Immunohistochemical detection of PIEZO1 and PIEZO2 in human digital Meissner´s corpuscles

Abstract

Background: The cutaneous end organ complexes or cutaneous sensory corpuscles are specialized sensory organs associated to low-threshold mechanoreceptors. Mechano-gated proteins forming a part of ion channels have been detected in both the axon and terminal glial cells of Meissner corpuscles, a specific cutaneous end organ complex in the human glabrous skin. The main candidates to mechanotransduction in Meissner corpuscles are members of the Piezo family of cationic ion channels. PIEZO2 has been detected in the axon of these sensory structures whereas no data exists about the occurrence and cell localization of PIEZO1. Methods: Skin samples (n = 18) from the palmar aspect of the distal phalanx of the first and second fingers were analysed (8 female and 10 males; age range 26 to 61 26–61 years). Double immunofluorescence for PIEZO1 and PIEZO2 together with axonal or terminal glial cell markers was captured by laser confocal microscopy, and the percentage of PIEZOs positive Meissner corpuscles was evaluated. Results: MCs from human fingers showed variable morphology and degree of lobulation. Regarding the basic immunohistochemical profile, in all cases the axons were immunoreactive for neurofilament proteins, neuron specific enolase and synaptophysin, while the lamellar cells displayed strong S100P immunoreactivity. PIEZO1 was detected co-localizing with axonal markers, but never with terminal glial cell markers, in the 56% of Meissner corpuscles; weak but specific immunofluorescence was additionally detected in the epidermis, especially in basal keratinocytes. Similarly, PIEZO2 immunoreactivity was found restricted to the axon in the 85% of Meissner corpuscles. PIEZO2 positive Merkel cells were also regularly found. Conclusions: PIEZO1 and PIEZO2 are expressed exclusively in the axon of a subpopulation of human digital Meissner corpuscles, thus suggesting that not only PIEZO2, but also PIEZO1 may be involved in the mechanotransduction from low-threshold mechanoreceptors. © 2023 The Authors