Role of Transient Receptor Potential Vanilloid 4 for the Development of Acute Lung Injury in Pneumococcal Pneumonia

In addition to the sense of taste and olfaction, chemesthesis, the sensation of irritation, pungency, cooling, warmth, or burning elicited by spices and herbs, plays a central role in food consumption. Many plant-derived molecules demonstrate their chemesthetic properties via the opening of transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential vanilloid 1 (TRPV1) channels. TRPA1 and TRPV1 are structurally related thermosensitive cation channels and are often co-expressed in sensory nerve endings. TRPA1 and TRPV1 can also indirectly influence some, but not all, primary taste qualities via the release of substance P and calcitonin gene-related peptide (CGRP) from trigeminal neurons and their subsequent effects on CGRP receptor expressed in Type III taste receptor cells. Here, we will review the effect of some chemesthetic agonists of TRPA1 and TRPV1 and their influence on bitter, sour, and salt taste qualities.

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Transient Receptor Potential Vanilloid 4 and Serum Glucocorticoid–regulated Kinase 1 Are Critical Mediators of Lung Injury in Overventilated Mice In Vivo

Anesthesiology ◽

10.1097/aln.0000000000001443 ◽

2017 ◽

Vol 126 (2) ◽

pp. 300-311 ◽

Cited By ~ 24

Author(s):

Laura Michalick ◽

Lasti Erfinanda ◽

Ulrike Weichelt ◽

Markus van der Giet ◽

Wolfgang Liedtke ◽

...

Keyword(s):

Lung Injury ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Cyclic Stretch ◽

Proximity Ligation Assay ◽

Functional Coupling ◽

Transient Receptor Potential Vanilloid ◽

Ventilator Induced Lung Injury ◽

Barrier Failure ◽

Transient Receptor

Abstract Background Mechanical ventilation can cause lung endothelial barrier failure and inflammation cumulating in ventilator-induced lung injury. Yet, underlying mechanotransduction mechanisms remain unclear. Here, the authors tested the hypothesis that activation of the mechanosensitive Ca2+ channel transient receptor potential vanilloid (TRPV4) by serum glucocorticoid–regulated kinase (SGK) 1 may drive the development of ventilator-induced lung injury. Methods Mice (total n = 54) were ventilated for 2 h with low (7 ml/kg) or high (20 ml/kg) tidal volumes and assessed for signs of ventilator-induced lung injury. Isolated-perfused lungs were inflated with continuous positive airway pressures of 5 or 15 cm H2O (n = 7 each), and endothelial calcium concentration was quantified by real-time imaging. Results Genetic deficiency or pharmacologic inhibition of TRPV4 or SGK1 protected mice from overventilation-induced vascular leakage (reduction in alveolar protein concentration from 0.84 ± 0.18 [mean ± SD] to 0.46 ± 0.16 mg/ml by TRPV4 antagonization), reduced lung inflammation (macrophage inflammatory protein 2 levels of 193 ± 163 in Trpv4−/−vs. 544 ± 358 pmol/ml in wild-type mice), and attenuated endothelial calcium responses to lung overdistension. Functional coupling of TRPV4 and SGK1 in lung endothelial mechanotransduction was confirmed by proximity ligation assay demonstrating enhanced TRPV4 phosphorylation at serine 824 at 18% as compared to 5% cyclic stretch, which was prevented by SGK1 inhibition. Conclusions Lung overventilation promotes endothelial calcium influx and barrier failure through a mechanism that involves activation of TRPV4, presumably due to phosphorylation at its serine 824 residue by SGK1. TRPV4 and SGK1 may present promising new targets for prevention or treatment of ventilator-induced lung injury.

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Streptozotocin-Induced Early Thermal Hyperalgesia is Independent of Glycemic State of Rats: Role of Transient Receptor Potential Vanilloid 1(TRPV1) and Inflammatory Mediators

Molecular Pain ◽

10.1186/1744-8069-7-52 ◽

2011 ◽

Vol 7 ◽

pp. 1744-8069-7-52 ◽

Cited By ~ 63

Author(s):

Mahendra Bishnoi ◽

Christine A Bosgraaf ◽

uvil Abooj ◽

Linlin Zhong ◽

Louis S Premkumar

Keyword(s):

Inflammatory Mediators ◽

Transient Receptor Potential ◽

Thermal Hyperalgesia ◽

Receptor Potential ◽

Transient Receptor Potential Vanilloid ◽

Transient Receptor

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Transient Receptor Potential Vanilloid in the Brain Gliovascular Unit: Prospective Targets in Therapy

Pharmaceutics ◽

10.3390/pharmaceutics13030334 ◽

2021 ◽

Vol 13 (3) ◽

pp. 334

Author(s):

Huilong Luo ◽

Xavier Declèves ◽

Salvatore Cisternino

Keyword(s):

Transient Receptor Potential ◽

Receptor Potential ◽

Brain Diseases ◽

Transient Receptor Potential Vanilloid ◽

Main Role ◽

Trpv Channels ◽

Gliovascular Unit ◽

Transient Receptor ◽

The Brain

The gliovascular unit (GVU) is composed of the brain microvascular endothelial cells forming blood–brain barrier and the neighboring surrounding “mural” cells (e.g., pericytes) and astrocytes. Modulation of the GVU/BBB features could be observed in a variety of vascular, immunologic, neuro-psychiatric diseases, and cancers, which can disrupt the brain homeostasis. Ca2+ dynamics have been regarded as a major factor in determining BBB/GVU properties, and previous studies have demonstrated the role of transient receptor potential vanilloid (TRPV) channels in modulating Ca2+ and BBB/GVU properties. The physiological role of thermosensitive TRPV channels in the BBB/GVU, as well as their possible therapeutic potential as targets in treating brain diseases via preserving the BBB are reviewed. TRPV2 and TRPV4 are the most abundant isoforms in the human BBB, and TRPV2 was evidenced to play a main role in regulating human BBB integrity. Interspecies differences in TRPV2 and TRPV4 BBB expression complicate further preclinical validation. More studies are still needed to better establish the physiopathological TRPV roles such as in astrocytes, vascular smooth muscle cells, and pericytes. The effect of the chronic TRPV modulation should also deserve further studies to evaluate their benefit and innocuity in vivo.

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