Open AccessRegulation of pancreatic β‐cell function and mass dynamics by prostaglandin signaling
Author(s) -
Carboneau Bethany A.,
Breyer Richard M.,
Gan Maureen
Publication year - 2017
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-017-0377-7
Subject(s) - prostacyclin , prostaglandin e2 receptor , receptor , g protein coupled receptor , microbiology and biotechnology , prostaglandin , signal transduction , pancreatic islets , thromboxane a2 , cell , thromboxane , endocrinology , medicine , biology , islet , insulin , biochemistry , platelet , agonist
Prostaglandins (PGs) are signaling lipids derived from arachidonic acid (AA), which is metabolized by cyclooxygenase (COX)‐1 or 2 and class‐specific synthases to generate PGD 2 , PGE 2 , PGF 2α , PGI 2 (prostacyclin), and thromboxane A 2 . PGs signal through G‐protein coupled receptors (GPCRs) and are important modulators of an array of physiological functions, including systemic inflammation and insulin secretion from pancreatic islets. The role of PGs in β‐cell function has been an active area of interest, beginning in the 1970s. Early studies demonstrated that PGE 2 inhibits glucose‐stimulated insulin secretion (GSIS), although more recent studies have questioned this inhibitory action of PGE 2 . The PGE 2 receptor EP3 and one of the G‐proteins that couples to EP3, Gα Z , have been identified as negative regulators of β‐cell proliferation and survival. Conversely, PGI 2 and its receptor, IP, play a positive role in the β‐cell by enhancing GSIS and preserving β‐cell mass in response to the β‐cell toxin streptozotocin (STZ). In comparison to PGE 2 and PGI 2 , little is known about the function of the remaining PGs within islets. In this review, we discuss the roles of PGs, particularly PGE 2 and PGI 2 , PG receptors, and downstream signaling events that alter β‐cell function and regulation of β‐cell mass.