P2X7 receptor is involved in lung injuries induced by ischemia-reperfusion in pulmonary arterial hypertension rats
Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease that ultimately leads to right heart failure and death. Current strategies are ineffective to prevent and cure PAH, especially in those who undergo cardiopulmonary bypass. P2 × 7 receptors (P2 × 7Rs) have been implied to participate in the pathogenesis of PAH and injuries induced by ischemia-reperfusion (IR). In the present study, we aimed to assess the potential therapeutic effects of anti-P2 × 7Rs on PAH and IR-induced lung injuries in rats and explore their underlying cellular and molecular mechanisms. In the present study, we have successfully established rat models with PAH and/or lung IR injuries. Immunohistochemical staining, western blot, and polymerase chain reaction were performed to detect the P2 × 7R expression in these models; P2 × 7R-specific inhibitor, Brilliant Blue G (BBG), was used to antagonize P2 × 7R, and enzyme-linked immunosorbent assay was used to help evaluate the P2 × 7R-mediated function in PAH with or without IR. Moreover, BBG, SB203580 (p38/MAPK inhibitor), and CD39 (adenosine triphosphate hydrolase) were applied to explore the inner signal pathway in vitro and in vivo. Our findings showed that P2 × 7R was involved in the development of PAH. By applying BBG, we have shown that the severity of PAH and IR was ameliorated through reducing the release of proinflammatory cytokines. Moreover, our results in vitro and in vivo indicated that P2 × 7R regulated the release of inflammatory mediators by the p38/MAPK signal pathway. Most important, CD39 showed the most dominant potential in improving inflammation in lung injuries caused by PAH and IR. In conclusion, the inhibition of P2 × 7R could effectively attenuate inflammation in lung injuries caused by PAH and IR in rats by reducing proinflammatory cytokines through regulating the p38/MAPK pathway.
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P2X7 receptor expression deletion appears to be beneficial in acute lung injury, asthma, lung inflammation, and fibrosis.
“In addition, P2X7 receptor expression deletion appears to be beneficial in case of acute lung injury, asthma, lung inflammation, and fibrosis [87–91].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [88]
P2X7 receptor knockout mice submitted to a model of lung fibrosis revealed reduced infiltration of inflammatory cells, cytokine release, apoptosis, and fibrosis, while P2X7 receptor agonists increased these deleterious processes.
“In addition, P2X7 receptor knockout mice submitted to a model of lung fibrosis revealed reduced infiltration of inflammatory cells, cytokine release, apoptosis, and fibrosis, while P2X7 receptor agonists increased these deleterious processes [88, 107].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [88]
Inhibition of the P2X7 receptor might decrease pathological traits mediated by the RAAS pressor axis and protect against brain and lung injury in COVID-19 patients.
“Since the P2X7 receptor is also involved in lung damage [87–89], neurodegenerative and psychiatric disorders [92, 95, 118], the hypothesis is reasonable that inhibition of this receptor might decrease pathological traits mediated by the RAAS pressor axis and protect against brain and lung injury in COVID-19 patients.”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [88]
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- Authors
- Duan, L., Hu, G.-H., Li, Y.-J., Zhang, C.-L., & Jiang, M.
- Affiliations
- Central South University (CN)
- Hunan Normal University (CN)
- Corresponding author
- Duan, Lian
- ORCID
- Jiang, Meng
- Venue
- Molecular Immunology
- Publisher
- Elsevier BV
- Published
- 2018-09
- Volume
- 101
- Pages
- 409-418
- ISSN
- 0161-5890 (ISSN-L)
- OpenAlex
- W2887229332
- Cited by
- 23
- References
- 52
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 4 · 2021: 6 · 2020: 8 · 2019: 1
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Hunan Provincial Science and Technology Department (2013SK3004)
- Natural Science Foundation of Hunan Province (13JJ3016)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Keywords
- P2X7 receptor, pulmonary arterial hypertension, lung ischemia-reperfusion injury, Brilliant Blue G, p38 MAPK signaling, CD39, inflammatory cytokines, lung inflammation, cardiopulmonary bypass
- MeSH terms
- Animals, Disease Models, Animal, Humans, Hypertension, Pulmonary, Pulmonary Artery, Reperfusion Injury, Cytokines, Monocrotaline, Rats, Sprague-Dawley, Inflammation Mediators, MAP Kinase Signaling System, Lung Injury, Receptors, Purinergic P2X7, Purinergic P2X Receptor Antagonists
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