ArticleArteriosclerosis, thrombosis, and vascular biology2011
Interleukin-10 released by CD4(+)CD25(+) natural regulatory T cells improves microvascular endothelial function through inhibition of NADPH oxidase activity in hypertensive mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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114 citing papers in PubMed, 170 citations in OpenAlex.
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- Bronchial anastomotic complications as a microvascular disruption in a mouse model of airway transplantation.Frontiers in immunology · 2025Review
- The role of T cells in vascular aging, hypertension, and atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2024Review
- Role of plasmacytoid dendritic cells in vascular dysfunction in mice with renovascular hypertension.Heliyon · 2024Article
- Immune and inflammatory mechanisms in hypertension.Nature reviews. Cardiology · 2024Review
- Modulator Effect of AT1 Receptor Knockdown on THP-1 Macrophage Proinflammatory Activity.Biology · 2024Article
- CD8American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Underlying Mechanisms and Treatment of Hypertension in Glomerular Diseases.Current hypertension reports · 2024Review
- Cross-talks between perivascular adipose tissue and neighbors: multifaceted nature of nereids.Frontiers in pharmacology · 2024Review
54 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWe previously demonstrated that a reduced number of CD(4+)CD(25+)-regulatory T cells (Tregs) was associated with microvascular dysfunction in hypertension. However, the underlying mechanism by which Tregs regulate vascular endothelial function remains unknown. METHODS AND
resultsControl and interleukin (IL)-10(-/-) knockout mice were infused with angiotensin II (400 ng/kg/min) for 2 weeks (hypertensive [HT] and HT-IL-10(-/-)). Endothelium-dependent relaxation (EDR) in response to acetylcholine was significantly reduced in mesenteric resistance artery (MRA) from HT and HT-IL-10(-/-) compared with control and IL-10(-/-) mice. Importantly, the incubation of MRA from HT mice with the conditioned media of cultured Tregs, isolated from control mice, reduced NADPH oxidase activity and improved EDR, whereas no effect was observed in MRA from control mice incubated with the same media. These effects were reversed when MRAs were preincubated with IL-10 antibody or IL-10 receptor antagonist, whereas incubation with transforming growth factor-β receptor antagonist had no effect. The transfer of cultured Tregs, isolated from control mice, into HT-IL-10(-/-) mice reduced systolic blood pressure (SBP) and NADPH oxidase activity and improved EDR in MRA compared with untreated HT-IL-10(-/-) mice. In vivo treatment of HT mice with IL-10 (1000 ng/mouse) significantly reduced SBP and NADPH oxidase activity and improved EDR in MRA compared with untreated HT mice. The transfer of cultured Tregs, isolated from IL-10(-/-) mice, into HT mice did not reduce SBP or NADPH oxidase activity or improve EDR. The incubation of MRA from HT mice with apocynin improved EDR, whereas NADPH oxidase substrate attenuated EDR in MRA from control mice, which was reversed with exogenous IL-10.
conclusionThese data demonstrate that IL-10 released from Tregs attenuates NADPH oxidase activity, which is a critical process in the improvement of microvascular endothelial function in hypertension, suggesting that Tregs/IL-10 could be a therapeutic target for treatment of vasculopathy in hypertension.
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