Early programmed cell death in human NT2 cell cultures during differentiation induced by all-trans-retinoic acid

2002 ◽  
Vol 71 (1) ◽  
pp. 38-45 ◽  
Author(s):  
I. Guillemain ◽  
G. Fontès ◽  
A. Privat ◽  
I. Chaudieu
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Programmed Cell Death ◽  
Cell Cultures ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

scholarly journals All-trans-retinoic acid-mediated cytoprotection in LLC-PK1 renal epithelial cells is coupled to p-ERK activation in a ROS-independent manner

2017 ◽  
Vol 313 (6) ◽  
pp. F1200-F1208 ◽  
Author(s):  
Jessica M. Sapiro ◽  
Terrence J. Monks ◽  
Serrine S. Lau
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Independent Manner ◽  
Toxicant Exposure ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Survival Pathways

Although all- trans-retinoic acid (ATRA) provides protection against a variety of conditions in vivo, particularly ischemia, the molecular mechanisms underpinning these effects remain unclear. The present studies were designed to assess potential mechanisms by which ATRA affords cytoprotection against renal toxicants in LLC-PK1 cells. Pretreatment of LLC-PK1 cells with ATRA (25 μM) for 24 h afforded cytoprotection against oncotic cell death induced by p-aminophenol (PAP), 2-(glutathion- S-yl)hydroquinone (MGHQ), and iodoacetamide but not against apoptotic cell death induced by cisplatin. Inhibition of protein synthesis with cycloheximide blunted ATRA protection, indicating essential cell survival pathways must be engaged before toxicant exposure to provide cytoprotection. Interestingly, ATRA did not prevent the PAP-induced generation of reactive oxygen species (ROS) nor did it alter glutathione levels. Moreover, ATRA had no significant effect on Nrf2 protein expression, and the Nrf2 inducers sulforaphane and MG132 did not influence ATRA cytoprotection, suggesting cytoprotective pathways beyond those that influence ROS levels contribute to ATRA protection. In contrast, ATRA rapidly (15 min) induced levels of the cellular stress kinases p-ERK and p-AKT at concentrations of ATRA (10 and 25 μM) required for cytoprotection. Consistent with a role for p-ERK in ATRA-mediated cytoprotection, inhibition of p-ERK with PD98059 reduced the ability of ATRA to afford protection against PAP toxicity. Collectively, these data suggest that p-ERK and its downstream targets, independent of ROS and antioxidant signaling, are important contributors to the cytoprotective effects of ATRA against oncotic cell death.

Effects of ?-all-trans retinoic acid on growth, proliferation, and cell death in a multicellular tumor spheroid model for squamous carcinomas

1990 ◽  
Vol 144 (2) ◽  
pp. 237-243 ◽  
Author(s):  
Peter G. Sacks ◽  
Victor Oke ◽  
Tracey Vasey ◽  
Dennise P. Calkins ◽  
Nicholas H. A. Terry
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Tumor Spheroid ◽  
Multicellular Tumor Spheroid ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

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.

45. Regulation of BcI-2 and cell death by all-trans retinoic acid in acute promyelocytic leukemic cells

1992 ◽  
Vol 46 (5-7) ◽  
pp. 260 ◽  
Author(s):  
C Chomiennc ◽  
S Barbey ◽  
N Balitrand ◽  
L Degos ◽  
L Sachs
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Leukemic Cells ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

Protective effect of all-trans retinoic acid on NMDA-induced neuronal cell death in rat retina

2010 ◽  
Vol 635 (1-3) ◽  
pp. 56-61 ◽  
Author(s):  
Kenji Sakamoto ◽  
Masahide Hiraiwa ◽  
Maki Saito ◽  
Tsutomu Nakahara ◽  
Yoji Sato ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinoic Acid ◽  
Protective Effect ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Retina ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid
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