Key result
IL-6 deletion prevents Ang II and salt-induced cardiac dysfunction in mice without altering blood pressure.
Why the study?
Does deletion of interleukin-6 prevent cardiac inflammation, fibrosis, and dysfunction in mice with Ang II-high salt-induced hypertension?
Does deletion of interleukin-6 prevent cardiac inflammation, fibrosis, and dysfunction in mice with Ang II-high salt-induced hypertension?
Deletion of interleukin-6 prevents cardiac dysfunction, inflammation, and fibrosis without affecting blood pressure in a mouse model of Ang II-high salt-induced hypertension.
IL-6 deletion attenuates hypertensive cardiac injury independent of BP in mice; leaves open clinical translation of targeted inhibition.
OBJECTIVE: Inflammation has been proposed as a key component in the development of hypertension and cardiac remodeling associated with different cardiovascular diseases. However, the role of the proinflammatory cytokine interleukin-6 in the chronic stage of hypertension is not well defined. Here, we tested the hypothesis that deletion of interleukin-6 protects against the development of hypertension, cardiac inflammation, fibrosis, remodeling and dysfunction induced by high salt diet and angiotensin II (Ang II). METHODS: Male C57BL/6J and interleukin-6-knock out (KO) mice were implanted with telemetry devices for blood pressure (BP) measurements, fed a 4% NaCl diet, and infused with either vehicle or Ang II (90 ng/min per mouse subcutaneously) for 8 weeks. We studied BP and cardiac function by echocardiography at baseline, 4 and 8 weeks. RESULTS: Myocyte cross-sectional area (MCSA), macrophage infiltration, and myocardial fibrosis were also assessed. BP increased similarly in both strains when treated with Ang II and high salt (Ang II-high salt); however, C57BL/6J mice developed a more severe decrease in left ventricle ejection fraction, fibrosis, and macrophage infiltration compared with interleukin-6-KO mice. No differences between strains were observed in MCSA, capillary density and MCSA to capillary density ratio. CONCLUSION: In conclusion, absence of interleukin -6 did not alter the development of Ang II-high salt-induced hypertension and cardiac hypertrophy, but it prevented the development of cardiac dysfunction, myocardial inflammation, and fibrosis. This indicates that interleukin-6 plays an important role in hypertensive heart damage but not in the development of hypertension.
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Gónzalez et al. (2014) studied Angiotensin II-high salt-induced hypertension and cardiac remodeling. Interleukin-6 deletion (IL-6 KO) vs. Wild-type C57BL/6J mice was evaluated on Blood pressure, cardiac function, myocardial fibrosis, and macrophage infiltration. Deletion of interleukin-6 in male mice prevented Ang II and high salt-induced cardiac dysfunction, myocardial inflammation, and fibrosis over 8 weeks, without altering blood pressure.
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