ArticleCNS neuroscience & therapeutics2017
The phosphoinositide-3 kinase signaling is involved in neuroinflammation in hypertensive rats.
Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- The brain-heart axis: effects of cardiovascular disease on the CNS and opportunities for central neuromodulation.Nature reviews. Neuroscience · 2026Review
- Aging aggravates cognitive dysfunction in spontaneously hypertensive rats by inducing cerebral microvascular endothelial dysfunction.PloS one · 2025Article
- Activation of Cannabinoid Type 2 Receptor in Microglia Reduces Neuroinflammation through Inhibiting Aerobic Glycolysis to Relieve Hypertension.Biomolecules · 2024Article
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- Effects and mechanism of renal denervation on ventricular arrhythmia after acute myocardial infarction in rats.BMC cardiovascular disorders · 2022Article
- ACE2 Rescues Impaired Autophagic Flux Through the PI3K/AKT Pathway After Subarachnoid Hemorrhage.Neurochemical research · 2022Article
- Influence of hypertension classification on hypertensive intracerebral hemorrhage location.Journal of clinical hypertension (Greenwich, Conn.) · 2021Article
- The Regulation Effect ofMediators of inflammation · 2021Review
- β-Arrestin1 Reduces Oxidative Stress via Nrf2 Activation in the Rostral Ventrolateral Medulla in Hypertension.Frontiers in neuroscience · 2021Article
- The Release of Nitric Oxide Is Involved in the β-Arrestin1-Induced Antihypertensive Effect in the Rostral Ventrolateral Medulla.Frontiers in physiology · 2021Article
- Gut microbiota and neuroinflammation in pathogenesis of hypertension: A potential role for hydrogen sulfide.Pharmacological research · 2020Review
- Angiotensin-Converting Enzyme 2 in the Rostral Ventrolateral Medulla Regulates Cholinergic Signaling and Cardiovascular and Sympathetic Responses in Hypertensive Rats.Neuroscience bulletin · 2019Article
- Spontaneous activities in baroreflex afferent pathway contribute dominant role in parasympathetic neurocontrol of blood pressure regulation.CNS neuroscience & therapeutics · 2018Article
- The phosphoinositide-3 kinase signaling is involved in neuroinflammation in hypertensive rats.CNS neuroscience & therapeutics · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsIt has been demonstrated that neuroinflammation is associated with cardiovascular dysfunction. The phosphoinositide-3 kinase (PI3K) signaling in the rostral ventrolateral medulla (RVLM), a key region for sympathetic outflow, is upregulated and contributes to increased blood pressure (BP) and sympathetic outflow in hypertension. This study was designed to determine the role of the PI3K signaling in neuroinflammation in the RVLM of hypertension.
methodsThe normotensive WKY rats were performed by intracisternal infusion of lipopolysaccharide (LPS) or angiotensin II (Ang II) for inducing neuroinflammation. Elisa was used to determine the level of proinflammatory cytokines. Western blot was employed to detect the protein expression of PI3K signaling pathway. Gene silencing of PI3K p110δ subunit and overexpression of angiotensin-converting enzyme 2 (ACE2) were realized by injecting related lentivirus into the RVLM.
resultsIn the spontaneously hypertensive rats (SHR), the PI3K signaling in the RVLM was upregulated compared with WKY, gene silencing of PI3K in the RVLM significantly reduced BP and renal sympathetic nerve activity (RSNA), but also decreased the levels of proinflammatory cytokines. In the WKY rats, central infusion of LPS and Ang II significantly elevated BP and RSNA, but also increased the levels of proinflammatory cytokines and PI3K signaling activation in the RVLM. These changes in the Ang II-induced hypertension were effectively prevented by gene silencing of PI3K in the RVLM. Furthermore, overexpression of ACE2 in the RVLM significantly attenuated high BP and neuroinflammation, as well as decreased the activation of PI3K signaling in hypertensive rats.
conclusionThis study suggests that the PI3K signaling in the RVLM is involved in neuroinflammation in hypertension and plays an important role in the renin-angiotensin system-mediated changes in neuroinflammation in the RVLM.
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