Bibliographic Details
| Title: |
STAT6 deficiency mitigates the severity of pulmonary arterial hypertension caused by chronic intermittent hypoxia by suppressing Th2-inducing cytokines. |
| Authors: |
Jiang, Pan1,2,3 (AUTHOR), Huang, Huai1 (AUTHOR), Liu, Zilong1 (AUTHOR), Xiang, Guiling1,4 (AUTHOR), Wu, Xiaodan1,5 (AUTHOR) ollow_the_line@163.com, Hao, Shengyu1,4 (AUTHOR) janet9yu@163.com, Li, Shanqun1,5 (AUTHOR) li.shanqun@zs-hospital.sh.cn |
| Source: |
Respiratory Research. 1/13/2025, Vol. 26 Issue 1, p1-14. 14p. |
| Subject Terms: |
*IMMUNOMODULATORS, *PULMONARY arterial hypertension, *SLEEP apnea syndromes, *HEART septum, *PULMONARY artery |
| Abstract: |
Background: Obstructive sleep apnea (OSA) is frequently associated with increased incidence and mortality of pulmonary hypertension (PH). The immune response contributes to pulmonary artery remodeling and OSA-related diseases. The immunologic factors linked to OSA-induced PH are not well understood. STAT6 is crucial in the signaling pathway that modulates immune response. However, the status of phosphorylated STAT6 (p-STAT6) in an OSA-induced PH mouse model remains largely unexplored. Methods: Chronic intermittent hypoxia (CIH) plays a crucial role in the progression of OSA. This study utilized a in vivo CIH model to examine the role of STAT6 in CIH-induced PH. Results: CIH mice exhibited pulmonary artery remodeling and pulmonary hypertension, indicated by increased right ventricular systolic pressure (RVSP), higher right ventricular to left ventricular plus septum (RV/LV + S) ratios, and significant morphological alterations compared to normoxic (Nor) mice. Increased p-STAT6 in the lungs and elevated p-STAT6 + IL-4 + producing T cells in CIH mice. STAT6 deficiency (STAT6-/-) improved PH and PA remodeling in CIH-induced PH mouse models.STAT6 deficiency impaired the T helper 2 (Th2) immune response, affecting IL-4 and IL-13 secretion. IL-4, rather than IL-13, activated STAT6 in human pulmonary artery smooth muscle cells (hPASMCs). STAT6 knockdown decreased the proliferation in IL-4 treated hPASMCs. Conclusion: These findings exhibit the critical role of STAT6 in the pathogenesis of CIH induced PH by regulating Th2 immune response.STAT6 could be a significant therapeutic target for OSA-related PH. [ABSTRACT FROM AUTHOR] |
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