scholarly journals All-Trans Retinoic Acid Increases Aquaporin 3 Expression in Human Vaginal Epithelial Cells

2016 ◽  
Vol 4 (4) ◽  
pp. e249-e254 ◽  
Author(s):  
Hyun-Suk Lee ◽  
Sun-Ouck Kim ◽  
Kyuyoun Ahn ◽  
Kwangsung Park
2015 ◽  
Vol 148 (4) ◽  
pp. S-880 ◽  
Author(s):  
Shubha Priyamvada ◽  
Arivarasu Natarajan Anbazhagan ◽  
Anoop Kumar ◽  
Tarunmeet Gujral ◽  
Alip Borthakur ◽  
...  

Placenta ◽  
2015 ◽  
Vol 36 (8) ◽  
pp. 881-887 ◽  
Author(s):  
C. Prat ◽  
D. Bouvier ◽  
A. Comptour ◽  
G. Marceau ◽  
C. Belville ◽  
...  

Placenta ◽  
2014 ◽  
Vol 35 (9) ◽  
pp. A45
Author(s):  
Cécile Prat ◽  
Aurélie Comptour ◽  
Damien Bouvier ◽  
Geoffroy Marceau ◽  
Corinne Belville ◽  
...  

2010 ◽  
Vol 299 (2) ◽  
pp. L215-L221 ◽  
Author(s):  
Angela Lee Linderholm ◽  
June Onitsuka ◽  
Changhong Xu ◽  
Maggie Chiu ◽  
Wai-Ming Lee ◽  
...  

DUOX1 and DUOX2 are members of the NADPH oxidase family that are specifically regulated to produce hydrogen peroxide in epithelia of the thyroid, gastrointestinal tract, and respiratory tract. The determinants of DUOX1 or DUOX2 expression in various tissues have not been established. Using respiratory tract epithelial cells as a model, we investigated changes in DUOX mRNA and protein expression during the first 10 days of differentiation. By comparing a respiratory tract cell line, HBE1, with primary tracheobronchial epithelial (TBE) cells, we determined that DUOX2 was significantly expressed only in cell conditions that included all- trans retinoic acid (ATRA). In HBE1 cells, DUOX2 mRNA increased 6-fold after ATRA treatment. Similarly, ATRA induced a 19-fold increase in DUOX2 mRNA expression in primary TBE cells with parallel increases in DUOX protein and DUOX-mediated H2O2 production as well. In addition, DUOX2 induction by rhinovirus required the presence of ATRA. ATRA had no effect on DUOX1 expression for all the conditions studied. Our data indicate that for respiratory epithelial cells, ATRA is important in the regulation of DUOX2 expression, function, and rhinovirus-mediated DUOX2 inducibility.


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