The Histamine 3 Receptor Is Expressed in the Heart and Its Activation Opposes Adverse Cardiac Remodeling in the Angiotensin II Mouse Model
Histamine is a basic amine stored in mast cells, with its release capable of activating one of four histamine receptors. The histamine 3 receptor (H<sub>3</sub>R) is known to be cardioprotective during acute ischemia by acting to limit norepinephrine release. However, a recent study repo...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2020-12-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/21/24/9757 |
| Summary: | Histamine is a basic amine stored in mast cells, with its release capable of activating one of four histamine receptors. The histamine 3 receptor (H<sub>3</sub>R) is known to be cardioprotective during acute ischemia by acting to limit norepinephrine release. However, a recent study reported that myofibroblasts isolated from the infarct zone of rat hearts responded to H<sub>3</sub>R activation by up-regulating collagen production. Thus, it is necessary to clarify the potential role of the H<sub>3</sub>R in relation to fibrosis in the heart. We identified that the mouse left ventricle (LV) expresses the H<sub>3</sub>R. Isolation of mouse cardiac fibroblasts determined that while angiotensin II (Ang II) increased levels of the H<sub>3</sub>R, these cells did not produce excess collagen in response to H<sub>3</sub>R activation. Using the Ang II mouse model of adverse cardiac remodeling, we found that while H<sub>3</sub>R blockade had little effect on cardiac fibrosis, activation of the H<sub>3</sub>R reduced cardiac fibrosis and macrophage infiltration. These findings suggest that when activated, the H<sub>3</sub>R is anti-inflammatory and anti-fibrotic in the mouse heart and may be a promising target for protecting against cardiac fibrosis. |
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| ISSN: | 1661-6596 1422-0067 |