ArticleAmerican journal of physiology. Cell physiology2020
Extracellular adenosine enhances pulmonary artery vasa vasorum endothelial cell barrier function via Gi/ELMO1/Rac1/PKA-dependent signaling mechanisms.
Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Modeling NDD-Associated NLGN2 Depletion Using CRISPR/Cas13 Reveals Exaggerated Process Elongation Mediated by the CCDC88A-G Protein-ELMO Axis.International journal of molecular sciences · 2026Article
- Signaling Through Girdin Underlies Excessive Cell Morphogenesis Resulting from Depletion of Neurodevelopmental Disorder-Related Neurexin-2.International journal of molecular sciences · 2026Article
- A hypothesis and evidence map for neuroimmune regulation of DOCK-family cytoskeletal programs in solid tumors.Frontiers in immunology · 2026Review
- Single-nucleus transcriptome profiling of skeletal muscle in Diqing Tibetan pigs with distinct body sizes.BMC genomics · 2025Article
- Extracellular purines in lung endothelial permeability and pulmonary diseases.Frontiers in physiology · 2024Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- On vasa vasorum: A history of advances in understanding the vessels of vessels.Science advances · 2022Review
- Pleiotropic and Potentially Beneficial Effects of Reactive Oxygen Species on the Intracellular Signaling Pathways in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2021Review
- P2Y Purinergic Receptors, Endothelial Dysfunction, and Cardiovascular Diseases.International journal of molecular sciences · 2020Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The vasa vasorum (VV), the microvascular network around large vessels, has been recognized as an important contributor to the pathological vascular remodeling in cardiovascular diseases. In bovine and rat models of hypoxic pulmonary hypertension (PH), we have previously shown that chronic hypoxia profoundly increased pulmonary artery (PA) VV permeability, associated with infiltration of inflammatory and progenitor cells in the arterial wall, perivascular inflammation, and structural vascular remodeling. Extracellular adenosine was shown to exhibit a barrier-protective effect on VV endothelial cells (VVEC) via cAMP-independent mechanisms, which involved adenosine A1 receptor-mediated activation of Gi-phosphoinositide 3-kinase-Akt pathway and actin cytoskeleton remodeling. Using VVEC isolated from the adventitia of calf PA, in this study we investigated in more detail the mechanisms linking Gi activation to downstream barrier protection pathways. Using a small-interference RNA (siRNA) technique and transendothelial electrical resistance assay, we found that the adaptor protein, engulfment and cell motility 1 (ELMO1), the tyrosine phosphatase Src homology region 2 domain-containing phosphatase-2, and atypical Gi- and Rac1-mediated protein kinase A activation are implicated in VVEC barrier enhancement. In contrast, the actin-interacting GTP-binding protein, girdin, and the p21-activated kinase 1 downstream target, LIM kinase, are not involved in this response. In addition, adenosine-dependent cytoskeletal rearrangement involves activation of cofilin and inactivation of ezrin-radixin-moesin regulatory cytoskeletal proteins, consistent with a barrier-protective mechanism. Collectively, our data indicate that targeting adenosine receptors and downstream barrier-protective pathways in VVEC may have a potential translational significance in developing pharmacological approach for the VV barrier protection in PH.
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