4.7 Article

Cardioprotective Effects of Palmitoleic Acid (C16:1n7) in a Mouse Model of Catecholamine-Induced Cardiac Damage Are Mediated by PPAR Activation

Journal

Publisher

MDPI
DOI: 10.3390/ijms222312695

Keywords

palmitoleic acid (C16; 1n7); lipokine; catecholamine; cardiac damage; PPAR; cardioprotective effects

Funding

  1. German Centre for Cardiovascular Research (DZHK) [BER 5.4 PR]
  2. Deutsche Gesellschaft fur Kardiologie (DKG)
  3. DZHK [BER 5.4 PR]
  4. Charite-Universitatsmedizin Berlin
  5. Berlin Institute of Health
  6. Entzuendungsprozesse [GR 5179/1-1]
  7. DFG [UH 275/1-1]
  8. ERC [ERC-2014-StG 638573]
  9. Deutsche Forschungsgemeinschaft (DFG) [KI 712/10-1]
  10. Bundesinstitut fur Risikobewertung (BMBF) [BfR1328-564]
  11. Einstein Foundation/Foundation Charite [EVF-BIH-2018-440]

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The study demonstrated that C16:1n7 has protective effects on the heart by regulating PPAR-specific signaling pathways and may be used for therapy against cardiac fibrosis and inflammation induced by catecholamines.
Palmitoleic acid (C16:1n7) has been identified as a regulator of physiological cardiac hypertrophy. In the present study, we aimed to investigate the molecular pathways involved in C16:1n7 responses in primary murine cardiomyocytes (PCM) and a mouse model of isoproterenol (ISO)-induced cardiac damage. PCMs were stimulated with C16:1n7 or a vehicle. Afterwards, RNA sequencing was performed using an Illumina HiSeq sequencer. Confirmatory analysis was performed in PCMs and HL-1 cardiomyocytes. For an in vivo study, 129 sv mice were orally treated with a vehicle or C16:1n7 for 22 days. After 5 days of pre-treatment, the mice were injected with ISO (25 mg/kg/d s. c.) for 4 consecutive days. Cardiac phenotyping was performed using echocardiography. In total, 129 genes were differentially expressed in PCMs stimulated with C16:1n7, including Angiopoietin-like factor 4 (Angptl4) and Pyruvate Dehydrogenase Kinase 4 (Pdk4). Both Angptl4 and Pdk4 are proxisome proliferator-activated receptor alpha/delta (PPAR alpha/delta) target genes. Our in vivo results indicated cardioprotective and anti-fibrotic effects of C16:1n7 application in mice. This was associated with the C16:1n7-dependent regulation of the cardiac PPAR-specific signaling pathways. In conclusion, our experiments demonstrated that C16:1n7 might have protective effects on cardiac fibrosis and inflammation. Our study may help to develop future lipid-based therapies for catecholamine-induced cardiac damage.

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