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The effects of retinoid status on TGF β expression during mouse embryogenesis

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Abstract

In a previous study we investigated the effects of RA excess on TGF β protein localization in early postimplantation stages of mouse development. Here we extend this investigation by comparing the effects of retinoid deficiency with those of excess, and by comparing the effects of altered retinoid status on TGF β protein and RNA transcript distribution. In vitamin A-deficient embryos, TGF β1 RNA and protein distribution were both unaltered compared with controls; conversely, TGF β2 protein levels were reduced while RNA levels remained normal. In RA-treated embryos, the previous study showed that intracellular TGF β1 levels were decreased, while those of extracellular TGF β1 were initially decreased but subsequently increased; here we found that TGF β1 RNA transcript levels were reduced following exposure to RA excess. TGF β2 showed a clear disparity between the effects of RA excess on protein and RNA transcript levels: RNA transcript distribution was unchanged or showed a slight increase in RA-treated embryos, whereas the previous results showed greatly reduced protein levels. The new results provide further evidence for interaction between retinoids and TGF βs during mouse development, and indicate that retinoids are capable of differentially regulating TGF β isoforms through mechanisms involving different stages in the process of TGF β synthesis and secretion. The long-term nature of the effects of transient exposure to RA excess suggests that the mechanisms of RA-TGF β interaction may be indirect.

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Mahmood, R., Flanders, K.C. & Morriss-Kay, G.M. The effects of retinoid status on TGF β expression during mouse embryogenesis. Anat Embryol 192, 21–33 (1995). https://doi.org/10.1007/BF00186988

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