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Conjugated linoleic acid may decrease arterial calcification via induction of heat shock proteins (1158.7)
Author(s) -
Hsieh TsungHsiu,
Xu Jen,
Hsieh YuChung,
Kao EJay,
Wu Yong,
Lim Kenneth,
Kong Tianqing,
Park Yeonhwa,
Lu Tzongshi
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1158.7
Subject(s) - conjugated linoleic acid , calcification , heat shock protein , linoleic acid , in vivo , chemistry , aorta , vascular smooth muscle , medicine , biochemistry , biology , smooth muscle , fatty acid , gene , microbiology and biotechnology
Vascular calcification (VC) is a significant contributor to cardiovascular mortality in patients with chronic kidney disease and chronic inflammatory conditions. Despite this, there are currently no ideal therapies directed at the prevention or treatment of VC in clinical practice. We recently reported that heat shock protein 72 (HSP72) could be induced in human arteries and prevent human aortic smooth muscle cell (HA‐SMC) calcification. Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of octadecadienoic acid (linoleic acid) with a conjugated double bond system, and cis9, trans11‐CLA form has been shown to have HSP72 inductive properties. In this study, we postulate that CLA may exert vasculo‐protective effects through induction of HSP72. Our results show that inducible HSP72 is significantly expressed following CLA treatment in HA‐SMCs, in vitro as well as in aorta from mice treated with CLA, in vivo. We next showed that JC‐1 complex, an indicator of mitochondrial membrane potential stability was preserved in HA‐SMCs treated with calcification medium following induction of HSP72 by CLA. In conclusion, induction of HSP72’s anti‐calcific effects by CLA involve stabilization of mitochondrial function. We suggest treatment strategies involving induction of HSP72 by CLA as a new approach to inhibit VC.