Switch from actin α1 to α2 expression and upregulation of biomarkers for pressure overload and cardiac hypertrophy in taurine-deficient mouse heart
-
Ulrich Warskulat
, Birgit Andrée , Jessica Lüsebrink , Karl Köhrer and Dieter Häussinger
Abstract
Taurine is the most abundant free amino acid in heart muscle and protects against heart failure. In the present study, the consequences of hereditary taurine deficiency on cardiac gene expression were examined in 2- and 15–16-month-old taurine transporter knockout (taut-/-) mice using a mouse-specific DNA microarray. This oligonucleotide-based microarray contains probes for 251 genes with relevance for heart function. Of these, 163 probes exhibited a reproducible hybridization signal and were analyzed. α-Actin type 1 mRNA levels were 70% lower in the heart of young and older taut-/- mice compared to wild-type controls. Interestingly, the hearts of taut-/- mice showed a switch from α-actin 1 to α-actin 2 expression, as confirmed by real-time PCR and Western blot analysis. In addition, mRNA levels of biomarkers for pressure overload and hypertension were upregulated in taut-/- hearts, i.e., atrial natriuretic factor (+848%), brain natriuretic peptide (+90%), cardiac ankyrin repeat protein (+118%), and procollagen 1a1, 1a2 and 3a1 (+40% at least). These results point to a stress situation in the heart of taut-/- mice under laboratory conditions, and it can be speculated that taut-/- hearts may be even more susceptible to failure in the wild when under exogenous stress.
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Articles in the same Issue
- Highlight: Redox signaling – mechanisms and biological impact
- Paper of the Year 2005: Award to Vanessa Ferreira Merino
- Two-site substrate recognition model for the Keap1-Nrf2 system: a hinge and latch mechanism
- Hypoxia and lipid signaling
- Glutathione peroxidases and redox-regulated transcription factors
- Redox regulation of the hypoxia-inducible factor
- The l-arginine nitric oxide pathway: avenue for a multiple-level approach to assess vascular function
- Protein oxidation and proteolysis
- Mitochondrial signaling, TOR, and life span
- Pathogenetic interplay between osmotic and oxidative stress: the hepatic encephalopathy paradigm
- Regulation of redox-sensitive exofacial protein thiols in CHO cells
- N-Ethylmaleimide-sensitive factor: a redox sensor in exocytosis
- Aspects of the biological redox chemistry of cysteine: from simple redox responses to sophisticated signalling pathways
- Singlet oxygen inactivates protein tyrosine phosphatase-1B by oxidation of the active site cysteine
- Regulatory effects of the mitochondrial energetic status on mitochondrial p66Shc
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- Incinerator fly ash provokes alteration of redox equilibrium and liberation of arachidonic acid in vitro
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- Switch from actin α1 to α2 expression and upregulation of biomarkers for pressure overload and cardiac hypertrophy in taurine-deficient mouse heart
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- The β12-β13 loop is a key regulatory element for the activity and properties of the catalytic domain of protein phosphatase 1 and 2B
- DNA-binding properties of the recombinant high-mobility-group-like AT-hook-containing region from human BRG1 protein
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