scholarly journals Transcriptional profiling reveals potential involvement of microvillous TRPM5-expressing cells in viral infection of the olfactory epithelium

2020 ◽  
Author(s):  
B. Dnate’ Baxter ◽  
Eric D. Larson ◽  
Laetitia Merle ◽  
Paul Feinstein ◽  
Arianna Gentile Polese ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Viral Infection ◽  
Olfactory Epithelium ◽  
Transient Receptor Potential ◽  
Transcriptional Profiling ◽  
Receptor Potential ◽  
Olfactory Nerve ◽  
Brush Cells ◽  
Solitary Chemosensory Cells ◽  
Transient Receptor

AbstractBackgroundUnderstanding viral infection of the olfactory epithelium is essential because the olfactory nerve is an important route of entry for viruses to the central nervous system. Specialized chemosensory epithelial cells that express the transient receptor potential cation channel subfamily M member 5 (TRPM5) are found throughout the airways and intestinal epithelium and are involved in responses to viral infection.ResultsHerein we performed deep transcriptional profiling of olfactory epithelial cells sorted by flow cytometry based on the expression of mCherry as a marker for olfactory sensory neurons and for eGFP in OMP-H2B::mCherry/TRPM5-eGFP transgenic mice (Mus musculus). We find profuse expression of transcripts involved in inflammation, immunity and viral infection in TRPM5-expressing microvillous cells.ConclusionOur study provides new insights into a potential role for TRPM5-expressing microvillous cells in viral infection of the olfactory epithelium. We find that, as found for solitary chemosensory cells (SCCs) and brush cells in the airway epithelium, and for tuft cells in the intestine, the transcriptome of TRPM5-expressing microvillous cells indicates that they are likely involved in the inflammatory response elicited by viral infection of the olfactory epithelium.

scholarly journals Transcriptional profiling reveals potential involvement of microvillous TRPM5-expressing cells in viral infection of the olfactory epithelium

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
B. Dnate’ Baxter ◽  
Eric D. Larson ◽  
Laetitia Merle ◽  
Paul Feinstein ◽  
Arianna Gentile Polese ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Viral Infection ◽  
Sensory Neurons ◽  
Olfactory Epithelium ◽  
Transient Receptor Potential ◽  
Transcriptional Profiling ◽  
Receptor Potential ◽  
Olfactory Nerve ◽  
Olfactory Sensory Neurons ◽  
Brush Cells

Abstract Background Understanding viral infection of the olfactory epithelium is essential because the olfactory nerve is an important route of entry for viruses to the central nervous system. Specialized chemosensory epithelial cells that express the transient receptor potential cation channel subfamily M member 5 (TRPM5) are found throughout the airways and intestinal epithelium and are involved in responses to viral infection. Results Herein we performed deep transcriptional profiling of olfactory epithelial cells sorted by flow cytometry based on the expression of mCherry as a marker for olfactory sensory neurons and for eGFP in OMP-H2B::mCherry/TRPM5-eGFP transgenic mice (Mus musculus). We find profuse expression of transcripts involved in inflammation, immunity and viral infection in TRPM5-expressing microvillous cells compared to olfactory sensory neurons. Conclusion Our study provides new insights into a potential role for TRPM5-expressing microvillous cells in viral infection of the olfactory epithelium. We find that, as found for solitary chemosensory cells (SCCs) and brush cells in the airway epithelium, and for tuft cells in the intestine, the transcriptome of TRPM5-expressing microvillous cells indicates that they are likely involved in the inflammatory response elicited by viral infection of the olfactory epithelium.

TRPC1 functions as a store-operated Ca2+ channel in intestinal epithelial cells and regulates early mucosal restitution after wounding

2006 ◽  
Vol 290 (4) ◽  
pp. G782-G792 ◽  
Author(s):  
Jaladanki N. Rao ◽  
Oleksandr Platoshyn ◽  
Vera A. Golovina ◽  
Lan Liu ◽  
Tongtong Zou ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Transient Receptor Potential ◽  
Intestinal Epithelial Cells ◽  
Critical Role ◽  
Receptor Potential ◽  
Mucosal Injury ◽  
Intestinal Epithelial ◽  
Epithelial Restitution ◽  
Transient Receptor

An increase in cytosolic free Ca2+ concentration ([Ca2+]cyt) results from Ca2+ release from intracellular stores and extracellular Ca2+ influx through Ca2+-permeable ion channels and is crucial for initiating intestinal epithelial restitution to reseal superficial wounds after mucosal injury. Capacitative Ca2+ entry (CCE) induced by Ca2+ store depletion represents a major Ca2+ influx mechanism, but the exact molecular components constituting this process remain elusive. This study determined whether canonical transient receptor potential (TRPC)1 served as a candidate protein for Ca2+-permeable channels mediating CCE in intestinal epithelial cells and played an important role in early epithelial restitution. Normal intestinal epithelial cells (the IEC-6 cell line) expressed TRPC1 and TPRC5 and displayed typical records of whole cell store-operated Ca2+ currents and CCE generated by Ca2+ influx after depletion of intracellular stores. Induced TRPC1 expression by stable transfection with the TRPC1 gene increased CCE and enhanced cell migration during restitution. Differentiated IEC-Cdx2L1 cells induced by forced expression of the Cdx2 gene highly expressed endogenous TRPC1 and TRPC5 and exhibited increased CCE and cell migration. Inhibition of TRPC1 expression by small interfering RNA specially targeting TRPC1 not only reduced CCE but also inhibited cell migration after wounding. These findings strongly suggest that TRPC1 functions as store-operated Ca2+ channels and plays a critical role in intestinal epithelial restitution by regulating CCE and intracellular [Ca2+]cyt.

scholarly journals Thermosensitive transient receptor potential channels in human corneal epithelial cells

2011 ◽  
Vol 226 (7) ◽  
pp. 1828-1842 ◽  
Author(s):  
Stefan Mergler ◽  
Fabian Garreis ◽  
Monika Sahlmüller ◽  
Peter S. Reinach ◽  
Friedrich Paulsen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Human Corneal Epithelial Cells ◽  
Potential Channels ◽  
Transient Receptor

PAR-2 activation enhances weak acid-induced ATP release through TRPV1 and ASIC sensitization in human esophageal epithelial cells

2015 ◽  
Vol 309 (8) ◽  
pp. G695-G702 ◽  
Author(s):  
Liping Wu ◽  
Tadayuki Oshima ◽  
Jing Shan ◽  
Hiroo Sei ◽  
Toshihiko Tomita ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Transient Receptor Potential ◽  
Atp Release ◽  
Receptor Potential ◽  
Weak Acid ◽  
Transient Receptor Potential Vanilloid ◽  
Esophageal Epithelial Cells ◽  
Transient Receptor ◽  
Esophageal Hypersensitivity ◽  
Interfering Rna

Esophageal visceral hypersensitivity has been proposed to be the pathogenesis of heartburn sensation in nonerosive reflux disease. Protease-activated receptor-2 (PAR-2) is expressed in human esophageal epithelial cells and is believed to play a role in inflammation and sensation. PAR-2 activation may modulate these responses through adenosine triphosphate (ATP) release, which is involved in transduction of sensation and pain. The transient receptor potential vanilloid receptor 1 (TRPV1) and acid-sensing ion channels (ASICs) are both acid-sensitive nociceptors. However, the interaction among these molecules and the mechanisms of heartburn sensation are still not clear. We therefore examined whether ATP release in human esophageal epithelial cells in response to acid is modulated by TRPV1 and ASICs and whether PAR-2 activation influences the sensitivity of TRPV1 and ASICs. Weak acid (pH 5) stimulated the release of ATP from primary human esophageal epithelial cells (HEECs). This effect was significantly reduced after pretreatment with 5-iodoresiniferatoxin (IRTX), a TRPV1-specific antagonist, or with amiloride, a nonselective ASIC blocker. TRPV1 and ASIC3 small interfering RNA (siRNA) transfection also decreased weak acid-induced ATP release. Pretreatment of HEECs with trypsin, tryptase, or a PAR-2 agonist enhanced weak acid-induced ATP release. Trypsin treatment led to the phosphorylation of TRPV1. Acid-induced ATP release enhancement by trypsin was partially blocked by IRTX, amiloride, or a PAR-2 antagonist. Conversely, acid-induced ATP release was augmented by PAR-2 activation through TRPV1 and ASICs. These findings suggested that the pathophysiology of heartburn sensation or esophageal hypersensitivity may be associated with the activation of PAR-2, TRPV1, and ASICs.

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