title: Effects of the angiotensin-(1-7) receptor Mas on cell proliferation and on the population of doublecortin positive cells within the dentate gyrus and the piriform cortex.
abstract: Aside from the well-known biologically active angiotensin II, other biologically active angiotensins have been discovered, including angiotensin IV and angiotensin-(1-7). Some years ago, we and others discovered that the Mas proto-oncogene encodes a G protein-coupled receptor being essential for angiotensin-(1-7) signaling. Mas is not only expressed in the periphery but also within the brain, e.g. in the dentate gyrus (DG) and the piriform cortex (PC). Since the DG is capable of adult neurogenesis, we examined the impact of a deletion of Mas upon adult neurogenesis. Deletion of Mas did not alter cell proliferation in the adult DG (as monitored with phosphohistone H3) and did not alter cell death (as monitored with activated Caspase 3). However, Mas deficiency resulted in an increase in the number of doublecortin (DCX) positive cells, indicating that lack of Mas increases the number of this cell population. Concerning the PC, it is discussed whether adult neurogenesis occurs under physiological conditions in this area. We could demonstrate that Mas deficiency has an impact on cell division and on the population of DCX-positive cells within the PC. Since Mas is not expressed before birth within the brain, our data may suggest that adult hippocampal neurogenesis and neurogenesis occurring during prenatal development share several common mechanisms, but are, at least in part, differentially regulated. Moreover, since deficiency for Mas increases the numbers of DCX-positive young neurons, blockage of Mas might be beneficial in stimulating neurogenesis in adults.
authors.affiliation: Institute of Anatomy and Cell Biology, Universitätsmedizin Greifswald, Friedrich Löffler Straße 23c, 17487 Greifswald, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Freund
authors.affiliation: Department of Pharmacology and Therapeutics, University College Cork, Cork, Ireland; Department of Pediatric Surgery, Centre for Fetal Medicine, Division of Women and Child Health, University of Leipzig, Leipzig, Germany; Department of Obstetrics, Centre for Fetal Medicine, Division of Women and Child Health, University of Leipzig, Leipzig, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Walther
authors.affiliation: Institute of Anatomy and Cell Biology, Universitätsmedizin Greifswald, Friedrich Löffler Straße 23c, 17487 Greifswald, Germany. Electronic address: oliver.vonbohlen@uni-greifswald.de.
authors.forename: O
authors.initials: O
authors.lastname: von Bohlen Und Halbach
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D053148:Caspase 3 / Q000378:metabolism; D002455:Cell Division / Q000502:physiology; D049109:Cell Proliferation; D018891:Dentate Gyrus / Q000502:physiology*; D000089622:Doublecortin Domain Proteins; D000089662:Doublecortin Protein; D006657:Histones / Q000378:metabolism; D007150:Immunohistochemistry; D051379:Mice; D018345:Mice, Knockout; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D055495:Neurogenesis; D009474:Neurons / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism*; D009833:Olfactory Pathways / Q000502:physiology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*
chemical_list: C000714847:Dcx protein, mouse; D000089622:Doublecortin Domain Proteins; D000089662:Doublecortin Protein; D006657:Histones; D008869:Microtubule-Associated Proteins; D009479:Neuropeptides; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; C505409:Casp3 protein, mouse; D053148:Caspase 3
keywords: Abercrombie's; Doublecortin; Hippocampus; Immunohistochemistry; Knockout; Mice