Stimulation and Inhibition of Angiogenesis by Placental Proliferin and Proliferin-Related Protein

• Published in: Science (American Association for the Advancement of Science) Vol. 266; no. 5190; pp. 1581 - 1584
• Main Authors: Jackson, Dowdy, Volpert, Olga V., Bouck, Noël, Daniel I. H. Linzer
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society for the Advancement of Science 02.12.1994; American Association for the Advancement of Science; The American Association for the Advancement of Science
• Subjects: Angiogenesis; Animal migration behavior; Animals; Biological and medical sciences; Cattle; Cell differentiation, maturation, development, hematopoiesis; Cell Movement - drug effects; Cell physiology; Cellular biology; CHO cells; Cornea; Cornea - blood supply; Culture Techniques; Endothelial cells; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Family (Sociological Unit); Female; Fibroblast Growth Factor 2 - pharmacology; Fundamental and applied biological sciences. Psychology; Glycoproteins - metabolism; Glycoproteins - pharmacology; Growth Substances - metabolism; Growth Substances - pharmacology; Hormones; Individualized Instruction; Intercellular Signaling Peptides and Proteins; Migration; Molecular and cellular biology; Neovascularization; Neovascularization, Pathologic; Placenta; Placenta - blood supply; Pregnancy; Pregnancy proteins; Pregnancy Proteins - pharmacology; Proteins; Rats; Reproduction; Tissue culture techniques; Ungulates; Cell proliferation; Angiogenesis; Vertebrata; Regulation(control); Mammalia; Placenta; Adenohypophyseal hormone; Prolactin; STH
• DOI: 10.1126/science.7527157
• ISSN: 0036-8075

In many mammalian species, the placenta is the site of synthesis of proteins in the prolactin and growth hormone family. Analysis of two such proteins, proliferin (PLF) and proliferin-related protein (PRP), revealed that they are potent regulators of angiogenesis; PLF stimulated and PRP inhibited endothelial cell migration in cell culture and neovascularization in vivo. The mouse placenta secretes an angiogenic activity during the middle of pregnancy that corresponds primarily to PLF, but later in gestation releases a factor that inhibits angiogenesis, which was identified as PRP. Incubation of placental tissue with PLF led to the specific binding of this hormone to capillary endothelial cells. Thus PLF and PRP may regulate the initiation and then the cessation of placental neovascularization.