Adenosine A(2A) and A(2B) Receptors Differentially Modulate Keratinocyte Proliferation: Possible Deregulation in Psoriatic Epidermis
![Thumbnail](/xmlui/bitstream/handle/10234/165877/Andres_JID_2017.pdf.jpg?sequence=6&isAllowed=y)
View/ Open
Impact
![Google Scholar](/xmlui/themes/Mirage2/images/uji/logo_google.png)
![Microsoft Academico](/xmlui/themes/Mirage2/images/uji/logo_microsoft.png)
Metadata
Show full item recordcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/36080
comunitat-uji-handle3:10234/36082
comunitat-uji-handle4:
INVESTIGACIONMetadata
Title
Adenosine A(2A) and A(2B) Receptors Differentially Modulate Keratinocyte Proliferation: Possible Deregulation in Psoriatic EpidermisAuthor (s)
Date
2017-01Publisher
ElsevierBibliographic citation
ANDRÉS, Rosa M., et al. Adenosine A 2A and A 2B Receptors Differentially Modulate Keratinocyte Proliferation: Possible Deregulation in Psoriatic Epidermis. Journal of Investigative Dermatology, 2017, vol. 137, no 1, p. 123-131.Type
info:eu-repo/semantics/articlePublisher version
http://www.sciencedirect.com/science/article/pii/S0022202X16322369Version
info:eu-repo/semantics/acceptedVersionAbstract
Adenosine is a potent regulator of inflammation and immunity, but the role of adenosine receptors in keratinocytes remains controversial. We determined that in addition to A2B receptors, human epidermal keratinocytes ... [+]
Adenosine is a potent regulator of inflammation and immunity, but the role of adenosine receptors in keratinocytes remains controversial. We determined that in addition to A2B receptors, human epidermal keratinocytes also express A2A receptors, although to a lower extent. Through the use of selective adenosine receptor agonists and antagonists, we showed that physiological concentrations of adenosine activate A2B receptors in normal human keratinocytes, inducing cell cycle arrest through the increase of intracellular calcium but not through cAMP signaling. In contrast, the selective activation of A2A receptors by CGS-21680 induces keratinocyte proliferation via p38–mitogen-activated protein kinase activation. Adenosine and selective A2A and A2B agonists presented anti-inflammatory profiles independent of adenosine receptors but mediated by membrane phosphatase activation. Finally, keratinocyte exposure to diverse inflammatory cytokines altered adenosine receptor expression by reducing A2B and increasing A2A, a pattern also observed in psoriatic epidermis. Because increased epidermal turnover and inflammatory response are characteristics of psoriatic disease, further studies are needed to assess the role and consequences of the altered adenosine receptor expression in lesional and nonlesional psoriatic keratinocytes. [-]
Is part of
Journal of Investigative Dermatology Volume 137, Issue 1, January 2017Rights
Copyright © 2017 Elsevier B.V. or its licensors or contributors.
http://rightsstatements.org/vocab/InC/1.0/
info:eu-repo/semantics/openAccess
http://rightsstatements.org/vocab/InC/1.0/
info:eu-repo/semantics/openAccess
This item appears in the folowing collection(s)
- MED_Articles [669]