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Merkel cells as putative regulatory cells in skin disorders: an in vitro study. | LitMetric

AI Article Synopsis

  • Merkel cells (MCs) have a role in both sensing mechanical changes and potentially influencing skin disorders through the release of neuropeptides and hormones.
  • In a new culture model with swine MCs, researchers found that MCs can proliferate and respond to bFGF by extending, but not to neurotrophins, indicating that these growth factors do not promote MC growth.
  • The study revealed that MCs can release vasoactive intestinal peptide (VIP) in response to certain stimuli; this release does not depend on calcium, suggesting that mechanisms for neuropeptide release and neurotransmitter exocytosis are distinct and may be regulated differently.

Article Abstract

Merkel cells (MCs) are involved in mechanoreception, but several lines of evidence suggest that they may also participate in skin disorders through the release of neuropeptides and hormones. In addition, MC hyperplasias have been reported in inflammatory skin diseases. However, neither proliferation nor reactions to the epidermal environment have been demonstrated. We established a culture model enriched in swine MCs to analyze their proliferative capability and to discover MC survival factors and modulators of MC neuroendocrine properties. In culture, MCs reacted to bFGF by extending outgrowths. Conversely, neurotrophins failed to induce cell spreading, suggesting that they do not act as a growth factor for MCs. For the first time, we provide evidence of proliferation in culture through Ki-67 immunoreactivity. We also found that MCs reacted to histamine or activation of the proton gated/osmoreceptor TRPV4 by releasing vasoactive intestinal peptide (VIP). Since VIP is involved in many pathophysiological processes, its release suggests a putative regulatory role for MCs in skin disorders. Moreover, in contrast to mechanotransduction, neuropeptide exocytosis was Ca(2+)-independent, as inhibition of Ca(2+) channels or culture in the absence of Ca(2+) failed to decrease the amount of VIP released. We conclude that neuropeptide release and neurotransmitter exocytosis may be two distinct pathways that are differentially regulated.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722079PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006528PLOS

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