Modulation of Piezo1 influences human skin architecture and oxytocin expression

Abstract

ObjectiveThroughout our existence, the skin senses and analyses the mechanical forces imposed by the environment. In response to these environmental forces, skin can deform itself and achieve a biological response. The subsequent cutaneous plasticity emerges from mechanical properties arising from the collective action of the skin cells, particularly keratinocytes, that govern the tensile strength via cell‐to‐cell adhesions and via cell–matrix adhesion structures. In addition to serving as force‐bearing entities, keratinocytes respond to forces by activating signalling pathways to control their own fate and function. To detect and adapt to mechanical signals, keratinocytes possess a panel of sensory receptors and junctional intercellular structures. Mechanically activated ion channel Piezo1 has been described as a force sensor and as being involved in pleasant touch perception. In this study, relationships between Piezo1 modulation and oxytocin synthesis were investigated.MethodsThe expression of Piezo1 in the skin was studied and compared with the expression of TRPV1. Dooku1 antagonist and Jedi1 agonist were used to modulate Piezo1. The level of E‐cadherin and oxytocin was monitored in ex vivo skin biopsies by immunodetection.ResultsTaken together, our results illustrate the major role of mechanosensitive ion channel Piezo1 in skin barrier integrity, and in peripheral oxytocin synthesis in the skin.ConclusionIn conclusion, this study highlights the relationships between pleasant touch, soft touch and local oxytocin synthesis.

Disrupted Neural Regeneration in Dry Eye Secondary to Ankylosing Spondylitis—With a Theoretical Link between Piezo2 Channelopathy and Gateway Reflex, WDR Neurons, and Flare-Ups

“…Moreover, Piezo2 channelopathy is theorized to be the microinjury that increases the IL-6 level [13,20], so it could be considered to be the IL-6 amplifier. In addition, it is important to note that the allostatic acute stress is theorized to be invoked by osteocalcin [2] or oxytocin [17], and indeed recent research shows that Piezo1 modulation has a role in the upregulation of oxytocin synthesis [83]. In summary, the overstimulation of microenvironmental (e.g., muscle spindle, Merkel cell-neurite complex, encapsulated mechanoceptor neuron terminals in the facet joints) Piezo1-Piezo2 mechanostransduction under allostasis could lead to Piezo2 channelopathy at proprioceptive terminals or in sensory terminals contributing to proprioception, hence resulting in the impairment of the Piezo2-Piezo1 crosstalk in these compartmental micromilieus and the initiation of inflammatory reflexes.…”