Premium
Longitudinal changes in ZnT‐1 protein abundance in response to moderately excess zinc in an in vitro blood‐brain barrier model
Author(s) -
Olley Bryony Jean,
Bobilya Dennis
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.a626-a
Subject(s) - in vitro , abundance (ecology) , zinc , blood–brain barrier , biology , chemistry , neuroscience , biochemistry , ecology , central nervous system , organic chemistry
Zinc (Zn) is one of several trace minerals essential to life. Zinc toxicity can upset body homeostasis, but zinc transporter proteins exist to protect against homeostatic imbalances in the body. Longitudinal studies have been performed to examine zinc transporter behavior and mRNA expression in a blood brain barrier (BBB) model. The moderately high Zn concentrations caused in increase in ZnT‐1 transporter expression and the cells of the BBB increased their capacity to transport zinc. The current study examined the longitudinal changes in the relative quantity of ZnT‐1 protein in brain capillary endothelial cells of the BBB in response to Zn. BCEC were isolated from Yucatan miniature swine and grown into an in vitro model of the BBB. The cells were exposed to a moderately excessive (50 μM) Zn environment for varying periods of time (0, 12, 24, 48, 72 & 96 h). Protein abundance was measured by Western analysis using an antibody generously provided by Lonnerdal and Kelleher (Univ. California, Davis). ZnT‐1 protein increased in abundance by approximately 50% within 24 h of Zn exposure, and remained at this elevated level throughout the remainder of the measurement period (96 h). This increase in ZnT‐1 transport proteins corresponds to changes in zinc transport kinetics and therefore implies that ZnT‐1 serves as a mediator of brain zinc homeostasis under conditions of moderate zinc excess.