ArticleImmunity, inflammation and disease2022
Inhibiting P2Y12 receptor relieves LPS-induced inflammation and endothelial dysfunction.
Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Memory deficits in hypertensive ApoE4 mice reversed by P2Y12 inhibition via different mechanisms in males and perimenopausal females.Research square · 2025Article
- Role and recent progress of P2Y12 receptor in cancer development.Purinergic signalling · 2025Review
- How selective antagonists and genetic modification have helped characterise the expression and functions of vascular P2Y receptors.Purinergic signalling · 2025Review
- Potential pharmaceuticals targeting neuroimmune interactions in treating acute lung injury.Clinical and translational medicine · 2024Review
- Platelet P2YBritish journal of pharmacology · 2024Review
- The Signaling Pathway of the ADP Receptor P2YInternational journal of molecular sciences · 2023Review
- Inhibiting P2Y12 receptor relieves LPS-induced inflammation and endothelial dysfunction.Immunity, inflammation and disease · 2022Article
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1 author at 1 institution in 1 country.
Funding
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Abstract
backgroundAcute lung injury (ALI) is characterized by abnormal inflammatory response without effective therapies. P2Y12 receptor (P2Y12R) plays a vital role in inflammatory response. This study intends to explore whether P2Y12R antagonists can inhibit LPS-induced inflammatory injury of human pulmonary microvascular endothelial cells (HPMVECs) and endothelial cell dysfunction.
methodsUsing a cell model of ALI, the role of P2Y12R was investigated in LPS-induced HPMVECs. The expression of P2Y12R was detected by RT-qPCR and Western blot analysis assay and TNF-α, IL-1β, and IL-6 levels were analyzed by RT-qPCR. NO levels were also analyzed through NO kit. The levels of NF-κB p65, P-IκB-α, and IκB-α, as well as p-AKT and eNOS levels were detected by Western blot analysis assay. Wound healing assay was performed to evaluate HPMVECs migration. FITC-dextran was used to evaluate endothelial cell permeability, and the analysis of adherens junction protein VE-cadherin and endothelial cell tight junction proteins ZO-1, Claudin 5 and Occludin expression was performed by RT-qPCR and Western blot analysis assay.
resultsIn vitro, LPS increased the expression levels of P2Y12R and pro-inflammatory mediators (TNF-α, IL-1β, and IL-6), followed by a decrease in HPMVECs migration. In addition, LPS led to an increase in endothelial cell permeability. P2Y12R antagonists Ticagrelor or clopidogrel treatment significantly reversed these effects of LPS.
conclusionThe inhibitor of P2Y12R was able to decrease inflammatory response, promote migration and improve endothelial cell function and permeability, suggesting a key role of P2Y12R in ALI.
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