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01.12.2012 | Original investigation | Ausgabe 1/2012 Open Access

Cardiovascular Diabetology 1/2012

Regional evidence of modulation of cardiac adiponectin level in dilated cardiomyopathy: pilot study in a porcine animal model

Zeitschrift:
Cardiovascular Diabetology > Ausgabe 1/2012
Autoren:
Chiara Caselli, Vincenzo Lionetti, Manuela Cabiati, Tommaso Prescimone, Giovanni D Aquaro, Virginia Ottaviano, Fabio Bernini, Letizia Mattii, Silvia Del Ry, Daniela Giannessi
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2840-11-143) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare they have no competing interests.

Authors’ contributions

As to the contribution of each author, CC and DG designed the study, analyzed and interpreted the results, and drafted the manuscript; GDA and FB were involved in the animal model; MC, TP and VO made substantial contributions to performing the experimental protocol; VL, LM and SDR were involved in revising the manuscript critically for important intellectual content. All authors participated in the discussion and interpretation of the results and in the final approval of the manuscript submitted.

Abstract

Background

The role of systemic and myocardial adiponectin (ADN) in dilated cardiomyopathy is still debated. We tested the regulation of both systemic and myocardial ADN and the relationship with AMP-activated protein kinase (AMPK) activity in a swine model of non-ischemic dilated cardiomyopathy.

Methods and results

Cardiac tissue was collected from seven instrumented adult male minipigs by pacing the left ventricular (LV) free wall (180 beats/min, 3 weeks), both from pacing (PS) and opposite sites (OS), and from five controls. Circulating ADN levels were inversely related to global and regional cardiac function. Myocardial ADN in PS was down-regulated compared to control (p < 0.05), yet ADN receptor 1 was significantly up-regulated (p < 0.05). No modifications of AMPK were observed in either region of the failing heart. Similarly, myocardial mRNA levels of PPARγ, PPARα, TNFα, iNOS were unchanged compared to controls.

Conclusions

Paradoxically, circulating ADN did not show any cardioprotective effect, confirming its role as negative prognostic biomarker of heart failure. Myocardial ADN was reduced in PS compared to control in an AMPK-independent fashion, suggesting the occurrence of novel mechanisms by which reduced cardiac ADN levels may regionally mediate the decline of cardiac function.
Zusatzmaterial
Authors’ original file for figure 1
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Authors’ original file for figure 2
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Authors’ original file for figure 3
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Authors’ original file for figure 4
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Literatur
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