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 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.

Retinoic acid regulates programmed cell death through BMP signalling

10.1038/10098 ◽  
1999 ◽  
Vol 1 (2) ◽  
pp. 125-126 ◽  
Author(s):  
J. Rodriguez-Leon ◽  
R. Merino ◽  
D. Macias ◽  
Y. Gañan ◽  
E. Santesteban ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Programmed Cell Death ◽  
Bmp Signalling

Tu1402 All-Trans Retinoic Acid (ATRA) Stimulates SLC26A3 Activity in Intestinal Epithelial Cells via a PI3K Signaling Pathway

2015 ◽  
Vol 148 (4) ◽  
pp. S-880 ◽  
Author(s):  
Shubha Priyamvada ◽  
Arivarasu Natarajan Anbazhagan ◽  
Anoop Kumar ◽  
Tarunmeet Gujral ◽  
Alip Borthakur ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Intestinal Epithelial Cells ◽  
Pi3k Signaling ◽  
Intestinal Epithelial ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Pi3k Signaling Pathway

scholarly journals Constitutive Expression of the Promyelocytic Leukemia–Associated Oncogene PML-RARα in TF1 Cells: Isoform-Specific and Retinoic Acid–Dependent Effects on Growth, bcl-2 Expression, and Apoptosis

Blood ◽  
1998 ◽  
Vol 91 (9) ◽  
pp. 3347-3356 ◽  
Author(s):  
James L. Slack ◽  
Min Yu
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Constitutive Expression ◽  
Promyelocytic Leukemia ◽  
Gm Csf ◽  
Functional Differences ◽  
All Trans Retinoic Acid ◽  
Erythroleukemia Cell ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony

Two major isoforms of PML-RARα are associated with (15;17)-positive acute promyelocytic leukemia (APL); however, functional differences between these isoforms have been difficult to define, and the molecular mechanism by which each isoform contributes to the pathogenesis of APL is not fully understood. To address these issues, the ‘short’ (S) and ‘long’ (L) isoforms of PML-RARα were constitutively expressed in the factor-dependent human erythroleukemia cell line, TF1. Expression of the L, but not the S, isoform inhibited growth of these cells in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF). In the absence of GM-CSF, the S isoform partially protected against apoptosis, while the L isoform accelerated cell death. Treatment with all-trans retinoic acid (ATRA) inhibited cell growth and caused apoptosis only in PML-RARα–expressing cells, and these effects of ATRA were more marked in cells expressing the L isoform. ATRA treatment also led to downregulation of bcl-2 and endogenous RARα in PML-RARα–expressing cells, but had little effect on the level of exogenously expressed PML-RARα. We conclude that (1) subtle differences exist in the biologic activities of the L and S isoforms of PML-RARα, and (2) both isoforms are capable of transducing an ATRA-mediated signal that leads to downregulation of bcl-2 and induction of programmed cell death.

scholarly journals Helicobacter pylori Induces Gastric Epithelial Cell Apoptosis in Association with Increased Fas Receptor Expression

1999 ◽  
Vol 67 (8) ◽  
pp. 4237-4242 ◽  
Author(s):  
Nicola L. Jones ◽  
Andrew S. Day ◽  
Hilary A. Jennings ◽  
Philip M. Sherman
Keyword(s):  
Cell Death ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Receptor Expression ◽  
Gastric Epithelial Cells ◽  
Ags Cells ◽  
Fas Receptor ◽  
Epithelial Cell Apoptosis ◽  
H Pylori

ABSTRACT The mechanisms involved in mediating the enhanced gastric epithelial cell apoptosis observed during infection withHelicobacter pylori in vivo are unknown. To determine whether H. pylori directly induces apoptosis of gastric epithelial cells in vitro and to define the role of the Fas-Fas ligand signal transduction cascade, human gastric epithelial cells were infected with H. pylori for up to 72 h under microaerophilic conditions. As assessed by both transmission electron microscopy and fluorescence microscopy, incubation with acagA-positive, cagE-positive, VacA-positive clinical H. pylori isolate stimulated an increase in apoptosis compared to the apoptosis of untreated AGS cells (16.0% ± 2.8% versus 5.9% ± 1.4%, P < 0.05) after 72 h. In contrast, apoptosis was not detected following infection withcagA-negative, cagE-negative, VacA-negative clinical isolates or a Campylobacter jejuni strain. In addition to stimulating apoptosis, infection with H. pylorienhanced Fas receptor expression in AGS cells to a degree comparable to that of treatment with a positive control, gamma interferon (12.5 ng/ml) (148% ± 24% and 167% ± 24% of control, respectively). The enhanced Fas receptor expression was associated with increased sensitivity to Fas-mediated cell death. Ligation of the Fas receptor with an agonistic monoclonal antibody resulted in an increase in apoptosis compared to the apoptosis of cells infected with the bacterium alone (38.5% ± 7.1% versus 16.0% ± 2.8%,P < 0.05). Incubation with neutralizing anti-Fas antibody did not prevent apoptosis of H. pylori-infected cells. Taken together, these findings demonstrate that the gastric pathogen H. pylori stimulates apoptosis of gastric epithelial cells in vitro in association with the enhanced expression of the Fas receptor. These data indicate a role for Fas-mediated signaling in the programmed cell death that occurs in response toH. pylori infection.

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