Activation of satellite glia in stellate ganglia from chronic heart failure rats

Huiyin Tu, Dongze Zhang, Michael C. Wadman, Yu Long Li

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Cardiac sympathetic overactivation is linked to ventricular arrhythmogenesis and is associated with mortality in patients with chronic heart failure (CHF). However, the sites and mechanisms responsible for increased cardiac sympathetic activity are still poorly understood. Our previous studies showed that CHF-elevated proinflammatory cytokine levels and macrophage expansion in stellate ganglia are critical factors for cardiac sympathoexcitation. Here we tested if activation of satellite glial cells (SGCs) contributes to macrophage expansion in stellate ganglia from CHF rats. Rat CHF was induced by surgical ligation of the left anterior descending coronary artery. SGCs and postsynaptic sympathetic neurons were respectively identified by anti-S100B and anti-tyrosine hydroxylase (TH) antibodies with immunofluorescence staining. As a marker of SGC activation, glial fibrillary acidic protein (GFAP) was measured by immunofluorescence double staining and Western blot analysis. Sympathetic neurons in stellate ganglia from both sham and CHF rats were totally surrounded by S100B-positive SGCs. However, However, a few GFAP-postive SGCs covered sympathetic neurons in sham stellate ganglia, whereas more GFAP-positive SGCs surrounded sympathetic neurons in CHF stellate ganglia. Western blot data showed that GFAP was elevated in stellate ganglia from CHF rats, compared to sham rats. From these results, we conclude that activation of SGCs in stellate ganglia is higher in CHF rats than that in sham rats, which might contribute to the neuroinflammation and sympathoexcitation in stellate ganglia.

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


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