Beta-carotene and apocarotenals promote retinoid signaling in BEAS-2B human bronchioepithelial cells.
Arch Biochem Biophys
; 455(1): 48-60, 2006 Nov 01.
Article
in En
| MEDLINE
| ID: mdl-17034753
ABSTRACT
High dose beta-carotene supplementation of smokers was associated with increased lung cancer risk in two intervention trials. It was proposed that generation of apocarotenals in smoke-exposed lungs impaired retinoic acid (RA) signaling, leading to squamous metaplasia and cell proliferation. To test this, we compared RA target gene regulation by retinoids, apocarotenals or beta-carotene by transcriptomics in BEAS-2B cells cultured to promote squamous differentiation. Retinoids, beta-carotene as well as apocarotenals induced known RA target genes. Retinoids upregulated involucrin, indicating that retinoids did not rescue BEAS-2B cells from squamous differentiation. Muc5AC, a marker for mucous differentiation, was transiently induced. beta-Carotene and apocarotenals less strongly induced involucrin and did not induce muc5AC. In summary, apocarotenals or beta-carotene upregulated RA target genes suggesting promotion, not inhibition, of RA signaling in BEAS-2B cells. Furthermore, apocarotenals and beta-carotene regulated gene expression independently of RA signaling. Squamous differentiation is not unequivocally linked to RA deficiency in BEAS-2B cells.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Retinoids
/
Carotenoids
/
Signal Transduction
/
Beta Carotene
Limits:
Humans
Language:
En
Journal:
Arch Biochem Biophys
Year:
2006
Document type:
Article
Affiliation country: