Transcriptomic changes by PACAP-38 and PACAP(6-38) on rat trigeminal ganglion cell culture. undefined

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a broadly-expressed neuropeptide which has diverse effects in both the peripheral and central nervous system. While its neuroprotective effects have been shown in a variety of disease models, both animal and human data support the role of PACAP in migraine headache generation. In rat trigeminal ganglion (TG) cells, both PACAP and its truncated derivative PACAP(6-38) could increase intracellular calcium levels even though the latter is an antagonist on the classical receptors of PACAP in most experimental settings. Our goal was to identify the common signaling pathway behind the effect of the two peptides on by transcriptomic analysis. Rat trigeminal ganglion cells cultured were incubated with 1 µM PACAP-38 or PACAP(6-38). Six and 24 hours later RNA was isolated and next-generation RNA sequencing as performed with Illumina NextGenSeq 550 Instrument followed by transcriptomic analysis. Statistical analysis was made with RStudio to identify differentially-expressed genes. Functional analysis was performed for gene annotation using the Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome databases. (3) Results: Both PACAP-38 and PACAP(6-38) treatments caused downregulation of NADH:ubiquinone oxidoreductase subunit B6 and upregulation of transient receptor potential cation channel, subfamily M, member 8 significantly. Target receptor at transcriptome levels was not detected.