Publication Database

Cardioprotective effects of palmitoleic acid (C16:1n7) in a mouse model of catecholamine-induced cardiac damage are mediated by PPAR activation (2021)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Betz, Iris Rosa

Qaiyumi, Sarah Julia

Goeritzer, Madeleine

Thiele, Arne

Brix, Sarah

Beyhoff, Niklas

Grune, Jana

Klopfleisch, Robert (WE 12)

Greulich, Franziska

Uhlenhaut, Nina Henriette

Kintscher, Ulrich

Foryst-Ludwig, Anna

Quelle

International journal of molecular sciences

Bandzählung: 22

Heftzählung: 23

Seiten: Artikel 12695

ISSN: 1422-0067

Sprache

Englisch

Verweise

URL (Volltext): https://www.mdpi.com/1422-0067/22/23/12695

DOI: 10.3390/ijms222312695

Pubmed: 34884498

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

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 α/δ (PPARα/δ) 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.