Corrigendum to "Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice".

[This corrects the article DOI: 10.1155/2020/5741047.].

Interleukin-9 Aggravates Isoproterenol-Induced Heart Failure by Activating Signal Transducer and Activator of Transcription 3 Signalling.

BACKGROUND: Previous studies have demonstrated that inflammation is closely related to the occurrence and development of heart failure (HF). As an inflammation-related cytokine, interleukin (IL)-9 has been reported to be involved in the development of cardiovascular diseases. However, the role of IL-9 in HF in response to isoproterenol (ISO) stimulation has barely been explored. Thus, this study aimed to investigate whether IL-9 participates in HF and the possible associated mechanisms. METHODS: Chronic ISO infusion was used to establish an HF model, and the IL-9 levels in mice and isolated cardiomyocytes were measured. In addition, ISO-treated mice received an injection of recombinant mouse IL-9 (rIL-9) or an antimouse IL-9 neutralizing monoclonal antibody (mAb) to investigate the effects of IL-9 on cardiac function, hypertrophy, and fibrosis. RESULTS: IL-9 levels were significantly increased in mice and isolated cardiomyocytes after ISO treatment. Treatment with rIL-9 resulted in aggravated cardiac dysfunction and amplified cardiac hypertrophy and fibrosis, whereas treatment with the anti-IL-9 neutralizing mAb ameliorated cardiac dysfunction and reduced cardiac hypertrophy and fibrosis in ISO-treated mice. In addition, ISO infusion-induced cardiac inflammation and cardiomyocyte apoptosis was aggravated by rIL-9 but prevented by the anti-IL-9 mAb. IL-9 did not activate signal transducer and activator of transcription (STAT)1 or STAT5 but induced STAT3 phosphorylation in ISO-induced HF. Moreover, S31-201, a specific STAT3 inhibitor, nearly abolished rIL-9-induced increases in cardiac dysfunction, hypertrophy, and fibrosis in response to ISO stimulation. CONCLUSIONS: IL-9 aggravated cardiac dysfunction and amplified cardiac hypertrophy and fibrosis in the ISO-induced HF model by activating STAT3 signalling. These data indicate that blocking IL-9 may be an attractive pharmacotherapeutic strategy for the treatment of cardiac hypertrophy and fibrosis induced by chronic ß-adrenergic receptor activation to limit the progression of HF.

Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice.

BACKGROUND: Multiple interleukin (IL) family members were reported to be closely related to hypertension. We aimed to investigate whether IL-9 affects angiotensin II- (Ang II-) induced hypertension in mice. METHODS: Mice were treated with Ang II, and IL-9 expression was determined. In addition, effects of IL-9 knockout (KO) on blood pressure were observed in Ang II-infused mice. To determine whether the effects of IL-9 on blood pressure was mediated by the signal transducer and activator of the transcription 3 (STAT3) pathway, Ang II-treated mice were given S31-201. Furthermore, circulating IL-9 levels in patients with hypertension were measured. RESULTS: Ang II treatment increased serum and aortic IL-9 expression in a dose-dependent manner; IL-9 levels were the highest in the second week and continued to remain high into the fourth week after the treatment. IL-9 KO downregulated proinflammatory cytokine expression, whereas it upregulated anti-inflammatory cytokine levels, relieved vascular dysfunction, and decreased blood pressure in Ang II-infused mice. IL-9 also reduced smooth muscle 22α (SM22α (SM22. CONCLUSIONS: IL-9 KO alleviates inflammatory response, prevents phenotypic transformation of smooth muscle, reduces vascular dysfunction, and lowers blood pressure via the STAT3 pathway in Ang II-infused mice. IL-9 might be a novel target for the treatment and prevention of clinical hypertension.

Comparison of effects of propofol versus sevoflurane for patients undergoing cardiopulmonary bypass cardiac surgery.

OBJECTIVE: To compare the effects of propofol versus sevoflurane on the outcomes of patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). METHODS: A total of 110 patients undergoing cardiac surgery with CPB in our hospital from January 2015 to June 2017 were randomly divided into 2 groups (n=55): Group A, in which anesthesia was maintained with sevoflurane, and Group B, in which anesthesia was maintained with propofol. The MMSE score before and after operation, perioperative laboratory index, incidence of postoperative cognitive dysfunction (POCD) and incidence of adverse events between the two groups were compared. RESULTS: The MMSE score was significantly higher in Group B than in Group A after anesthesia (p<0.05). Serum levels of the brain injury markers neuron-specific enolase, S100ß and matrix metalloproteinase 9 were significantly lower in Group B than in Group A (p<0.05). POCD incidence at 12 hour and 24 hour after operation was significantly lower in Group B than in Group A (p<0.05). There were no significant differences in the incidence of low cardiac output and thoracotomy bleeding between two groups. CONCLUSION: Compared with sevoflurane, the use of propofol during cardiac surgery with CPB can efficiently improve postoperative cognitive function without increasing the risk of adverse reactions.