Premium
Copper transporter (Ctr1) expression in mouse tissue is impacted by age and dietary copper
Author(s) -
Kuo Yien Ming,
Gybina Anna A,
Gitschier Jane,
Prohaska Joseph R
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a553-c
Subject(s) - choroid plexus , kidney , staining , myenteric plexus , biology , epithelium , immunohistochemistry , immunocytochemistry , copper , chemistry , endocrinology , medicine , central nervous system , organic chemistry , immunology , genetics
Distribution of the copper transporter, Ctr1, a transmembrane protein responsible for cellular copper uptake, was determined in adult mice and in suckling mice nursed by either copper‐adequate (Cu+) or copper‐deficient (Cu‐) dams. In adult mice, immunohistochemical analyses detected abundant Ctr1 protein in liver canaliculi; kidney cortex tubules; small intestinal enterocytes; the choroid plexus and capillaries of brain; intercalated disks of heart; mature spermatozoa; epithelium of mammary ducts; and the pigment epithelium (RPE), outer limiting membrane (OLM), and outer plexiform layer (OPL) of the retina. Duodenal Ctr1 distribution was different in the adult compared to suckling mice; adult mice demonstrated strong intracellular staining of the enterocyte whereas apical staining predominated in the suckling mice. In Cu‐ mice at postnatal day 16 (P16), Ctr1 staining was augmented in kidney, duodenum, and choroid plexus, compared to Cu+ mice. Cu‐ mice had lower hemoglobin (56% of Cu+), and lower copper concentration (% of Cu+) in liver (15%), brain (26%), and kidney (65%). These results suggest that Ctr1 protein is expressed in multiple tissues and found in higher levels in selected organs following perinatal copper deficiency. Enhanced Ctr1 levels and redistribution might compensate, partially, for the decrease in copper supply. Mechanisms for the enhancement in Ctr1 staining remain to be established. Supported in part by NIH grant HD 39708 to JRP and HHMI (JG).