Wound healing involves physical, chemical and immunological processes. Transient receptor potential (TRP) and other ion channels are implicated in epidermal re-epithelization. Ion movement across ion channels can induce transmembrane potential that leads to transepithelial potential (TEP) changes. TEP is present in epidermis surrounding the lesion decreases and induces an endogenous direct current generating an epithelial electric field (EF) that could be implicated in wound re-epithelialization. TRP channels are involved in the activation of immune cells during mainly the inflammatory phase of wound healing. The aim of the study was to review the mechanisms of ion channel involvement in wound healing in in vivo experiments in murine (mice, rats) and how can this process be influenced. This review used the latest results published in scientific journals over the last year and this year to date (1 January 2023-31 December 3000) in order to include the in-press articles. Some types of TRP channels, such as TRPV1, TRPV3 and TRPA1, are expressed in immune cells and can be activated by inflammatory mediators. The most beneficial effects in wound healing are produced using agonists of TRPV1, TRPV4 and TRPA1 channels or by inhibiting with antagonists, antisense oligonucleotides or knocking down TRPV3 and TRPM8 channels.

Transient Receptor Potential (TRP) channels, essential for sensing environmental stimuli, are widely distributed. Among them, thermosensory TRP channels play a crucial role in temperature sensing and regulation. Sebastes schlegelii, a significant aquatic economic species, exhibits sensitivity to temperature across multiple aspects. In this study, we identified 18 SsTRP proteins using whole-genome scanning. Motif analysis revealed motif 2 in all TRP proteins, with conserved motifs in subfamilies. TRP-related domains, anchored repeats, and ion-transmembrane domains were found. Chromosome analysis showed 18 TRP genes on 11 chromosomes and a scaffold. Phylogenetics classified SsTRPs into four subfamilies: TRPM, TRPA, TRPV, and TRPC. In diverse organisms, four monophyletic subfamilies were identified. Additionally, we identified key TRP genes with significantly upregulated transcription levels under short-term (30 min) and long-term (3 days) exposure at 24 °C (optimal elevated temperature) and 27 °C (critical high temperature). We propose that genes upregulated at 30 min may be involved in the primary response process of temperature sensing, while genes upregulated at 3 days may participate in the secondary response process of temperature perception. This study lays the foundation for understanding the regulatory mechanisms of TRPs responses to environmental stimuli in S. schlegelii and other fishes.

Quantification of the vasodilation after topical application of capsaicin or cinnamaldehyde is often implemented to indirectly assess Transient Receptor Potential (TRP) Vanilloid 1 (TRPV1) or Ankyrin 1 (TRPA1) functionality respectively. This method has been well-established on the human forearm. However, to enable TRP functionality assessments in distal peripheral neuropathy, the vascular response upon TRP activation on dorsal finger skin was characterized.
Two doses of cinnamaldehyde (3 % and 10 % v/v) and capsaicin (300 μg and 1000 μg) were topically applied (20 μL) on the skin of the mid three proximal phalanges in 17 healthy men. The dose-response, and inter-hand and inter-period reproducibility of the dermal blood flow (DBF) increase was assessed using Laser Speckle Contrast Imaging (LSCI) during 60 min post-application. Linear mixed models explored dose-driven differences, whereas the intra-class correlation coefficient (ICC) estimated the reproducibility of the vascular response.
Both doses of cinnamaldehyde and capsaicin induced a robust, dose-dependent increase in DBF. The vascular response to cinnamaldehyde 10 % on finger skin, expressed as area under the curve, correlated well over time (ICC = 0.66) and excellently between hands (ICC = 0.87). Similarly, the response to capsaicin 1000 μg correlated moderately over time (ICC = 0.50) and well between hands (ICC = 0.73).
The vascular response upon topical cinnamaldehyde and capsaicin application on finger skin is an alternative approach for measurements on forearm skin. Thereby, it is a promising vascular read-out to investigate the pathophysiology, and TRP involvement in particular, of specific peripheral neuropathic pain syndromes.

Ion channels play a crucial role in a wide range of biological processes, including cell cycle regulation and cancer progression. In particular, the transient receptor potential (TRP) family of channels has emerged as a promising therapeutic target due to its involvement in several stages of cancer development and dissemination. TRP channels are expressed in a large variety of cells and tissues, and by increasing cation intracellular concentration, they monitor mechanical, thermal, and chemical stimuli under physiological and pathological conditions. Some members of the TRP superfamily, namely vanilloid (TRPV), canonical (TRPC), melastatin (TRPM), and ankyrin (TRPA), have been investigated in different types of cancer, including breast, prostate, lung, and colorectal cancer. TRP channels are involved in processes such as cell proliferation, migration, invasion, angiogenesis, and drug resistance, all related to cancer progression. Some TRP channels have been mechanistically associated with the signaling of cancer pain. Understanding the cellular and molecular mechanisms by which TRP channels influence cancer provides new opportunities for the development of targeted therapeutic strategies. Selective inhibitors of TRP channels are under initial scrutiny in experimental animals as potential anti-cancer agents. In-depth knowledge of these channels and their regulatory mechanisms may lead to new therapeutic strategies for cancer treatment, providing new perspectives for the development of effective targeted therapies.

UNASSIGNED: Transient receptor potential (TRP) channels have been found to have significant implications in neuronal outgrowth, survival, inflammatory neurogenic pain, and various epileptogenic processes. Moreover, there is a growing body of evidence indicating that transient receptor potential (TRP) channels have a significant impact on epilepsy and its drug-resistant subtypes.
UNASSIGNED: We postulated that EGb 761 would modulate TRPA1 channels, thereby exhibiting anti-inflammatory and neuroprotective effects in a neuroblastoma cell line. Our rationale was to investigate the impact of EGb 761 in a controlled model of pentylenetetrazole-induced generalized epilepsy.
UNASSIGNED: We evaluated the neuroprotective, antioxidant and anti-apoptotic effects of EGb 761 both before and after the pentylenetetrazole application in a neuroblastoma cell line. Specifically, we focused on the effects of EGB 761 on the activity of Transient receptor potential (TRP) channels.
UNASSIGNED: EGb 761 applications both before and after the pentylenetetrazole incubation period reduced Ca release and restored apoptosis, ROS changes, mitochondrial depolarization and caspase levels, suggesting a prominent prophylactic and therapeutic effect of EGb 761 in the pentylenetetrazole-induced epileptogenesis process.
UNASSIGNED: Our basic mechanistic framework for elucidating the pathophysiological significance of fundamental ion mechanisms in a pentylenetetrazole treated neuroblastoma cell line provided compelling evidence for the favorable efficacy and safety profile of Egb 761 in human-relevant in vitro model of epilepsy. To the best of our knowledge, this is the first study to investigate the combined effects of EGb 761 and pentylenetetrazole on TRP channels and measure their activation level in a relevant model of human epileptic diseases.

High fat, western-style diets increase vascular oxidative stress. We hypothesized that smooth muscle cells and endothelial cells adapt during the consumption of high fat diets to become more resilient to acute oxidative stress. Male C57Bl/6J mice were fed a western-style diet high in fat and processed carbohydrates (WD), a high fat diet that induces obesity (DIO), or their respective control (CD) and standard (SD) diets for 16 weeks. Posterior cerebral arteries (PCAs) were isolated and pressurized for study. During acute exposure to H2O2 (200 µM), smooth muscle cell and endothelial cell death were reduced in PCAs from WD, but not DIO mice. WD selectively attenuated mitochondrial membrane potential depolarization and vessel wall Ca2+ influx during H2O2 exposure. Selective inhibition of transient receptor potential (TRP) V4 or TRPC3 channels reduced smooth muscle cell and endothelial cell death in concert with the vessel wall [Ca2+]i response to H2O2 for PCAs from CD mice and eliminated differences between CD and WD. Inhibiting Src kinases reduced smooth muscle cell death along with [Ca2+]i response to H2O2 only in PCAs from CD mice and eliminated differences between diets. However, Src kinase inhibition did not alter endothelial cell death. These findings indicate that consuming a WD, but not high fat alone, leads to adaptations that limit Ca2+ influx and vascular cell death during exposure to acute oxidative stress.

The perception of pungency can be attributed to the combination of pain and heat, and it has critical impacts on food flavor and food consumption preferences. Many studies have reported a variety of pungent ingredients with different Scoville heat units (SHU), and the mechanism of pungent perception was revealed in vivo and in vitro. The worldwide use of spices containing pungent ingredients has led to an increasing awareness of their effects on basic tastes. However, the interaction between basic tastes and pungency perception based on structure-activity relationship, taste perception mechanism and neurotransmission lacks review and summary, considering its brighter prospects in food flavor. Thus, in this review, common pungency substances and pungency evaluation methods, and the mechanism of pungency perception is presented, and the interaction between basic tastes and pungency perception and the possible factors of their interaction are reviewed in detail. Pungent stimuli are mainly transduced through transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential fixed hormone isoform (TRPA1) activated by stimulants. Using modern detection techniques combined with sensory standards, different substances produce different degrees of pungent stimulation, ranging from 104 to 107 SHU/g. Pungent stimuli can affect taste receptor or channel protein conformation and regulate taste bud cell sensitivity by producing neurotransmission products. The products of neurotransmission and taste receptor cell activation in turn act on taste perception. When there are simultaneous effects of taste perception, pungency stimulation may enhance the perception of salty at a certain concentration, with a mutual inhibition effect with sour, sweet, and bitter taste, while its interaction with umami taste is not obvious. However, due to the complexity of perception and the uncertainty of many perceptual receptors or channels, the current studies of interactions are still controversial. Based on the understanding of the mechanism and influencing factors, the availability of pungency substances is proposed in the perspective of food industry in order to achieve new development.

Maintaining the correct ionic gradient from extracellular to intracellular space via several membrane-bound transporters is critical for maintaining overall cellular homeostasis. One of these transporters is the transient receptor potential (TRP) channel family that consists of six putative transmembrane segments systemically expressed in mammalian tissues. Upon the activation of TRP channels by brain disease, several cations are translocated through TRP channels. Brain disease, especially ischemic stroke, epilepsy, and traumatic brain injury, triggers the dysregulation of ionic gradients and promotes the excessive release of neuro-transmitters and zinc. The divalent metal cation zinc is highly distributed in the brain and is specifically located in the pre-synaptic vesicles as free ions, usually existing in cytoplasm bound with metallothionein. Although adequate zinc is essential for regulating diverse physiological functions, the brain-disease-induced excessive release and translocation of zinc causes cell damage, including oxidative stress, apoptotic cascades, and disturbances in energy metabolism. Therefore, the regulation of zinc homeostasis following brain disease is critical for the prevention of brain damage. In this review, we summarize recent experimental research findings regarding how TRP channels (mainly TRPC and TRPM) and zinc are regulated in animal brain-disease models of global cerebral ischemia, epilepsy, and traumatic brain injury. The blockade of zinc translocation via the inhibition of TRPC and TRPM channels using known channel antagonists, was shown to be neuroprotective in brain disease. The regulation of both zinc and TRP channels may serve as targets for treating and preventing neuronal death.

As one of the most prevalent and disabling brain disorders, epilepsy is characterized by spontaneous seizures that result from aberrant, excessive hyperactivity of a group of highly synchronized brain neurons. Remarkable progress in epilepsy research and treatment over the first two decades of this century led to a dramatical expansion in the third-generation antiseizure drugs (ASDs). However, there are still over 30% of patients suffering from seizures resistant to the current medications, and the broad unbearable adversative effects of ASDs significantly impair the quality of life in about 40% of individuals affected by the disease. Prevention of epilepsy in those who are at high risks is another major unmet medical need, given that up to 40% of epilepsy patients are believed to have acquired causes. Therefore, it is important to identify novel drug targets that can facilitate the discovery and development of new therapies engaging unprecedented mechanisms of action that might overcome these significant limitations. Also over the last two decades, calcium signaling has been increasingly recognized as a key contributory factor in epileptogenesis of many aspects. The intracellular calcium homeostasis involves a variety of calcium-permeable cation channels, the most important of which perhaps are the transient receptor potential (TRP) ion channels. This review focuses on recent exciting advances in understanding of TRP channels in preclinical models of seizure disorders. We also provide emerging insights into the molecular and cellular mechanisms of TRP channels-engaged epileptogenesis that might lead to new antiseizure therapies, epilepsy prevention and modification, and even a cure.

Transient receptor potential (TRP) proteins are a large group of ion channels that control many physiological functions in our body. These channels are considered potential therapeutic drug targets for various diseases such as neurological disorders, cancers, cardiovascular disease, and many more. The Nobel Prize in Physiology/Medicine in the year 2021 was awarded to two scientists for the discovery of TRP and PIEZO ion channels. Improving our knowledge of technologies for their study is essential. In the present study, we reviewed the role of TRP channel types in the control of normal physiological functions as well as disease conditions. Also, we discussed the current and novel technologies that can be used to study these channels successfully. As such, Flux assays for detecting ionic flux through ion channels are among the core and widely used tools for screening drug compounds. Technologies based on these assays are available in fully automated high throughput set-ups and help detect changes in radiolabeled or non-radiolabeled ionic flux. Aurora\'s Ion Channel Reader (ICR), which works based on label-free technology of flux assay, offers sensitive, accurate, and reproducible measurements to perform drug ranking matching with patch-clamp (gold standard) data. The non-radiolabeled trace-based flux assay coupled with the ICR detects changes in various ion types, including potassium, calcium, sodium, and chloride channels, by using appropriate tracer ions. This technology is now considered one of the very successful approaches for analyzing ion channel activity in modern drug discovery. It could be a successful approach for studying various ion channels and transporters, including the different members of the TRP family of ion channels.