Alternative splicing of CRH‐R1 receptors in human and mouse skin: identification of new variants and their differential expression

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Abstract
We identified four new isoforms of human CRH‐R1 (e‐h) and three of mouse (mCRH‐R1c, e, and f). In all new forms exon 6 was missing. Human CRH‐R1e was characterized by the deletion of exons 3 and 4; exon 12 from CRH‐R1f; exon 11, 27 base pairs (bp) of exon 10 and 28 bp of exon 12 from CRH‐R1g and CRH‐R1h by the addition of a cryptic exon. In mouse CRH‐R1c exon 3 was spliced out; in mCRH‐R1e exons 3 and 4 and in mCRH‐R1f exon 11 were spliced from mRNA. CRH‐R1 was expressed in all skin specimens in patterns dependent on the cell type, physiological status, and presence of pathology. CRH‐R1α, the most prevalent form, was detected in almost all samples. Ultraviolet radiation (UV) changed the splicing pattern and induced or increased expression of CRH‐R1α in cultured skin cells. Continuing UV treatment of succeeding generations of cells resulted in a progressive increase in the number of CRH‐R1 isoforms, which suggests that receptor heterogeneity might favor cell survival. TPA (phorbol 12‐myristate 13‐acetate), forskolin, dbcAMP (N6, 2′‐O‐dibutyryladenosine 3′:5′‐cyclic monophospate sodium), and IBMX (3‐isobutyl‐1‐methylxanthine) also changed the splicing pattern. We suggest that a polymorphism of CRH‐R1 expression is related to anatomic location, skin physiological or pathologic status, specific cell type, and external stress (UV), and that cAMP‐dependent pathways and TPA may regulate CRH‐R1.
Funding Information
  • National Science Foundation (IBN-049087)

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