ArticleBritish journal of pharmacology2009
Endothelin-converting enzyme 1 promotes re-sensitization of neurokinin 1 receptor-dependent neurogenic inflammation.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Broadening the View: Substance P and Its Metabolism in Pruritus-Related Diseases.The Journal of dermatology · 2026Review
- Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets.Brain sciences · 2024Review
- Electroacupuncture Alleviates Diabetic Neuropathic Pain and Downregulates p-PKC and TRPV1 in Dorsal Root Ganglions and Spinal Cord Dorsal Horn.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Susceptibility ofFrontiers in pediatrics · 2022Article
- Neuroimmune Interaction: A Widespread Mutual Regulation and the Weapons for Barrier Organs.Frontiers in cell and developmental biology · 2022Review
- Neuroimmune Pathophysiology in Asthma.Frontiers in cell and developmental biology · 2021Review
- G-Protein-Coupled Receptors Are Dynamic Regulators of Digestion and Targets for Digestive Diseases.Gastroenterology · 2019Review
- Endothelin-converting enzyme 2 differentially regulates opioid receptor activity.British journal of pharmacology · 2015Article
- Endothelin-converting enzyme 1 and β-arrestins exert spatiotemporal control of substance P-induced inflammatory signals.The Journal of biological chemistry · 2014Article
- Opioid receptor function is regulated by post-endocytic peptide processing.The Journal of biological chemistry · 2014Article
- Neural peptidase endothelin-converting enzyme 1 regulates endothelin 1-induced pruritus.The Journal of clinical investigation · 2014Article
- Tachykinins and their receptors: contributions to physiological control and the mechanisms of disease.Physiological reviews · 2014Review
- Endothelin-converting enzymes degrade intracellular β-amyloid produced within the endosomal/lysosomal pathway and autophagosomes.The Journal of biological chemistry · 2013Article
- Roles of proteolysis in regulation of GPCR function.British journal of pharmacology · 2013Review
- Endothelin-converting enzymes and related metalloproteases in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2013Review
- Neurotensin-induced proinflammatory signaling in human colonocytes is regulated by β-arrestins and endothelin-converting enzyme-1-dependent endocytosis and resensitization of neurotensin receptor 1.The Journal of biological chemistry · 2012Article
- Do the urinary bladder and large bowel interact, in sickness or in health? ICI-RS 2011.Neurourology and urodynamics · 2012Review
- Desensitization, trafficking, and resensitization of the pituitary thyrotropin-releasing hormone receptor.Frontiers in neuroscience · 2012Article
- Endothelin-converting enzyme-1 regulates trafficking and signalling of the neurokinin 1 receptor in endosomes of myenteric neurones.The Journal of physiology · 2011Article
- Protein phosphatase 2A mediates resensitization of the neurokinin 1 receptor.American journal of physiology. Cell physiology · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeThe metalloendopeptidase endothelin-converting enzyme 1 (ECE-1) is prominently expressed in the endothelium where it converts big endothelin to endothelin-1, a vasoconstrictor peptide. Although ECE-1 is found in endosomes in endothelial cells, the role of endosomal ECE-1 is unclear. ECE-1 degrades the pro-inflammatory neuropeptide substance P (SP) in endosomes to promote recycling and re-sensitization of its neurokinin 1 (NK(1)) receptor. We investigated whether ECE-1 regulates NK(1) receptor re-sensitization and the pro-inflammatory effects of SP in the endothelium. EXPERIMENTAL APPROACH: We examined ECE-1 expression, SP trafficking and NK(1) receptor re-sensitization in human microvascular endothelial cells (HMEC-1), and investigated re-sensitization of SP-induced plasma extravasation in rats. KEY
resultsHMEC-1 expressed all four ECE-1 isoforms (a-d), and fluorescent SP trafficked to early endosomes containing ECE-1b/d. The ECE-1 inhibitor SM-19712 prevented re-sensitization of SP-induced Ca2+ signals in HMEC-1 cells. Immunoreactive ECE-1 and NK(1) receptors co-localized in microvascular endothelial cells in the rat. SP-induced extravasation of Evans blue in the urinary bladder, skin and ears of the rat desensitized when the interval between two SP injections was 10 min, and re-sensitized after 480 min. SM-19712 inhibited this re-sensitization. CONCLUSIONS AND IMPLICATIONS: By degrading endocytosed SP, ECE-1 promotes the recycling and re-sensitization of NK(1) receptors in endothelial cells, and thereby induces re-sensitization of the pro-inflammatory effects of SP. Thus, ECE-1 inhibitors may ameliorate the pro-inflammatory actions of SP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.