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Published on: July 18, 2014
Galectin-3 aggravates pulmonary arterial hypertension via immunomodulation in congenital heart disease
Qiang Shen1, Wei Chen2, Jun Liu1
1Department of Cardiology, University of South China Affiliated Huaihua Hospital, Huaihua 418000, PR China.
Insights
Galectin-3 (Gal-3) facilitates pulmonary artery remodeling and congenital heart disease-pulmonary arterial hypertension (CHD-PAH) progression by activating Th2 immune responses. This study elucidates Gal-3
Area of Science:
- Immunology
- Cardiovascular Research
- Molecular Biology
Background:
- Pulmonary arterial hypertension (PAH) is a severe condition linked to right ventricular failure and mortality.
- Congenital heart disease (CHD) frequently coexists with varying degrees of PAH.
- Galectin-3 (Gal-3) is implicated in both PAH and CHD pathogenesis.
Purpose of the Study:
- To investigate the specific mechanism of Galectin-3 (Gal-3) in congenital heart disease-pulmonary arterial hypertension (CHD-PAH).
- To explore the role of Gal-3 in pulmonary artery remodeling and disease progression in vivo.
Main Methods:
- Analysis of T-cell subsets, cytokine levels, and Gal-3 in patients with CHD-PAH.
- Establishment of CHD-PAH mouse models with Gal-3 manipulation (restored or depleted).
- Evaluation of systolic pulmonary artery pressure (sPAP), right ventricular hypertrophy index (RVHI), inflammatory markers, and pulmonary artery smooth muscle cell (PASMC) proliferation.
- Assessment of CD4+ T-cell transfer effects in Gal-3 knockdown mice.
Main Results:
- Gal-3 levels were significantly upregulated in patients with CHD-PAH.
- Restored Gal-3 increased sPAP, RVHI, and PASMC proliferation by activating Th2 immune responses (elevated IL-4, IL-5, IL-13) and the AKT pathway.
- Adoptive transfer of CD4+ T cells exacerbated CHD-PAH in Gal-3 knockdown mice, promoting perivascular infiltration.
Conclusions:
- Galectin-3 plays a facilitating role in pulmonary artery remodeling and the progression of CHD-PAH.
- Gal-3 promotes disease progression through the activation of Th2 immune responses.
- Targeting Gal-3 may offer a therapeutic strategy for CHD-PAH.
Abstract:
Pulmonary arterial hypertension (PAH) is reported to contribute to right ventricular failure and death. PAH of variable degrees is often related to congenital heart disease (CHD). Galectin-3 (Gal-3) has been proven to be of great importance in PAH and CHD. Therefore, we investigated the specific mechanism of Gal-3 in CHD-PAH. Patients with CHD-PAH were enrolled to detect the changes of T-cell subsets, cytokine levels, and other related inflammatory cells in the plasma and to assess the Gal-3 levels in the serum. Next, CHD-PAH mouse models were established and treated with restored or depleted Gal-3 to evaluate the systolic pulmonary artery pressure (sPAP) and right ventricular hypertrophy index (RVHI), to determine levels of IL-4, IL-5, IL-13, AKT and p-AKT along with proliferation of pulmonary artery smooth muscle cells (PASMCs). Finally, we explored the effects of adoptive transfer of CD4+T cells on CHD-PAH in mice with Gal-3 knockdown to further investigate the role of Gal-3 in vivo. Initially, Gal-3 was up-regulated in patients with CHD-PAH. Subsequently, it was demonstrated that restored Gal-3 increased sPAP and RVHI, and promoted proliferation of PASMCs by activating the immune response with elevated levels of IL-4, IL-5, IL-13 and p-AKT. Finally, adoptive transfer of CD4+T cells promoted CD4+T cell perivascular infiltration and the progression of CHD-PAH in mice with Gal-3 knockdown. Collectively, the current study suggests a facilitating role of Gal-3 in pulmonary artery remodeling and progression of CHD-PAH via activation of Th2.
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