ABSTRACT
Pituitary adenylate cyclase activating polypeptide (PACAP) was first isolated from ovine hypothalamus and was known to stimulate the release of growth factor in various cells. Recently, we reported the cellular localization of PACAP and its type I (PAC1 ) receptor in rat placenta during pregnancy. Placenta is a critical organ that synthesizes several growth factors and angiogenic factors for the fetal development and its own growth. However, there is little information regarding the cellular localization of PACAP and its receptor in human placenta at various gestations. The aim of the present study was to define the expression and distribution of PACAP and PAC1 receptor mRNAs in the human placenta during the pregnancy period. PACAP and PAC1 receptor mRNAs were expressed in stroma cells of stem villi and terminal villi. At the early stage, on 7 and 14 weeks, PACAP and PAC1 receptor genes were moderately expressed in stroma cells surrounding the blood vessels within stem villi. These genes were strongly expressed in stroma cells of stem villi and terminal villi on 24 and 38 weeks. The expression of these genes was increased as gestation advanced, and localized in the same areas. Localization of PACAP and PAC1 receptor demonstrate the evidence that PACAP may play an important role, as an autoregulator or pararegulator via its PAC1 receptor. In conclusion, our findings strongly suggest that PACAP may have a critical role in physiological function of the placenta for gestational maintenance and fetal growth.
Subject(s)
Female , Humans , Pregnancy , Chorionic Villi/metabolism , Gene Expression , Nerve Growth Factors/biosynthesis , Neuropeptides/biosynthesis , Neurotransmitter Agents/biosynthesis , Pituitary Adenylate Cyclase-Activating Polypeptide , Placenta/metabolism , Pregnancy Trimester, First , Pregnancy Trimester, Second , RNA, Messenger , Receptors, Cell Surface/biosynthesis , Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide , Receptors, Pituitary Adenylate Cyclase-Activating PolypeptideABSTRACT
Desde 1934 se realizaron estudios analizando los efectos que sobre las células sensitivas y neuronas motoras espinales que inervaban las extremidades de animales, producía la extirpación de primordios nerviosos. Las observaciones obtenidas de estos estudios (después de algunos años) permitieron el descubrimiento de un factor promotor del crecimiento neuronal, al cual se designó como factor de crecimiento neuronal (NGF). El NFG es la sustancia mejor caracterizada dentro de una familia de moléculas que se requieren para la supervivencia y el desarrollo de neuronas durante etapas embrionarias del crecimiento y durante la vida adulta. Se ha observado que, bajo ciertas circunstancias, la infusión exógena de BGF puede promover la supervivencia neuronal y la regeneración axonal, por lo cual, en la actualidad, se ha intentado la utilización de este factor para mejorar algunas condiciones patológicas en las cuales el principal componente es el daño neuronal, pudiendo producirse este último por diferentes mecanismos. Dado lo anterior, se ha postulado que la administración de BGF recombinante humano pudiera ser, en el futuro, de utilidad para el tratamiento de enfermedades del sistema nervioso central y periférico, ya que en algunos de los estudios realizados se ha demostrado que este factor puede tener efectos benéficos