Lysophosphatidic acid modulates prostaglandin signalling in bovine steroidogenic luteal cells.
We examined whether lysophosphatidic acid affects prostaglandin biosynthesis, transport, and signalling in bovine steroidogenic luteal cells. The aim of the present study was to determine the influence of LPA on PGE2 and PGF2α synthesis and on the expression of enzymes involved in PG biosynthesis (PTGS2, mPGES-1, cPGES, mPGES-2, PGFS and 9-KPR), prostaglandin transporter (PGT), and prostaglandin receptors (EP1, EP2, EP3, EP4 and FP) in bovine steroidogenic luteal cells. We found that LPA inhibited PGF2α synthesis in steroidogenic luteal cells. Moreover, LPA increased mPGES1 and cPGES and decreased PGFS expression in cultured bovine steroidogenic luteal cells. Additionally, LPA stimulated EP2 and EP4 receptor and PGT expression. This study suggests that LPA activity in the bovine CL directs the physiological intraluteal balance between the two main prostanoids towards luteotropic PGE2.
Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Ilona
I
Kowalczyk-Zieba
Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Dorota
D
Boruszewska
Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Emilia
E
Sinderewicz
Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland.
Katarzyna
K
Grycmacher
Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland. Electronic address: i.woclawek-potocka@pan.olsztyn.pl.
Izabela
I
Woclawek-Potocka
D000003:Abattoirs; D000818:Animals; D001692:Biological Transport; D002417:Cattle; D002478:Cells, Cultured; D003612:Dairying; D015237:Dinoprost / Q000037:antagonists & inhibitors / Q000378:metabolism; D015232:Dinoprostone / Q000819:agonists / Q000378:metabolism; D030762:Estrous Cycle / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation; D006911:Hydroxyprostaglandin Dehydrogenases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D019746:Intramolecular Oxidoreductases / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D008184:Luteal Cells / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000378:metabolism; D008246:Lysophospholipids / Q000378:metabolism*; D027361:Organic Anion Transporters / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D000071876:Prostaglandin-E Synthases; D058307:Receptors, Prostaglandin E, EP2 Subtype / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D058309:Receptors, Prostaglandin E, EP4 Subtype / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
D007527:Isoenzymes; D008246:Lysophospholipids; D027361:Organic Anion Transporters; D058307:Receptors, Prostaglandin E, EP2 Subtype; D058309:Receptors, Prostaglandin E, EP4 Subtype; D007986:Luteinizing Hormone; D015237:Dinoprost; D006911:Hydroxyprostaglandin Dehydrogenases; C031051:prostaglandin-F synthase; D019746:Intramolecular Oxidoreductases; D000071876:Prostaglandin-E Synthases; D015232:Dinoprostone; C032881:lysophosphatidic acid
Cow; Lysophosphatidic acid; Prostaglandins; Steroidogenic cells