Premium
Changes in hepatic gene expression in dogs with experimentally induced nutritional iron deficiency
Author(s) -
Fry Michael M.,
Kirk Claudia A.,
Liggett Jason L.,
Daniel Gregory B.,
Baek Seung Joon,
Gouffon Julia S.,
Chimakurthy Pradeep M.,
Rekapalli Bhanu
Publication year - 2009
Publication title -
veterinary clinical pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 51
eISSN - 1939-165X
pISSN - 0275-6382
DOI - 10.1111/j.1939-165x.2008.00081.x
Subject(s) - hepcidin , calreticulin , gene expression , biology , gene , transferrin receptor , microarray analysis techniques , microarray , fold change , gene expression profiling , ferroportin , ferritin , microbiology and biotechnology , transferrin , regulation of gene expression , dna microarray , endocrinology , genetics , immunology , biochemistry , endoplasmic reticulum , inflammation
Background and Objective: We investigated hepatic gene expression in dogs with experimentally induced nutritional iron deficiency (ID). Our hypothesis was that ID would result in decreased hepcidin gene expression, and possibly in altered expression of other genes associated with iron metabolism. Methods: Liver biopsies were collected from each of 3 dogs before induction of ID, at the point of maximal ID, and after resolution of ID. Using Affymetrix microarray technology and analytical tools specifically designed for microarray data, we identified genes that had at least a 2‐fold change in expression in response to ID. Four genes were selected for further analysis by reverse transcriptase PCR (RT‐PCR). Results: Dogs with ID had markedly decreased expression of the hepcidin gene (mean decrease of 40‐fold for one probe and >100‐fold for another probe) and increased expression of the transferrin receptor gene (mean increase of >7‐fold). There was also mildly decreased expression of the “similar to calreticulin” gene and a gene of unknown function. Results of RT‐PCR analysis were consistent with microarray findings. Conclusion: Changes in hepcidin and transferrin receptor gene expression were consistent with the known biology of iron metabolism. The decrease in expression of a gene identified as “similar to calreticulin,” while not statistically significant, was consistent with the findings of other investigators that suggest iron plays a role in calreticulin expression.