ABSTRACT
Figure 6 Expression of mRNA for various retinoid-binding proteins in cultured human keratinocytes (reverse transcription coupled to the polymerase chain reaction). Amplification products were electrophoresed on 7% acrylamide gels, stained with ethidium bromide, and photographed under UV Lane 1, molecular weight (base pairs) markers; 2, reference (GAPDH) for normalization of staining; 3, RBP; 4, CRBPI; 5, CRABPI; 6, CRABPII; 7, RXRa; 8, RARa; 9, RAR!3; and 10, RARy. (Modified from Refs. 162 and 247.)
proteins (CRABP I and CRBPI and CRABPI are ubiquitously Pvr•rP.~ . .,P.I11 but their type II counterparts appear to have a much more restricted distribution (213,214). Figure 6 shows the mRNA expression of various retinoid-binding proteins in cultured human keratinocytes using reverse transcription polymerase chain reaction for amplification (162). Distinct bands corresponding to the mRNAs for CRBPI and CRABPII are seen. The much weaker expression of mRNA for CRABPI is consistent with negative findings using less sensitive Northern blot and in situ hybridization techniques (215,216). Also, CRABPI (but not the other binding proteins) is downregulated in rapidly proliferating, undifferentiated keratinocytes
The quantitative data on the distribution of cellular retinoid-binding in the skin must be with some caution. Older techniques did not dis~ criminate the various of CRBP and CRABP, but the general mm~r"""" was that the former was present throughout the skin, whereas the latter protein was almost confined to epidermis (218,219). In both proteins have been demonstrated in sebaceous glands and in skin fibroblasts (220,221). In comparison with several other tissues, notably liver, intestine, and testis (213), low total levels are found in normal skin (219,220,222).
