The recently identified
adipocytokine omentin was previously found to be expressed mainly in human omental and visceral adipose tissues. As such, reduced plasma concentrations of omentin were revealed to be associated with increased risks of
cardiovascular diseases. Omentin has also been previously demonstrated to exert anti-inflammatory effects. By contrast,
resistin is a
protein that has been associated with
obesity and type-2
diabetes mellitus, and the serum concentration of
resistin is increased significantly in these populations.
Resistin is involved in mediating
inflammation development, where they can promote
cardiac hypertrophy in humans through
toll-like receptor 4 (TLR4)-related signaling. In the present study, the potential effects of omentin on
resistin-induced
hypertrophy in H9c2 cardiomyoblasts were investigated. In the absence/presence of omentin, H9c2 cardiomyoblasts were treated with
resistin. Omentin was found to significantly inhibit
resistin-induced increases in the surface area of H9c2 cardiomyoblasts as determined by immunofluorescence. In addition, omentin significantly inhibited
resistin-induced increases in the
mRNA expression of
atrial natriuretic factor,
brain natriuretic peptide, β-
myosin heavy chain (which is a characteristic feature of
cardiac hypertrophy) and TLR4, which was determined using reverse-transcription-quantitative PCR. According to western blotting results, omentin significantly inhibited
resistin-induced ERK phosphorylation, which is an important mediator of cardiomyoblast
hypertrophy. Furthermore, omentin significantly inhibited
resistin-induced
protein expression of TLR4,
myeloid differentiation factor 88 (MyD88) and NF-κB phosphorylation, both of which are important members of inflammatory signaling. To conclude, data from the present study suggest that omentin can inhibit
resistin-induced H9c2 cardiomyoblast
hypertrophy through inhibition of the TLR4/MyD88/NF-κB signaling pathway. Therefore, omentin serve as an attractive therapeutic target against
resistin-induced
cardiac hypertrophy.