Prostaglandin E2 Enhances Gap Junctional Intercellular Communication in Clonal Epithelial Cells

Prostaglandins are a group of lipids that produce diverse physiological and pathological effects. Among them, prostaglandin E2 (PGE2) stands out for the wide variety of functions in which it participates. To date, there is little information about the influence of PGE2 on gap junctional intercellula...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-05, Vol.22 (11), p.5813
Main Authors: Ogazon Del Toro, Alejandro, Jimenez, Lidia, Serrano Rubi, Mauricio, Castillo, Aida, Hinojosa, Lorena, Martinez Rendon, Jacqueline, Cereijido, Marcelino, Ponce, Arturo
Format: Article
Language:English
Subjects:
Adenylyl Cyclases - metabolism
Animals
Cell Communication - drug effects
Cyclic AMP - metabolism
Cyclic AMP-Dependent Protein Kinases - metabolism
Dinoprostone - pharmacology
Dogs
Dose-Response Relationship, Drug
dye transfer
epithelia
Epithelial Cells - cytology
Epithelial Cells - drug effects
Epithelial Cells - metabolism
gap junction
Gap Junctions - drug effects
Gap Junctions - metabolism
Madin Darby Canine Kidney Cells
prostaglandin E2
Receptors, Prostaglandin E, EP2 Subtype - metabolism
Signal Transduction - drug effects
Time Factors
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Summary:Prostaglandins are a group of lipids that produce diverse physiological and pathological effects. Among them, prostaglandin E2 (PGE2) stands out for the wide variety of functions in which it participates. To date, there is little information about the influence of PGE2 on gap junctional intercellular communication (GJIC) in any type of tissue, including epithelia. In this work, we set out to determine whether PGE2 influences GJIC in epithelial cells (MDCK cells). To this end, we performed dye (Lucifer yellow) transfer assays to compare GJIC of MDCK cells treated with PGE2 and untreated cells. Our results indicated that (1) PGE2 induces a statistically significant increase in GJIC from 100 nM and from 15 min after its addition to the medium, (2) such effect does not require the synthesis of new mRNA or proteins subunits but rather trafficking of subunits already synthesized, and (3) such effect is mediated by the E2 receptor, which, in turn, triggers a signaling pathway that includes activation of adenylyl cyclase and protein kinase A (PKA). These results widen the knowledge regarding modulation of gap junctional intercellular communication by prostaglandins.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22115813