Biology subjects

Derouiche, S.

Publications and source records attributed to Derouiche, S..

3 recordsLinked to original sources

bioRxiv2023

Involvement of TRPV4 in temperature-dependent perspiration in mice

Reports indicate that an interaction between TRPV4 and anoctamin 1 could be widely involved in water efflux of exocrine glands, suggesting that the interaction could play a role in perspiration. In secretory cells of sweat glands present in mouse foot pads, TRPV4 clearly colocalized with cytokeratin 8, anoctamin 1 (ANO1) and aquaporin-5 (AQP5). Mouse sweat glands showed TRPV4-dependent cytosolic Ca2+ increases that was inhibited by menthol. Acetylcholine-stimulated sweating in foot pads was temperature-dependent in wild-type, but not in TRPV4-deficient mice, and was inhibited by menthol both in wild-type and TRPM8KO mice. The basal sweating without acetylcholine stimulation was inhibited by an ANO1 inhibitor. Sweating could be important for maintaining friction forces in mouse foot pads, and this possibility is supported by the finding that wild-type mice climbed up a slippery slope more easily than TRPV4-deleted mice. Furthermore, TRPV4 expression was significantly higher in controls and normohidrotic skin from patients with AIGA (acquired idiopathic generalized anhidrosis) compared to anhidrotic skin from patients with AIGA. Collectively, TRPV4 is likely involved in temperature-dependent perspiration via interactions with ANO1, and TRPV4 itself or the TRPV4/ANO 1 complex would be targets to develop agents that regulate perspiration.

physiology↗

bioRxiv2020

Lipooligosaccharide, Vag8, and pertussis toxin of Bordetella pertussis cooperatively cause coughing in mice

Whooping cough, a contagious respiratory disease caused by Bordetella pertussis, is characterized by paroxysmal coughing; however, the mechanism has not been studied because of the lack of versatile animal models that reproduce the cough. Here, we present a mouse model that reproduces coughing after intranasal inoculation with the bacteria or its components and demonstrate that lipooligosaccharide (LOS), pertussis toxin (PTx), and Vag8 of the bacteria cooperatively function to cause coughing. LOS-induced bradykinin sensitized a transient receptor potential ion channel, TRPV1, which acts as a sensor to evoke the cough reflex. Vag8 further increased bradykinin levels by inhibiting the C1 esterase inhibitor, the major downregulator of the contact system, which generates bradykinin. PTx inhibits intrinsic negative regulation systems for TRPV1 through inactivation of Gi GTPases. Our findings provide a basis for answering long-standing questions on the pathophysiology of the pertussis cough.

microbiology↗

bioRxiv2020

Inhibition of TRPV1 and TRPA1 by mosquito and mouse saliva

Arthropods are the largest group of living organisms and among them, mosquitoes spread parasites and viruses causing deathly diseases. Mosquitos painless piercing is due to the thinness of their fascicle, but mosquito saliva might also contribute to it. We found that mosquito and mouse saliva inhibit TRPV1 and TRPA1 channels, either heterologously expressed in HEK293T cells or endogenously expressed in native mouse sensory neurons. We have also identified sialorphin as a candidate antinociceptive peptide as it showed similar effects on TRPV1 and TRPA1. Finally, we confirmed the antinociceptive effects of saliva and sialorphin in vivo by observing decreased pain-related behaviors in mice coinjected with these substances. Similar inhibitory effects of mosquito and mouse saliva suggest that the antinociceptive effects of saliva are universal, which could explain why many animals including humans often lick their wounds. These findings would lead to the development of novel anti-nociceptive agents.

cell biology↗