Abstract
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.
Highlights
We considered the number of cells stained as a result of having injected a single cell (number of stained cells per trial (NSCPT)) as an estimate of gap junctional intercellular communication (GJIC)
From seminal fluid in 1930 [81,82,83], prostaglandins have become one of the most widely investigated substances, due in large part to the wide range of physiological and pathological processes in which they participate [84,85]. One proof of their importance is that a wide variety of drugs have been developed around them with widely different purposes, such as the control of inflammation, fever, pain, childbirth pain, rheumatoid arthritis, and blood clotting, starting with aspirin and later with other medications known as nonsteroidal anti-inflammatory drugs (NSAIDs) that, as aspirin does, work by inhibiting the activity of cyclo-oxygenase enzymes (COX-1 or COX-2) [86,87,88]
Prostaglandins are known to be involved in a wide variety of clinical phenomena and much information has been gathered about the signaling cascades they trigger, some aspects of their effects at the cellular and molecular levels remain poorly described and understood
Summary
PGs are a class member of the family of eicosanoids, which include leukotrienes and thromboxanes [1]. PGs are produced enzymatically, by cyclo-oxygenases (COXs), and from arachidonic acid, a 20-carbon polyunsaturated, essential fatty acid [2,3]. These compounds are produced by almost every cell of animal species. In most cases, they act as autocrine and paracrine hormone-like mediators (i.e., they signal at or immediately adjacent to their site of synthesis) [4,5]. Playing a role as signaling starters of diverse signaling pathways, PGs are involved in a variety of effects in numerous physiological and pathological processes [6,7], among which inflammation stands out [8,9] but which include cancer [10,11], heart disease [12,13], labor and delivery [14,15,16], hypertension [17,18], asthma and allergic diseases [19], migraine [20], sleep [21], bone metabolism [22,23], rheumatoid arthritis [24], and blood flow and the formation of blood clots [25], among many others
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