scholarly journals Regulation of the induction of ornithine decarboxylase in keratinocytes by retinoids

1995 ◽  
Vol 309 (1) ◽  
pp. 159-165 ◽  
Author(s):  
Z S Zheng ◽  
G Z Xue ◽  
J H Prystowsky
Keyword(s):  
Retinoic Acid ◽  
Ornithine Decarboxylase ◽  
Egf Receptor ◽  
Neutralizing Antibody ◽  
Mrna Levels ◽  
Egf Receptors ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Epidermal Growth ◽  
Dose Dependent Increase

Treatment of SV40-transformed keratinocytes (Z114) with epidermal growth factor (EGF) resulted in an increase in ornithine decarboxylase (ODC) activity and a dose-dependent increase in ODC mRNA levels. Pretreatment of keratinocytes with all-trans-retinoic retinoic acid inhibited the EGF induction of ODC activity. In both quiescent and EGF-stimulated cells, all-trans-retinoic acid inhibited ODC gene transcription and lowered ODC mRNA levels, whereas glyceraldehyde phosphate dehydrogenase expression remained unaffected. Treatment with all-trans-retinoic acid for 24 h resulted in a dose- and time-dependent decrease of up to 52% in EGF binding to EGF receptors and a 30-75% decrease in EGF-receptor quantity. In addition, when cells were treated with both UV radiation and all-trans-retinoic acid, their effects were additive in causing a decrease in EGF binding. Blocking of EGF receptors with a neutralizing antibody for EGF receptors inhibited the induction of ODC activity by EGF. The effects of several other retinoids, including Ro15-0778, etretinate, Ro13-7410, etarotene, Ro40-8757, 13-cis-retinoic acid and acitretin, were also studied to determine their effects on EGF binding and ODC activity. Two of these other retinoids, 13-cis-retinoic acid and Ro13-7410, inhibited EGF binding the most (35-46%, P < 0.001); several others (etarotene, Ro40-8757 and etretinate) were less effective (7-16%), but significantly decreased EGF binding (P < 0.05), and two retinoids (Ro15-0778 and acitretin) showed no significant effect on EGF binding. In contrast, all of the retinoids tested inhibited the induction of ODC activity by EGF, although etretinate and Ro15-0778 were less effective. EGF signal transduction is important in ODC gene regulation, and retinoids are significant modulators of this pathway.

scholarly journals All-trans retinoic acid reverses phorbol ester resistance in a human myeloid leukemia cell line

Blood ◽  
1994 ◽  
Vol 83 (2) ◽  
pp. 490-496 ◽  
Author(s):  
KD Yang ◽  
T Mizobuchi ◽  
SM Kharbanda ◽  
R Datta ◽  
E Huberman ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cell Line ◽  
Leukemia Cell Line ◽  
Nonspecific Esterase ◽  
Mrna Levels ◽  
Monocytic Differentiation ◽  
Granulocytic Differentiation ◽  
Protein Levels ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

Treatment of human HL-60 leukemic cells with 12-O-tetradecanoylphorbol- 13-acetate (TPA) is associated with activation of protein kinase C (PKC) and induction of monocytic differentiation. An HL-60 variant cell line, termed HL-525, derived from long-term exposure to TPA (Homma et al, Proc Natl Acad Sci USA 83: 7316, 1986) is resistant to TPA-induced differentiation and displays decreased PKC beta expression compared with the HL-60 parent line. However, this variant exhibits features of granulocytic differentiation, including nitroblue tetrazolium reduction, when exposed to all-trans retinoic acid (ATRA). Whereas treatment of HL-525 cells with ATRA or TPA alone had no effect on features of monocytic differentiation, these agents in combination resulted in cellular adhesion, nonspecific esterase staining, and induction of the c-fms (monocyte growth factor receptor) gene. In order to measure PKC expression associated with the reversal of TPA resistance by ATRA, we exposed HL-525 cells to ATRA and analyzed PKC- mRNA and protein levels. Exposure of HL-525 cells to ATRA for 3 days resulted in induction of PKC beta transcripts, whereas there was little change in PKC alpha mRNA levels. ATRA treatment was also associated with an increase in PKC activity and an induction of cytosolic PKC beta protein levels. These findings are consistent with the hypothesis that ATRA reverses TPA resistance in HL-525 cells by enhancing the expression of PKC.

Mechanism of all trans-retinoic acid and glucocorticoid regulation of surfactant protein mRNA

1998 ◽  
Vol 274 (4) ◽  
pp. L560-L566 ◽  
Author(s):  
Thomas N. George ◽  
Olga L. Miakotina ◽  
Kelli L. Goss ◽  
Jeanne M. Snyder
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Half Life ◽  
Normal Function ◽  
Mrna Levels ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Mrna Half Life

The surfactant proteins (SPs) are required for the normal function of pulmonary surfactant, a lipoprotein substance that prevents alveolar collapse at end expiration. We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line. Cortisol, at 10−6M, caused a significant inhibition of SP-A mRNA to levels that were 60–70% of controls and a five- to sixfold increase in the levels of SP-B mRNA. RA alone (10−6M) had no effect on SP-A mRNA levels and modestly reduced the inhibitory effect of cortisol. RA alone and the combination of cortisol and RA both significantly increased SP-B mRNA levels. RA had no effect on the rate of SP-A gene transcription or on SP-A mRNA stability. Cortisol alone and the combination of cortisol and RA significantly inhibited the rate of SP-A gene transcription but had no effect on SP-A mRNA half-life. RA at 10−6 M had no effect on the rate of SP-B gene transcription but prolonged SP-B mRNA half-life. Cortisol alone and the combination of cortisol and RA caused a significant increase in the rate of SP-B gene transcription and also caused a significant increase in SP-B mRNA stability. We conclude that RA has no effect on SP-A gene expression and increases SP-B mRNA levels by an effect on SP-B mRNA stability and not on the rate of SP-B gene transcription. In addition, the effects of the combination of RA and cortisol were generally similar to those of cortisol alone.

scholarly journals All-trans retinoic acid reverses phorbol ester resistance in a human myeloid leukemia cell line

Blood ◽  
1994 ◽  
Vol 83 (2) ◽  
pp. 490-496 ◽  
Author(s):  
KD Yang ◽  
T Mizobuchi ◽  
SM Kharbanda ◽  
R Datta ◽  
E Huberman ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cell Line ◽  
Leukemia Cell Line ◽  
Nonspecific Esterase ◽  
Mrna Levels ◽  
Monocytic Differentiation ◽  
Granulocytic Differentiation ◽  
Protein Levels ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

Abstract Treatment of human HL-60 leukemic cells with 12-O-tetradecanoylphorbol- 13-acetate (TPA) is associated with activation of protein kinase C (PKC) and induction of monocytic differentiation. An HL-60 variant cell line, termed HL-525, derived from long-term exposure to TPA (Homma et al, Proc Natl Acad Sci USA 83: 7316, 1986) is resistant to TPA-induced differentiation and displays decreased PKC beta expression compared with the HL-60 parent line. However, this variant exhibits features of granulocytic differentiation, including nitroblue tetrazolium reduction, when exposed to all-trans retinoic acid (ATRA). Whereas treatment of HL-525 cells with ATRA or TPA alone had no effect on features of monocytic differentiation, these agents in combination resulted in cellular adhesion, nonspecific esterase staining, and induction of the c-fms (monocyte growth factor receptor) gene. In order to measure PKC expression associated with the reversal of TPA resistance by ATRA, we exposed HL-525 cells to ATRA and analyzed PKC- mRNA and protein levels. Exposure of HL-525 cells to ATRA for 3 days resulted in induction of PKC beta transcripts, whereas there was little change in PKC alpha mRNA levels. ATRA treatment was also associated with an increase in PKC activity and an induction of cytosolic PKC beta protein levels. These findings are consistent with the hypothesis that ATRA reverses TPA resistance in HL-525 cells by enhancing the expression of PKC.

Retinoic acid alters EGF receptor expression during palatogenesis

Development ◽  
1988 ◽  
Vol 102 (4) ◽  
pp. 853-867 ◽  
Author(s):  
B.D. Abbott ◽  
E.D. Adamson ◽  
R.M. Pratt
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Epithelial Cells ◽  
Programmed Cell Death ◽  
Egf Receptor ◽  
Receptor Expression ◽  
Egf Receptors ◽  
Receptor Localization ◽  
All Trans Retinoic Acid ◽  
Fetal Mice

Various growth factors are necessary for normal embryonic development and EGF receptors are present in developing palatal shelves of embryonic/fetal mice at least from day 12 of gestation. The medial epithelium of the palatal shelf undergoes a series of developmental events which do not occur in the oral and nasal epithelia. In utero and in organ culture, the control palatal medial epithelium shows a developmental decline in EGF receptors, demonstrated both by a decrease in the binding of antibody to EGF receptors and a decrease in the binding of 125I-EGF; decreases which are not observed in cells of the adjacent oral or nasal epithelium. During this period, medial cells cease DNA synthesis and undergo programmed cell death. Medial epithelial cells exposed to all-trans-retinoic acid continue to express EGF receptors, bind EGF, proliferate, fail to undergo programmed cell death and exhibit a morphology typical of nasal cells. The data suggest that this disturbance by retinoic acid of EGF receptor localization and subsequent alterations in differentiation of the epithelial cells plays a role in the retinoic-acid-mediated induction of cleft palate.

scholarly journals Differential effects of 9-cis and all-trans retinoic acid on the induction of retinoic acid receptor-β and cellular retinoic acid-binding protein II in human neuroblastoma cells

1994 ◽  
Vol 304 (1) ◽  
pp. 147-154 ◽  
Author(s):  
C P F Redfern ◽  
P E Lovat ◽  
A J Malcolm ◽  
A D J Pearson
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Mrna Levels ◽  
Human Neuroblastoma ◽  
Acid Receptor ◽  
Acid Binding Protein ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
High Concentrations ◽  
Crabp Ii

The objective of this study was to compare the properties of 9-cis and all-trans retinoic acid with respect to the induction of expression of retinoic acid receptor beta (RAR-beta) and cellular retinoic acid-binding protein (CRABP) II in human neuroblastoma SH SY 5Y cells. RAR-beta and CRABP II mRNA was induced by both all-trans and 9-cis retinoic acid in SH SY 5Y cells. Induction was rapid, detectable within 2-4 h, and inhibited by actinomycin D. Time-courses of induction for RAR-beta and CRABP II differed: RAR-beta mRNA levels reached a maximum 4-6 h after adding all-trans or 9-cis retinoic acid, whereas CRABP II mRNA levels increased over at least 18 h. These differences were attributed to the longer half-life of CRABP II mRNA (20 h) compared with RAR-beta mRNA (3.9 h). The dose-response characteristics of all-trans and 9-cis retinoic acid were different: all-trans was effective at nanomolar concentrations, whereas 10-fold higher levels of 9-cis retinoic acid were required to achieve comparable induction of RAR-beta and CRABP II. Conversely, at high concentrations, 9-cis retinoic acid gave a greater induction of RAR-beta and CRABP II than all-trans. The induction of RAR-beta and CRABP II by all-trans retinoic acid was maintained in the subsequent absence of all-trans retinoic acid, whereas induction by 9-cis retinoic acid was dependent on its continued presence in the culture medium. These results suggest that, at high concentrations, 9-cis retinoic acid may produce its transcriptional effects via retinoid X receptor (RXR) homodimers. This has implications for the cellular functions of 9-cis retinoic acid and its use as a biological response modifier.

scholarly journals All-trans Retinoic Acid-induced Abnormal Hippocampal Expression of Synaptic Genes SynDIG1 and DLG2 is Correlated with Anxiety or Depression-Like Behavior in Mice

2020 ◽  
Vol 21 (8) ◽  
pp. 2677
Author(s):  
Xin-Ya Qin ◽  
Hui Fang ◽  
Qing-Hong Shan ◽  
Cong-Cong Qi ◽  
Jiang-Ning Zhou
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Central Area ◽  
Synaptic Function ◽  
Anxiety And Depression ◽  
Mrna Levels ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Potential Link ◽  
Novel Target

Clinical reports suggest a potential link between excess retinoids and development of depression. Although it has been shown that all-trans retinoic acid (ATRA) administration induces behavioral changes, further insight into how ATRA is involved is lacking. The hippocampus seems to be a major target of retinoids, and abnormal synaptic plasticity of the hippocampus is involved in depression. We examined two genes associated with synaptic function, discs large homolog 2 (DLG2), and synapse differentiation-inducing gene protein 1 (SynDIG1) in terms of hippocampal expression and correlation with behavior. Three different doses of ATRA were injected into young mice and 10 mg/kg ATRA was found to induce depression-like behavior. In the hippocampus, DLG2 mRNA was significantly decreased by ATRA. mRNA levels were positively correlated with central area duration and distance in the open-field test. Increased SynDIG1 mRNA levels were observed. There was a negative correlation between SynDIG1 mRNA levels and mobility time in the forced swimming test. Retinoic acid receptor γ mRNA was significantly positively correlated with DLG2 and negatively correlated with SynDIG1. To summarize, ATRA administration induced anxiety- and depression-like behavior accompanied by a decreased expression of DLG2 and an increased expression of SynDIG1. Moreover, DLG2 was correlated with anxiety-like behavior and SynDIG1 was correlated with depression-like behavior. These results might constitute a novel target underlying ATRA-induced anxiety- and depression-like behavior.

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