Citation

Price JA, Rogers JV, Plahovinsak JL, Wendling MQ, Perry MR, Reid FM, Graham JS. Cutan. Ocul. Toxicol. 2012; 31(4): 323-331.

Affiliation

Battelle Biomedical Research Center , Columbus, OH , USA.

Copyright

(Copyright © 2012, Informa - Taylor and Francis Group)

DOI

10.3109/15569527.2012.679374

PMID

22533443

Abstract

Chlorine is an industrial chemical that can cause cutaneous burns. Understanding the molecular mechanisms of tissue damage and wound healing is important for the selection and development of an effective post-exposure treatment. This study investigated the effect of cutaneous chlorine vapor exposure using a weanling swine burn model and microarray analysis. Ventral abdominal sites were exposed to a mean calculated chlorine vapor concentration of 2.9 g/L for 30 min. Skin samples were harvested at 1.5 h, 3 h, 6 h, and 24 h post-exposure and stored in RNAlater(®) until processing. Total RNA was isolated, processed, and hybridized to Affymetrix GeneChip(®) Porcine Genome Arrays. Differences in gene expression were observed with respect to sampling time. Ingenuity Pathways Analysis revealed seven common biological functions among the top ten functions of each time point, while canonical pathway analysis revealed 3 genes (IL-6, IL1A, and IL1B) were commonly shared among three significantly altered signaling pathways. The transcripts encoding all three genes were identified as common potential therapeutic targets for Phase II/III clinical trial, or FDA-approved drugs. The present study shows transcriptional profiling of cutaneous wounds induced by chlorine exposure identified potential targets for developing therapeutics against chlorine-induced skin injury.

Language: en