Ryanodine Receptors Are Expressed in Epidermal Keratinocytes and Associated with Keratinocyte Differentiation and Epidermal Permeability Barrier Homeostasis

Denda, Sumiko; Kumamoto, Junichi; Takei, Kentaro; Tsutsumi, Moe; Aoki, Hideaki; Denda, Mitsuhiro

doi:10.1038/jid.2011.256

Cited by 27 publications

(25 citation statements)

References 31 publications

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“…This Ca 2+ gradient depends on a competent epidermal barrier (Mauro et al, 1998; Menon and Elias, 1991; Menon et al, 1994), which in turn is formed by keratinocyte Ca 2+ uptake, release, and influx (Feingold and Denda, 2012; Hu et al, 2000; Man et al, 1997). Studies from our group (Celli et al, 2010) and others (Adams et al, 2012; Cornelissen et al, 2007; Denda et al, 2012) have identified intracellular, rather than extracellular, calcium stores as the main components of the epidermal calcium gradient, and shown that ER Ca 2+ release alone can control barrier repair processes (Celli et al, 2011). …”

Section: Introductionmentioning

confidence: 98%

Endoplasmic Reticulum Calcium Regulates Epidermal Barrier Response and Desmosomal Structure

Celli

Crumrine

Meyer

et al. 2016

Journal of Investigative Dermatology

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Ca2+ fluxes direct keratinocyte differentiation, cell-to-cell adhesion, migration, and epidermal barrier homeostasis. We previously showed that intracellular Ca2+ stores constitute a major portion of the calcium gradient especially in the stratum granulosum. Loss of the calcium gradient triggers epidermal barrier homeostatic responses. In this report, using unfixed ex vivo epidermis and human epidermal equivalents we show that endoplasmic reticulum (ER) Ca2+ is released in response to barrier perturbation, and that this release constitutes the major shift in epidermal Ca2+ seen after barrier perturbation. We find that ER Ca2+ release correlates with a transient increase in extracellular Ca2+. Lastly, we show that ER calcium release resulting from barrier perturbation triggers transient desmosomal remodeling, seen as an increase in extracellular space and a loss of the desmosomal intercellular midline. Topical application of thapsigargin, which inhibits the ER Ca2+ ATPase activity without compromising barrier integrity, also leads to desmosomal remodeling and loss of the midline structure. These experiments establish the ER Ca2+ store as a master regulator of the Ca2+ gradient response to epidermal barrier perturbation, and suggest that ER Ca2+ homeostasis also modulates normal desmosomal reorganization, both at rest and after acute barrier perturbation.

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Section: Introductionmentioning

confidence: 98%

Endoplasmic Reticulum Calcium Regulates Epidermal Barrier Response and Desmosomal Structure

Celli

Crumrine

Meyer

et al. 2016

Journal of Investigative Dermatology

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“…As epidermal keratinocytes express ryanodine receptors (24), the endogenous mechanism of OT secretion from epidermal keratinocytes might be similar to that of hypothalamus. OT release by ATPcS was blocked by the removal of Ca…”

Section: Discussionmentioning

confidence: 99%

Oxytocin is expressed in epidermal keratinocytes and released upon stimulation with adenosine 5′‐[γ‐thio]triphosphate in vitro

Denda¹,

Takei

Kumamoto

et al. 2012

Experimental Dermatology

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Oxytocin is a neuropeptide produced primarily in the hypothalamus and is best known for its roles in parturition and lactation. It also influences behaviour, memory and mental state. Recent studies have suggested a variety of roles for oxytocin in peripheral tissues, including skin. Here we show that oxytocin is expressed in human skin. Immunohistochemical studies showed that oxytocin and its carrier protein, neurophysin I, are predominantly localized in epidermis. RT-PCR confirmed the expression of oxytocin in both skin and cultured epidermal keratinocytes. We also show that oxytocin is released from keratinocytes after application of adenosine 5′-[c-thio]triphosphate (ATPcS, a stable analogue of ATP) in a dose-dependent manner. The ATPcS-induced oxytocin release was inhibited by removal of extracellular calcium, or by the P2X receptor antagonist 2′,3′-O-(2,4,6-trinitrophenyl)adenosine 5′-triphosphate (TNP-ATP). These results suggest that oxytocin is produced in human epidermal keratinocytes and is released in response to calcium influx via P2X receptors.Abbreviations: ATPcS, adenosine 5′-[c-thio]triphosphate; OT, oxytocin; RT, reverse transcription; TNP-ATP, 2′,3′-O-(2,4,6-trinitrophenyl) adenosine 5′-triphosphate.

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“…Loss of Orai1 results in inhibited directional migration of keratinocytes [95]. Moreover, expression of RyRs in human keratinocytes has been linked to keratinocyte differentiation and epidermal barrier homeostasis [96]. Application of a RyR agonist or antagonist delays or enhances skin barrier recovery respectively [96].…”

Section: Calcium Signaling In Muscle Regenerationmentioning

confidence: 99%

“…Moreover, expression of RyRs in human keratinocytes has been linked to keratinocyte differentiation and epidermal barrier homeostasis [96]. Application of a RyR agonist or antagonist delays or enhances skin barrier recovery respectively [96]. Further studies will help determine whether the importance of Ca 2+ activity in regeneration is universal and will identify the particular Ca 2+ dynamics that facilitate regeneration in different tissues.…”

Section: Calcium Signaling In Muscle Regenerationmentioning

confidence: 99%

Calcium signaling in skeletal muscle development, maintenance and regeneration

et al. 2016

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Skeletal muscle-specific stem cells are pivotal for tissue development and regeneration. Muscle plasticity, inherent in these processes, is also essential for daily life activities. Great advances and efforts have been made in understanding the function of the skeletal muscle-dedicated stem cells, called muscle satellite cells, and the specific signaling mechanisms that activate them for recruitment in the repair of the injured muscle. Elucidating these signaling mechanisms may contribute to devising therapies for muscular injury or disease. Here we review the studies that have contributed to our understanding of how calcium signaling regulates skeletal muscle development, homeostasis and regeneration, with a focus on the calcium dynamics and calcium-dependent effectors that participate in these processes.

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Ryanodine Receptors Are Expressed in Epidermal Keratinocytes and Associated with Keratinocyte Differentiation and Epidermal Permeability Barrier Homeostasis

Cited by 27 publications

References 31 publications

Endoplasmic Reticulum Calcium Regulates Epidermal Barrier Response and Desmosomal Structure

Endoplasmic Reticulum Calcium Regulates Epidermal Barrier Response and Desmosomal Structure

Oxytocin is expressed in epidermal keratinocytes and released upon stimulation with adenosine 5′‐[γ‐thio]triphosphate in vitro

Calcium signaling in skeletal muscle development, maintenance and regeneration

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