Differential effect of galanin on proliferation of PC12 and B104 cells

• Published in: Neuroreport Vol. 18; no. 13; p. 1379
• Main Authors: Cheng, Shuang, Yuan, Chong-Gang
• Format: Journal Article
• Language: English
• Published: England 27.08.2007
• Subjects: Animals; Bradykinin - analogs & derivatives; Bradykinin - pharmacology; Cell Proliferation - drug effects; Dose-Response Relationship, Drug; Drug Interactions; Galanin - metabolism; Galanin - pharmacology; Gene Expression - drug effects; L-Lactate Dehydrogenase - metabolism; Neuroblastoma; PC12 Cells; Peptide Fragments - pharmacology; Rats; Receptors, Galanin - antagonists & inhibitors; Receptors, Galanin - genetics; Receptors, Galanin - metabolism; Reverse Transcriptase Polymerase Chain Reaction - methods; RNA, Messenger - metabolism; Tetrazolium Salts; Thiazoles
• ISSN: 0959-4965; 1473-558X
• DOI: 10.1097/WNR.0b013e3282c489cc

The effect of galanin (GAL) on neural cell proliferation was studied using PC12 and B104 cells. Reverse transcription-PCR was used to determine the expression of GAL and GAL receptors and a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay of cell viability was employed to detect the effects of GAL on cell proliferation. These studies revealed firstly that PC12 cells express mRNAs encoding all three GAL receptors (GalR1-3) but not GAL mRNA, whereas B104 cells express GAL, GalR2 and GalR3 mRNAs, but not GalR1 mRNA; and secondly that GAL inhibited the proliferation of PC12 cells, but in contrast significantly activated the proliferation of B104 cells. Moreover, these effects of GAL were blocked by M35, a nonselective, chimera peptide antagonist of GAL receptors. These data suggest that GAL can alter neural cell proliferation via GAL receptor activation, and that different GAL receptors and/or cellular complements of receptors produce different net effects via activation of different signaling pathways.