Deletion of the basigin gene results in reduced mitochondria in the neural retina

Document Type

Article

Publication Date

8-30-2013

Abstract

Basigin-null mice are characterized as blind from the time of eye opening, with degeneration of the retina beginning at 8. weeks of age, and progressing until the entire photoreceptor cell layer is destroyed. It is likely that a metabolic deficiency underlies the blindness and degeneration phenotypes, as it has been determined that Basigin-null mice do not express the transporter protein monocarboxylate transporter one on the membrane of photoreceptor cells and inner segments, nor Müller cells of the neural retina, as is observed in normal mice. The purpose of the present study was to assess the health of mitochondria in normal and Basigin-null mice, specifically to determine if mitochondria within the Basigin-null mouse neural retina are metabolically active. This was achieved via a measurement of cytochrome C concentration and the expression of autophagy-specific proteins via ELISA analyses. Additionally, Mitotracker dyes were used to assess the number and relative activity of mitochondria. It was determined that cytochrome C concentrations and expression of autophagy-specific proteins were not increased in Basigin-null animals, as compared to control animals. Also, while Basigin-null mice do have metabolically active mitochondria, the amount of mitochondria was greatly reduced, when compared to control animals. The results suggest that a reduction in mitochondria is a result, rather than the cause, of the metabolic deficiency observed in Basigin-null mice, and likely occurs because of reduced metabolic activity in the absence of MCT1 expression. © 2013 Elsevier Inc.

Publication Title

Biochemical and Biophysical Research Communications

Volume

438

Issue

3

First Page

546

Last Page

550

Digital Object Identifier (DOI)

10.1016/j.bbrc.2013.07.092

PubMed ID

23906756

ISSN

0006291X

E-ISSN

10902104

Link to Full Text

Share

COinS