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VIP and the potent analog, stearyl‐Nle 17 ‐VIP, induce proliferation of keratinocytes
Author(s) -
Granoth Ruth,
Fridkin Mati,
Gozes Illana
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01628-8
Subject(s) - hacat , vasoactive intestinal peptide , autocrine signalling , keratinocyte , pituitary adenylate cyclase activating peptide , paracrine signalling , receptor , biology , microbiology and biotechnology , cell culture , nitric oxide , chemistry , endocrinology , medicine , neuropeptide , biochemistry , genetics
Vasoactive intestinal polypeptide (VIP) exhibits effects on cell proliferation. Here, VIP, as well as the related peptide, pituitary adenylate cyclase activating peptide (PACAP), promoted human keratinocyte division. Stearyl‐Nle 17 ‐VIP (SNV) was identified as a superior mitogen for the keratinocytic cell line, HaCaT, both in potency (fM–nM concentrations) and efficacy. Reverse transcription‐polymerase chain reaction detected in keratinocytes only PACAP mRNA and the relevant type 1 (VPAC 1 R) and type 2 (VPAC 2 R) receptors, while VIP and the third receptor (PAC 1 ) transcripts were absent. Upon serum deprivation of HaCaT, the VPAC 1 R mRNA was apparently increased, while the VPAC 2 R transcript remained constant. Incubation of HaCaT with VIP or SNV increased nitric oxide and cGMP formation. In contrast to VIP, SNV did not augment cAMP. Thus, the paracrine VIP, and autocrine PACAP, related pathways leading to keratinocyte proliferation may involve VPAC 1 R/VPAC 2 R and nitric oxide/cGMP production.