| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1926931 | Archives of Biochemistry and Biophysics | 2007 | 5 Pages |
Total gastrectomy (TG) causes cobalamin (Cbl) deficiency followed by increases in tumor necrosis factor (TNF)-α levels in the spinal cord (SC) of the rat. In order to understand how Cbl deficiency may influence cell Cbl transport, we have measured by immunoblotting protein levels of the receptor for the Cbl–transcobalamin (TC) complex (TC-R) in both animal and cell models. TC-R protein levels were elevated in the total membranes of duodenal mucosa, kidneys, liver, and SC of rats made Cbl-deficient (Cbl-D) by means of TG or feeding with a Cbl-D diet. Postoperative Cbl-replacement treatment normalized the TC-R protein levels in each of the tested organs, regardless of whether this treatment was given during the first two post-TG or during the third and fourth post-TG mo. In Caco-2 cells, progressively increasing TNF-α concentrations supplemented to culture medium induced an up-regulation of TC-R protein levels. We provide the first evidence of the regulation of a Cbl-specific receptor by the vitamin itself in some rat organs.
