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Updated: Aug 15, 2026
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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
Protein oxidation and age-dependent alterations in calcium homeostasis
1Biochemistry and Biophysics Section, Department of Molecular Bioscience, University of Kansas, Lawrence, KS 66045-2106, USA. tsquier@ukans.edu
Summary
Aging impairs calcium homeostasis due to protein damage, affecting cellular function and increasing disease risk. Reversible modifications offer potential therapeutic targets for age-related conditions.
Area of Science:
- Biochemistry
- Cellular Biology
- Gerontology
Background:
- Aging is linked to impaired calcium homeostasis, contributing to reduced cellular function and age-related diseases.
- Calcium regulatory proteins, crucial for cellular signaling, undergo age-related functional decline.
- Post-translational modifications and structural changes in these proteins are key to understanding aging.
Purpose of the Study:
- To identify age-related post-translational modifications in calcium regulatory proteins.
- To elucidate the structural changes and functional consequences of these modifications.
- To explore the potential for reversing these modifications to treat age-related diseases.
Main Methods:
- Analysis of methionine oxidation in calmodulin (CaM) during aging in brain tissue.
- Investigation of tyrosine nitration in sarcoplasmic reticulum Ca-ATPase (SERCA2a) in muscle during aging.
- Assessment of changes in plasma membrane Ca-ATPase (PM-Ca-ATPase) activity.
Main Results:
- Oxidation of methionines in CaM impairs its ability to activate target proteins like PM-Ca-ATPase.
- Nitration of tyrosines in SERCA2a leads to decreased Ca-ATPase function in aging muscle.
- These protein dysfunctions correlate with increased intracellular calcium levels in senescent cells.
Conclusions:
- Age-related post-translational modifications of calcium regulatory proteins contribute to cellular dysfunction.
- These modifications may be reversible by specific intracellular repair enzymes.
- Reversible oxidation might enhance cellular survival under oxidative stress by reducing energy demand, with ATP depletion potentially underlying age-related calcium dysregulation.
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