Mitochondrial Ferritin Expression in Adult Mouse Tissues

Mitochondrial ferritin (FtMt) is a novel ferritin type specifically targeted to mitochondria. It is highly expressed in the human testis and in sideroblasts from patients with sideroblastic anemia, but other organs have not been studied. To study its expression in the main organs of the mouse, we fi...

Full description

Saved in:
Bibliographic Details
Published in:The journal of histochemistry and cytochemistry 2007-11, Vol.55 (11), p.1129-1137
Main Authors: Santambrogio, Paolo, Biasiotto, Giorgio, Sanvito, Francesca, Olivieri, Stefano, Arosio, Paolo, Levi, Sonia
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Enzyme-Linked Immunosorbent Assay
Ferritins - biosynthesis
Immunohistochemistry
Male
Mice
Mitochondrial Proteins - biosynthesis
Molecular Sequence Data
Organ Specificity
Recombinant Proteins - biosynthesis
Testis - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Mitochondrial ferritin (FtMt) is a novel ferritin type specifically targeted to mitochondria. It is highly expressed in the human testis and in sideroblasts from patients with sideroblastic anemia, but other organs have not been studied. To study its expression in the main organs of the mouse, we first used RT-PCR and then produced recombinant mouse FtMt and specific antibodies. Immunohistochemistry analyses confirmed that FtMt is highly expressed in mouse testis, particularly in spermatocytes and interstitial Leydig cells. The protein was also identified in other organs including heart, brain, spinal cord, kidney, and pancreatic islet of Langerhans but not in liver and splenocytes, which have iron storage function and express high levels of cytosolic ferritins. Results indicate that the primary function of ferritin FtMt is not involved in storing cellular or body iron, but its association with cell types characterized by high metabolic activity and oxygen consumption suggests a role in protecting mitochondria from iron-dependent oxidative damage.
ISSN:0022-1554
1551-5044
DOI:10.1369/jhc.7A7273.2007