title: Temporal effects in porcine skin following bromine vapor exposure.
abstract: Bromine is an industrial chemical that causes severe cutaneous burns. When selecting or developing effective treatments for bromine burns, it is important to understand the molecular mechanisms of tissue damage and wound healing. This study investigated the effect of cutaneous bromine vapor exposure on gene expression using a weanling swine burn model by microarray analysis. Ventral abdominal sites were exposed to a mean calculated bromine vapor concentration of 0.51 g/L for 7 or 17 min. At 6 h, 48 h, and 7 days post-exposure, total RNA from skin samples was isolated, processed, and analyzed with Affymetrix GeneChip® Porcine Genome Arrays (N = 3 per experimental group). Differences in gene expression were observed with respect to exposure duration and sampling time. Ingenuity Pathways Analysis (IPA) revealed four common biological functions (cancer, cellular movement, cell-to-cell signaling and interaction, and tissue development) among the top ten functions of each experimental group, while canonical pathway analysis revealed 9 genes (ARG2, CCR1, HMOX1, ATF2, IL-8, TIMP1, ESR1, HSPAIL, and SELE) that were commonly shared among four significantly altered signaling pathways. Among these, the transcripts encoding HMOX1 and ESR1 were identified using IPA as common potential therapeutic targets for Phase II/III clinical trial or FDA-approved drugs. The present study describes the transcriptional responses to cutaneous bromine vapor exposure identifying molecular networks and genes that could serve as targets for developing therapeutics for bromine-induced skin injury.
authors.affiliation: Battelle Biomedical Research Center, Columbus, Ohio 43201, USA. priceja@battelle.org
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Price
authors.forename: James V
authors.initials: JV
authors.lastname: Rogers
authors.forename: Morgan Q S
authors.initials: MQ
authors.lastname: Wendling
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Plahovinsak
authors.forename: Mark R
authors.initials: MR
authors.lastname: Perry
authors.forename: Frances M
authors.initials: FM
authors.lastname: Reid
authors.forename: Robyn C
authors.initials: RC
authors.lastname: Kiser
authors.forename: John S
authors.initials: JS
authors.lastname: Graham
mesh_terms: D000818:Animals; D001966:Bromine / Q000633:toxicity*; D002057:Burns, Chemical / Q000378:metabolism* / Q000473:pathology; D018076:DNA, Complementary / Q000235:genetics; D003627:Data Interpretation, Statistical; D004195:Disease Models, Animal; D005260:Female; D020869:Gene Expression Profiling; D020411:Oligonucleotide Array Sequence Analysis; D012313:RNA / Q000235:genetics; D012867:Skin / Q000293:injuries* / Q000378:metabolism* / Q000473:pathology; D034421:Sus scrofa; D014158:Transcription, Genetic / Q000187:drug effects*; D014835:Volatilization; D014945:Wound Healing
chemical_list: D018076:DNA, Complementary; D012313:RNA; D001966:Bromine