Effect of Immune Modulation Therapy on Cardiac Function and
            <i>T-bet</i>
            /
            <i>GATA-3</i>
            Gene Expression in Aging Male Patients with Chronic Cardiac Insufficiency

Han, Lina; Guo, S.L.; Li, Tieling; Ding, Guo-Lei; Ma, Jin

doi:10.2217/imt.12.139

Cited by 7 publications

(4 citation statements)

References 29 publications

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“…CRP levels are elevated in CHF and increasing levels are associated with increasing morbidity and mortality in ischemic and non-ischemic etiologies (Nakagomi et al, 2010). In this study, we found higher levels of NT-proBNP and CRP in the two DCM groups than in the normal control group, and in our previous study, NT-proBNP and CRP levels were negatively correlated with LVEF (Han et al, 2013). The DCM heart presumably undergoes a complex series of changes in neurohumoral mechanisms such as the sympathetic nervous and renin-angiotensin-aldosterone systems to compensate for the reduction in cardiac contractility, which are likely to affect cardiac gene expression resulting in electrical remodeling, ultimately evolving to cardiac arrhythmia, pump failure, and sudden death (Tsutamoto et al, 2011).…”

Section: Discussionsupporting

confidence: 64%

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Han¹,

Guo²,

Lin³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to analyze the incidence and types of arrhythmia and their relationship with the severity and prognosis of chronic heart failure (CHF) in patients with dilated cardiomyopathy (DCM), and to investigate the therapeutic effect of torasemide versus furosemide on CHF and incidence of arrhythmia. DCM patients with NYHA cardiac function II-IV were continuously monitored using a 24-h dynamic electrocardiogram (Holter), and arrhythmia incidence was analyzed by computer automatic analysis combined with manual assessment. In total, 125 participants were evenly divided into two groups: torasemide group which received 10 mg oral torasemide once daily) and regular anti-heart failure treatment (N = 65), and furosemide group which received torasemide (20 mg once daily orally) and regular antiheart failure treatment (N = 60). Another 60 normal healthy persons served as the normal control group. Incidence and severity of arrhythmia increased when degree of CHF was elevated. Size of left atrium was related to atrial fibrillation and size of left ventricle was related to malignant arrhythmia. At 3 months after treatment, cardiac function in both groups improved and incidence and severity of arrhythmia in both groups were reduced. However, left ventricular ejection fraction (LVEF) was higher in the torasemide group than in the furosemide group, while incidence of arrhythmia was lower in the torasemide group. Arrhythmias frequently occurred in patients with DCM and HF. Type of cardiac arrhythmia is closely related to ventricular enlargement and cardiac function grade. Torasemide is better for improving cardiac function to reduce arrhythmia and CHF compared to furosemide.

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Section: Discussionsupporting

confidence: 64%

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Han¹,

Guo²,

Lin³

et al. 2014

Genet. Mol. Res.

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“…Interferon-γ (IFN-γ) is the signature cytokine of Th1 cells and interleukin-4 (IL-4) is the corresponding signature cytokine of Th2 cells. GATA-binding protein 3 (GATA-3) is a Th2-specific transcription factor, which is upregulated during Th2 differentiation (9,10). The transcription factor T-box expressed in T cells (T-bet) controls the expression of the hallmark Th1 cytokine IFN-γ (11).…”

Section: Cd4mentioning

confidence: 99%

Fusion protein of tapasin and hepatitis B core antigen 18-27 enhances T helper cell type 1/2 cytokine ratio and antiviral immunity by inhibiting suppressors of cytokine signaling family members 1/3 in hepatitis B virus transgenic mice

Tang

Chen

Zhang

et al. 2014

Molecular Medicine Reports

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Abstract. Persistent hepatitis B virus (HBV) infection ischaracterized by a weak adaptive immune response, which is considered to be due to an imbalance of T helper cell types 1 and 2 (Th1/Th2). Suppressors of cytokine signaling (SOCS) family members, particularly SOCS1 and SOCS3, have been demonstrated to be important in the regulation of T cell differentiation. Previous studies by our group showed that the expressed and purified fusion protein of cytoplasmic transduction peptide (CTP) and HBV core antigen 18-27 (HBcAg18-27)-tapasin was able to enter the cytoplasm of bone marrow-derived dendritic cells (BMDCs), promoting the maturation of BMDCs and efficiently enhancing T cell immune responses in vitro. In the present study, HBcAg-specific immune responses induced by CTP-HBcAg18-27-tapasin in HBV were assessed in transgenic mice, and SOCS1 and SOCS3 were identified as negative regulators of this response. The Th1/Th2 cytokine ratio was analyzed by ELISA. The expression of T cell-specific T-box transcription factor (T-bet) and GATA-binding protein 3 (GATA-3), SOCS1 and SOCS3 were detected by real-time quantitative polymerase chain reaction and western blot analysis. The results demonstrated that CTP-HBcAg18-27-tapasin significantly increased the Th1/Th2 cytokine ratio in HBV transgenic mice. CTP-HBcAg18-27-tapasin immunization more efficiently suppressed the expression of serum hepatitis B surface antigen (HBsAg), HBV DNA as well as liver HBsAg and HBcAg in HBV transgenic mice. Furthermore, CTP-HBcAg18-27-tapasin promotes T-bet but reduces GATA-3 expression. In addition, the expression of SOCS1 and SOCS3 was significantly downregulated in the CTP-HBcAg18-27-tapasin group compared with the control groups. In conclusion, the present study demonstrated that CTP-HBcAg18-27-tapasin enhanced the Th1/Th2 cytokine ratio and antiviral immunity by suppressing SOCS1/3 in HBV transgenic mice.

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“…GATA-3 is a transcription factor revealed to be specifically expressed in Th2 cells, whereas T-box protein expressed in T cells (T-bet) is a transcription factor specifically expressed in Th1 cells. GATA-3 and T-bet have been reported to modulate gene expression during T cell differentiation, thus serving a critical role in the development of Th1 and Th2 lineages ( 4 , 5 ). However, the molecular mechanisms underlying allergic rhinitis are complex and involve other pathways apart from an aberrant Th2 response.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of astragaloside IV against ovalbumin-induced allergic rhinitis are mediated by T-box protein expressed in T cells/GATA-3 and forkhead box protein 3/retinoic acid-related orphan nuclear receptor γt

Chen

Jiang

et al. 2017

Molecular Medicine Reports

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3-O-β-D-xylopyranosyl-6-O-β-D-glucopyranosyl-cycloastragenol, or Astragaloside IV (AST), is one of the major active ingredients isolated from Astragalus membranaceous with distinct pharmacological effects, and possesses anti-inflammatory, immunoregulatory and antifibrotic properties. However, the effects of AST on allergic rhinitis remain to be elucidated. The present study aimed to examine the effects of AST on immunoglobulin (Ig) E-mediated allergic reactions in vivo, by using a mouse model of allergic rhinitis established via repetitive sensitization and intranasal challenge with ovalbumin (OVA). Intragastric administration of AST (25 mg/kg or 50 mg/kg) or dexamethasone (DEX; 3 mg/kg) significantly alleviated the inflammatory response, nasal symptoms and mucosa remodeling, and decreased the serum levels of OVA-specific IgE in allergic mice. Furthermore, treatment with AST or DEX significantly suppressed the mRNA and protein expression levels of the transcription factor GATA-3 and retinoic acid receptor-related orphan nuclear receptor (ROR)γt in tissue samples isolated from the spleen and nasal mucosa of mice with allergic rhinitis. Conversely, mRNA and protein expression levels of T-box protein expressed in T cells (T-bet) and forkhead box protein 3 (Foxp3) were upregulated in the spleen and nasal mucosa of mice with allergic rhinitis following treatment with AST or DEX, and spleen protein levels of signal transducer and activator of transcription 3 followed a similar trend. In addition, treatment with AST was associated with fewer adverse events compared with treatment with DEX. The present results suggested that treatment with AST may attenuate OVA-induced allergic rhinitis via regulating the expression of the transcription factors GATA-3, RORγt, T-bet and Foxp3, which commit T helper cells to the Th1 phenotype. Therefore, AST may represent an alternative therapeutic approach for the treatment of patients with allergic rhinitis.

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Effect of Immune Modulation Therapy on Cardiac Function and T-bet / GATA-3 Gene Expression in Aging Male Patients with Chronic Cardiac Insufficiency

Abstract: Immune modulation improved cardiac function of CCI patients and was associated with amelioration of T-helper superficial transcription factor polarization and its related cytokine imbalance. Immune modulation might be a new treatment strategy for aging CCI patients.

Cited by 7 publications

References 29 publications

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Torasemide reduces dilated cardiomyopathy, complication of arrhythmia, and progression to heart failure

Fusion protein of tapasin and hepatitis B core antigen 18-27 enhances T helper cell type 1/2 cytokine ratio and antiviral immunity by inhibiting suppressors of cytokine signaling family members 1/3 in hepatitis B virus transgenic mice

Protective effects of astragaloside IV against ovalbumin-induced allergic rhinitis are mediated by T-box protein expressed in T cells/GATA-3 and forkhead box protein 3/retinoic acid-related orphan nuclear receptor γt

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