Abstract：Objective To investigate the effect of corticosterone on the expression of the neuronal migration protein lissencephaly 1 (LIS1) in developing cerebral cortical neurons of fetal rats. Methods The primary cultured cerebral cortical neurons of fetal Wistar rats were divided into control group, low-dose group, and high-dose group. The neurons were exposed to the medium containing different concentrations of corticosterone (0 μmol/L for the control group, 0.1 μmol/L for the low-dose group, and 1.0 μmol/L for the high-dose group). The neurons were collected at 1, 4, and 7 days after intervention. Western blot and immunocytochemical staining were used to observe the change in LIS1 expression in neurons. Results Western blot showed that at 7 days after intervention, the low-and high-dose groups had significantly higher expression of LIS1 in the cytoplasm and nucleus of cerebral cortical neurons than the control group (P < 0.05), and the high-dose group had significantly lower expression of LIS1 in the cytoplasm of cerebral cortical neurons than the low-dose group (P < 0.05). Immunocytochemical staining showed that at 1, 4, and 7 days after corticosterone intervention, the high-dose group had a significantly lower mean optical density of LIS1 than the control group and the low-dose group (P < 0.05). At 7 days after intervention, the low-dose group had a significantly lower mean optical density of LIS1 than the control group (P < 0.05). Conclusions Corticosterone downregulates the expression of the neuronal migration protein LIS1 in developing cerebral cortical neurons of fetal rats cultured in vitro, and such effect depends on the concentration of corticosterone and duration of corticosterone intervention.
LUO Sen-Lin,BO Tao,LIU Tong et al. Effect of corticosterone on lissencephaly 1 expression in developing cerebral cortical neurons of fetal rats cultured in vitro[J]. CJCP, 2017, 19(9): 1008-1013.
Sweet DG, Carnielli V, Greisen G, et al. European consensus guidelines on the management of respiratory distress syndrome-2016 update[J]. Neonatology, 2017, 111(2):107-125.
[2]
Doyle LW, Ehrenkranz RA, Halliday HL. Early (< 8 days) postnatal corticosteroids for preventing chronic lung disease in preterm infants[J]. Cochrane Database Syst Rev, 2014, (5):CD001146.
[3]
Onland W, Offringa M, van Kaam A. Late (≥ 7 days) inhalation corticosteroids to reduce bronchopulmonary dysplasia in preterm infants[J]. Cochrane Database Syst Rev, 2012, (4):CD002311.
[4]
Doyle LW, Ehrenkranz RA, Halliday HL. Dexamethasone treatment after the first week of life for bronchopulmonary dysplasia in preterm infants:a systematic review[J]. Neonatology, 2010, 98(4):289-296.
[5]
ter Wolbeek M, de Sonneville LM, de Vries WB, et al. Early life intervention with glucocorticoids has negative effects on motor development and neuropsychological function in 14-17 year-old adolescents[J]. Psychoneuroendocrinology, 2013, 38(7):975-986.
[6]
Cheong JL, Burnett AC, Lee KJ, et al. Association between postnatal dexamethasone for treatment of bronchopulmonary dysplasia and brain volumes at adolescence in infants born very preterm[J]. J Pediatr, 2014, 164(4):737-743.e1.
[7]
Solecki DJ. Sticky situations:recent advances in control of cell adhesion during neuronal migration[J]. Curr Opin Neurobiol, 2012, 22(5):791-798.
[8]
Moon HM, Wynshaw-Boris A. Cytoskeleton in action:lissencephaly, a neuronal migration disorder[J]. Wiley Interdiscip Rev Dev Biol, 2013, 2(2):229-245.
[9]
Clark GD. Platelet-activating factor acetylhydrolase and brain development[J]. Enzymes, 2015, 38:37-42.
[10]
Pandey JP, Smith DS. A Cdk5-dependent switch regulates Lis1/Ndel1/dynein-driven organelle transport in adult axons[J]. J Neurosci, 2011, 31(47):17207-17219.
[11]
Nishimura YV, Shikanai M, Hoshino M, et al. Cdk5 and its substrates, Dcx and p27kip1, regulate cytoplasmic dilation formation and nuclear elongation in migrating neurons[J]. Development, 2014, 141(18):3540-3550.
[12]
Chen X, Zhang J, Zhao J, et al. Lis1 is required for the expansion of hematopoietic stem cells in the fetal liver[J]. Cell Res, 2014, 24(8):1013-1016.
[13]
Zimdahl B, Ito T, Blevins A, et al. Lis1 regulates asymmetric division in hematopoietic stem cells and in leukemia[J]. Nat Genet, 2014, 46(3):245-252.
[14]
Lanctot AA, Peng CY, Pawlisz AS, et al. Spatially dependent dynamic MAPK modulation by the Nde1-Lis1-Brap complex patterns mammalian CNS[J]. Dev Cell, 2013, 25(3):241-255.
[15]
Bahi-Buisson N, Guerrini R. Diffuse malformations of cortical development[J]. Handb Clin Neurol, 2013, 111:653-665.
[16]
Fry AE, Cushion TD, Pilz DT. The genetics of lissencephaly[J]. Am J Med Genet C Semin Med Genet, 2014, 166C(2):198-210.
[17]
Liu JS. Molecular genetics of neuronal migration disorders[J]. Curr Neurol Neurosci Rep, 2011, 11(2):171-178.
[18]
Pawlisz AS, Feng Y. Three-dimensional regulation of radial glial functions by Lis1-Nde1 and dystrophin glycoprotein complexes[J]. PLoS Biol, 2011, 9(10):e1001172.
[19]
Moon HM, Youn YH, Pemble H, et al. LIS1 controls mitosis and mitotic spindle organization via the LIS1-NDEL1-dynein complex[J]. Hum Mol Genet, 2014, 23(2):449-466.
[20]
Sebe JY, Bershteyn M, Hirotsune S, et al. ALLN rescues an in vitro excitatory synaptic transmission deficit in Lis1 mutant mice[J]. J Neurophysiol, 2013, 109(2):429-436.
[21]
Garcia-Lopez R, Pombero A, Dominguez E, et al. Developmental alterations of the septohippocampal cholinergic projection in a lissencephalic mouse model[J]. Exp Neurol, 2015, 271:215-227.
[22]
Moore KD, Chen R, Cilluffo M, et al. Lis1 reduction causes tangential migratory errors in mouse spinal cord[J]. J Comp Neurol, 2012, 520(6):1198-1211.
[23]
Lockrow JP, Holden KR, Dwivedi A, et al. LIS1 duplication:expanding the phenotype[J]. J Child Neurol, 2012, 27(6):791-795.
[24]
Arabadzisz D, Diaz-Heitjz R, Knuesel I, et al. Primate early life stress leads to long-term mild hippocampal decreases in corticosteroid receptor expression[J]. Biol Psychiatry, 2010, 67(11):1106-1109.
[25]
Moors M, Bose R, Johansson-Haque K, et al. Dickkopf 1 mediates glucocorticoid-induced changes in human neural progenitor cell proliferation and differentiation[J]. Toxicol Sci, 2012, 125(2):488-495.
[26]
Mutsaers HA, Tofighi R. Dexamethasone enhances oxidative stress-induced cell death in murine neural stem cells[J]. Neurotox Res, 2012, 22(2):127-137.
[27]
Malaeb SN, Stonestreet BS. Postnatal glucocorticoid-induced hypomyelination, gliosis, and neurologic deficits are dose-dependent, preparation-specific, and reversible[J]. Exp Neurol, 2016, 278:1-3.
[28]
Claessens SE, Belanoff JK, Kanatsou S, et al. Acute effects of neonatal dexamethasone treatment on proliferation and astrocyte immunoreactivity in hippocampus and corpus callosum:towards a rescue strategy[J]. Brain Res, 2012, 1482:1-12.
[29]
Oliveira M, Rodrigues AJ, Leão P, et al. The bed nucleus of stria terminalis and the amygdala as targets of antenatal glucocorticoids:implications for fear and anxiety responses[J]. Psychopharmacology (Berl), 2012, 220(3):443-453.
[30]
Ko MC, Hung YH, Ho PY, et al. Neonatal glucocorticoid treatment increased depression-like behaviour in adult rats[J]. Int J Neuropsychopharmacol, 2014, 17(12):1995-2004.
[31]
Tijsseling D, Camm EJ, Richter HG, et al. Statins prevent adverse effects of postnatal glucocorticoid therapy on the developing brain in rats[J]. Pediatr Res, 2013, 74(6):639-645.
[32]
Bhatt AJ, Feng Y, Wang J, et al. Dexamethasone induces apoptosis of progenitor cells in the subventricular zone and dentate gyrus of developing rat brain[J]. J Neurosci Res, 2013, 91(9):1191-1202.
[33]
Tijsseling D, Camm EJ, Richter HG, et al. Statins prevent adverse effects of postnatal glucocorticoid therapy on the developing brain in rats[J]. Pediatr Res, 2013, 74(6):639-645.
[34]
Caffino L, Calabrese F, Giannotti G, et al. Stress rapidly dysregulates the glutamatergic synapse in the prefrontal cortex of cocaine-withdrawn adolescent rats[J]. Addict Biol, 2015, 20(1):158-169.
[35]
Pagnamenta AT, Lise S, Harrison V, et al. Exome sequencing can detect pathogenic mosaic mutations present at low allele frequencies[J]. J Hum Genet, 2012, 57(1):70-72.
[36]
Classen S, Goecke T, Drechsler M, et al. A novel inverted 17p13.3 microduplication disrupting PAFAH1B1(LIS1) in a girl with syndromic lissencephaly[J]. Am J Med Genet A, 2013, 161A(6):1453-1458.
[37]
Lockrow JP, Holden KR, Dwivedi A, et al. LIS1 duplication:expanding the phenotype[J]. J Child Neurol, 2012, 27(6):791-795.
[38]
Nishi M, Kawata M. Dynamics of glucocorticoid receptor and mineralocorticoid receptor:implications from live cell imaging studies[J]. Neuroendocrinology, 2007, 85(3):186-192.
