Iron, ferritin and proteins of the methionine-centered redox cycle in young and old rat hearts

Baruch Bulvik; Leonid Grinberg; Ron Eliashar; Eddy Berenshtein; Mordechai (Mottie) Chevion

doi:10.1016/j.mad.2008.10.002

Iron, ferritin and proteins of the methionine-centered redox cycle in young and old rat hearts

Baruch Bulvik, Leonid Grinberg, Ron Eliashar, Eddy Berenshtein, Mordechai (Mottie) Chevion^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

22 Scopus citations

Abstract

Progressive oxidation of cellular components constitutes a major mechanism of the aging process. An emerging paradigm of redox signaling suggests that low level oxidants activate protective pathways resulting in prolonged cell survival. This report centers on the study of cardiac muscle in young and old rats, including (i) the expression of ferritin (Ft) the major iron storage protein, and (ii) the expression of the major proteins of the methionine-centered redox cycle (MCRC), which controls the cellular methionine redox status. Total amounts of Ft (protein) and its mRNA encoding for Ft L-subunit (Ft-L) were higher in the aged hearts, indicating that the iron-binding capacity of myocardial Ft increased with age. Among the proteins of the MCRC, methionine sulfoxide reductases A and B (MsrA, MsrB) and MsrA mRNA were significantly higher in hearts of old rats with a significant decrease in MsrA activity. The observed up-regulation of the expression of Msr and Ft-L could represent a protective response to the increased oxidative stress in the aging myocardium.

Original language	English
Pages (from-to)	139-144
Number of pages	6
Journal	Mechanisms of Ageing and Development
Volume	130
Issue number	3
DOIs	https://doi.org/10.1016/j.mad.2008.10.002
State	Published - Mar 2009
Externally published	Yes

Bibliographical note

Funding Information:
This study was supported by grants from the Israel Science Foundation (ISF 585/02 and 316/05), and from the ‘Dr. Abraham Moshe and Paula Pepka Bergman Memorial Fund’. MC is the incumbent of the Dr. William Ganz Chair for Heart Studies at the Hebrew University of Jerusalem.

Keywords

Aging
Ferritin subunits
Methionine sulfoxide reductase
Thioredoxin
Thioredoxin reductase

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10.1016/j.mad.2008.10.002

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title = "Iron, ferritin and proteins of the methionine-centered redox cycle in young and old rat hearts",

abstract = "Progressive oxidation of cellular components constitutes a major mechanism of the aging process. An emerging paradigm of redox signaling suggests that low level oxidants activate protective pathways resulting in prolonged cell survival. This report centers on the study of cardiac muscle in young and old rats, including (i) the expression of ferritin (Ft) the major iron storage protein, and (ii) the expression of the major proteins of the methionine-centered redox cycle (MCRC), which controls the cellular methionine redox status. Total amounts of Ft (protein) and its mRNA encoding for Ft L-subunit (Ft-L) were higher in the aged hearts, indicating that the iron-binding capacity of myocardial Ft increased with age. Among the proteins of the MCRC, methionine sulfoxide reductases A and B (MsrA, MsrB) and MsrA mRNA were significantly higher in hearts of old rats with a significant decrease in MsrA activity. The observed up-regulation of the expression of Msr and Ft-L could represent a protective response to the increased oxidative stress in the aging myocardium.",

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AU - Chevion, Mordechai (Mottie)

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AB - Progressive oxidation of cellular components constitutes a major mechanism of the aging process. An emerging paradigm of redox signaling suggests that low level oxidants activate protective pathways resulting in prolonged cell survival. This report centers on the study of cardiac muscle in young and old rats, including (i) the expression of ferritin (Ft) the major iron storage protein, and (ii) the expression of the major proteins of the methionine-centered redox cycle (MCRC), which controls the cellular methionine redox status. Total amounts of Ft (protein) and its mRNA encoding for Ft L-subunit (Ft-L) were higher in the aged hearts, indicating that the iron-binding capacity of myocardial Ft increased with age. Among the proteins of the MCRC, methionine sulfoxide reductases A and B (MsrA, MsrB) and MsrA mRNA were significantly higher in hearts of old rats with a significant decrease in MsrA activity. The observed up-regulation of the expression of Msr and Ft-L could represent a protective response to the increased oxidative stress in the aging myocardium.

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Iron, ferritin and proteins of the methionine-centered redox cycle in young and old rat hearts

Abstract

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Keywords

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