miR-208a as a Biomarker of Isoproterenol-induced Cardiac Injury in Sod2+/− and C57BL/6J Wild-type Mice

This investigation examined microRNA-208a (miR-208a) as a potential biomarker of isoproterenol (ISO)-induced cardiac injury in superoxide dismutase-2 (Sod2+/− ) and the wild-type mice, and the potential sensitivity of Sod2+/− mice to ISO-induced toxicity. A single intraperitoneal injection of ISO wa...

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Bibliographic Details
Published in:Toxicologic pathology 2014-10, Vol.42 (7), p.1117-1129
Main Authors: Liu, Ling, Aguirre, Shirley A., Evering, Winston E. N., Hirakawa, Brad P., May, Jeffrey R., Palacio, Kimbie, Wang, Jianying, Zhang, Yizhong, Stevens, Gregory J.
Format: Article
Language:English
Subjects:
Animals
Biomarkers - blood
Cardiac Myosins - blood
Cardiomyopathies - chemically induced
Cardiomyopathies - pathology
Caspase 3 - metabolism
Female
Heart - drug effects
Heart - physiopathology
Isoproterenol - toxicity
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
MicroRNAs - blood
Myosin Heavy Chains - blood
Superoxide Dismutase - metabolism
Troponin I - blood
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Summary:This investigation examined microRNA-208a (miR-208a) as a potential biomarker of isoproterenol (ISO)-induced cardiac injury in superoxide dismutase-2 (Sod2+/− ) and the wild-type mice, and the potential sensitivity of Sod2+/− mice to ISO-induced toxicity. A single intraperitoneal injection of ISO was administered to age-matched wild-type and Sod2+/− mice at 0, 80, or 160 mg/kg. Plasma miR-208a, cardiac troponin I (cTnI), and ISO systemic exposure were measured at various time points postdose. Hearts were collected for histopathology examination and for tissue expression of miR-208a and myosin heavy chain 7. ISO administration caused increases in cTnI and miR-208a plasma levels that correlated with myocardial damage; however, the magnitude of increase differed according to the types of mice. At similar ISO systemic exposure, the magnitude of cTnI was greater in wild-type mice compared to Sod2+/ − mice; however, the magnitude of miR-208a was greater in Sod2+/− mice than that of the wild-type mice. Myocardial degeneration occurred at ≥3 hr in the wild-type and ≥6 hr in Sod2+/ − mice. At ≥24 hr after ISO administration, miR-208a appeared superior to cTnI in indicating myocardial injury in both wild-type and Sod2+/− mice. Sod2+/− mice were not more sensitive than wild-type mice to ISO-induced toxicity.
ISSN:0192-6233
1533-1601
DOI:10.1177/0192623314525684