier dysfunction by activation of the RhoA-Rho-associated kinase signaling pathway.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 69 citations in OpenAlex.
- Advanced multifunctional thermo- and electro-stimulative hydrogels for bone regeneration.Materials today. Bio · 2026Review
- Type 2 diabetes Reprograms Bone Marrow Hematopoiesis and Dysregulates Immune Signaling in Response to Stroke.bioRxiv : the preprint server for biology · 2025Article
- ROS-scavenging nanomaterials as emerging tools for bone tissue regeneration: A comprehensive review of recent progress.Acta pharmaceutica Sinica. B · 2025Review
- Association of the lipidome with type 1 diabetes and the mediated effect of metabolites: A Mendelian randomization study.Medicine · 2025Article
- Single-cell RNA sequencing reveals a distinct profile of bone immune microenvironment and decreased osteoclast differentiation in type 2 diabetic mice.Genes & diseases · 2024Article
- Improved prediction of long-term kidney outcomes in people with type 2 diabetes by levels of circulating haematopoietic stem/progenitor cells.Diabetologia · 2023Article
- Impaired Hematopoietic Stem/Progenitor Cell Traffic and Multi-organ Damage in Diabetes.Stem cells (Dayton, Ohio) · 2022Article
- Hematopoietic Progenitors and the Bone Marrow Niche Shape the Inflammatory Response and Contribute to Chronic Disease.International journal of molecular sciences · 2022Review
- A cohort study of circulating progenitor cells after ST-segment elevation and non-ST segment elevation myocardial infarction in non-diabetic and diabetic patients.Frontiers in cardiovascular medicine · 2022Article
- Protective Effect and Mechanism of Traditional Chinese Medicine on Myocardial Ischemia Reperfusion Injury.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Salvianic Acid A Regulates High-Glucose-Treated Endothelial Progenitor Cell Dysfunction via the AKT/Endothelial Nitric Oxide Synthase (eNOS) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Skeleton-vasculature chain reaction: a novel insight into the mystery of homeostasis.Bone research · 2021Review
- Cell Therapy for Critical Limb Ischemia: Advantages, Limitations, and New Perspectives for Treatment of Patients with Critical Diabetic Vasculopathy.Current diabetes reports · 2021Review
- Review
- High Glucose Activates YAP Signaling to Promote Vascular Inflammation.Frontiers in physiology · 2021Article
- Activation of Bone Marrow Adaptive Immunity in Type 2 Diabetes: Rescue by Co-stimulation Modulator Abatacept.Frontiers in immunology · 2021Article
- Regulation of JAM2 Expression in the Lungs of Streptozotocin-Induced Diabetic Mice and Human Pluripotent Stem Cell-Derived Alveolar Organoids.Biomedicines · 2020Article
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- Article
- When Good Guys Turn Bad: Bone Marrow's and Hematopoietic Stem Cells' Role in the Pathobiology of Diabetic Complications.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDiabetes mellitus causes bone marrow (BM) microangiopathy. This study aimed to investigate the mechanisms responsible for BM endothelial dysfunction in diabetes mellitus. METHODS AND
resultsThe analysis of differentially expressed transcripts in BM endothelial cells (BMECs) from type-1 diabetic and nondiabetic mice showed an effect of diabetes mellitus on signaling pathways controlling cell death, migration, and cytoskeletal rearrangement. Type-1 diabetic-BMECs displayed high reactive oxygen species levels, increased expression and activity of RhoA and its associated protein kinases Rho-associated kinase 1/Rho-associated kinase 2, and reduced Akt phosphorylation/activity. Likewise, diabetes mellitus impaired Akt-related BMEC functions, such as migration, network formation, and angiocrine factor-releasing activity, and increased vascular permeability. Moreover, high glucose disrupted BMEC contacts through Src tyrosine kinase phosphorylation of vascular endothelial cadherin. These alterations were prevented by constitutively active Akt (myristoylated Akt), Rho-associated kinase inhibitor Y-27632, and Src inhibitors. Insulin replacement restored BMEC abundance, as assessed by flow cytometry analysis of the endothelial marker MECA32, and endothelial barrier function in BM of type-1 diabetic mice.
conclusionsRedox-dependent activation of RhoA/Rho-associated kinase and Src/vascular endothelial cadherin signaling pathways, together with Akt inactivation, contribute to endothelial dysfunction in diabetic BM. Metabolic control is crucial for maintenance of endothelial cell homeostasis and endothelial barrier function in BM of diabetic mice.
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