Immunoreactivity of MAPK Signaling in a Rat Model of Intrauterine Growth Retardation Induced by Uterine Artery Ligation.

BACKGROUND/AIM: Intrauterine growth retardation (IUGR) causes very low birth weight and is related to the morbidity and mortality of the newborn. In our previous study, expression of brain-derived neurotrophic factor (BDNF) was found reduced in the cerebral cortex and dentate gyrus of fetuses with IUGR. BDNF protected cortical neurons against hypoxic injury via activation of the extracellular signal-related kinase (ERK) pathway. The aim of the current study was to observe the immunoreactivity of ERK in mature neurons and proliferating cells.

MATERIALS AND

METHODS

Uterine artery ligation was performed at 17 days of gestation (dg). Rat fetuses were obtained at 21 dg using cesarean section. Fetuses were designated either to the growth retardation (GR) group when removed from the horn with uterine artery ligation, or to the control group when removed from the other horn with the untied artery. Immunohistochemistry was performed with primary antibodies on paraffin-embedded forebrain sections.

RESULTS

The density and proportion of cells expressing PCNA, ERK, and phosphate ERK in the subventricular zone (SVZ) was not different between the control and GR group. The density and proportion of NeuN- and phosphate ERK-positive cells in the cerebral parietal cortex was lower in the GR group, compared to the control group.

CONCLUSION

Although IUGR had no effect on the proliferation of cells in the SVZ, it reduced neuronal survival in the cerebral parietal cortex, which was associated with the decrease of pERK-positive cell density and proportion in the cerebral cortex.