scholarly journals Tsc2 disruption in mesenchymal progenitors results in tumors with vascular anomalies overexpressing Lgals3

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Peter J Klover ◽  
Rajesh L Thangapazham ◽  
Jiro Kato ◽  
Ji-an Wang ◽  
Stasia A Anderson ◽  
...  
Keyword(s):  
Lung Function ◽  
Tuberous Sclerosis Complex ◽  
Serum Levels ◽  
Limb Bud ◽  
Mesenchymal Progenitors ◽  
Expression Signature ◽  
Mtorc1 Signaling ◽  
Impaired Lung Function ◽  
Galectin 3

Increased mTORC1 signaling from TSC1/TSC2 inactivation is found in cancer and causes tuberous sclerosis complex (TSC). The role of mesenchymal-derived cells in TSC tumorigenesis was investigated through disruption of Tsc2 in craniofacial and limb bud mesenchymal progenitors. Tsc2cKOPrrx1-cre mice had shortened lifespans and extensive hamartomas containing abnormal tortuous, dilated vessels prominent in the forelimbs. Abnormalities were blocked by the mTORC1 inhibitor sirolimus. A Tsc2/mTORC1 expression signature identified in Tsc2-deficient fibroblasts was also increased in bladder cancers with TSC1/TSC2 mutations in the TCGA database. Signature component Lgals3 encoding galectin-3 was increased in Tsc2-deficient cells and serum of Tsc2cKOPrrx1-cre mice. Galectin-3 was increased in TSC-related skin tumors, angiomyolipomas, and lymphangioleiomyomatosis with serum levels in patients with lymphangioleiomyomatosis correlating with impaired lung function and angiomyolipoma presence. Our results demonstrate Tsc2-deficient mesenchymal progenitors cause aberrant morphogenic signals, and identify an expression signature including Lgals3 relevant for human disease of TSC1/TSC2 inactivation and mTORC1 hyperactivity.

The role of galectin-3 and LP(A) in atherosclerosis: A combined analysis of serum levels and plaque characteristics

2018 ◽  
Vol 275 ◽  
pp. e48-e49
Author(s):  
D. Palma ◽  
M.D. Di Taranto ◽  
M. Savoia ◽  
R. de Falco ◽  
F.P. D'Armiento ◽  
...  
Keyword(s):  
Serum Levels ◽  
Combined Analysis ◽  
Galectin 3

The CRP genotype, serum levels and lung function in men: the Caerphilly Prospective Study

2010 ◽  
Vol 120 (8) ◽  
pp. 347-355 ◽  
Author(s):  
Charlotte E. Bolton ◽  
Wiebke Schumacher ◽  
John R. Cockcroft ◽  
Nicholas J. Timpson ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Lung Function ◽  
Prospective Study ◽  
Causal Effect ◽  
Serum Levels ◽  
Forced Expiratory Volume ◽  
Reverse Causality ◽  
Lung Function Decline ◽  
Impaired Lung Function ◽  
Serum Crp

Systemic CRP (C-reactive protein) has been associated with impaired lung function. A causal relationship would increase the value of CRP as both a diagnostic and therapeutic tool. We assessed the association between lung function parameters, circulating CRP and CRP polymorphisms using Mendelian randomization in efforts to attribute causality to known associations. Spirometric parameters of FEV1 (forced expiratory volume in 1 s) and FVC (forced vital capacity) were determined in 2173 men participating in the Caerphilly Prospective Study. Lung function measures on 1021 participants were available at follow-up (mean, 16.8 years later). Serum CRP levels were measured at baseline, and three CRP polymorphisms were analysed. Haplotype analysis was performed. Serum CRP levels at baseline were inversely associated with contemporaneous FEV1 and FVC as well as at follow-up (P<0.001) even after adjustment for conventional confounders. Serum CRP was associated with FEV1 decline (P=0.04). All three CRP polymorphisms (rs1800947, rs1130864 and rs1205) predicted serum CRP; however, there were no clear associations of the polymorphisms or haplotypes with lung function or with lung function decline. In conclusion, serum CRP was associated with lung function cross-sectionally; however, CRP polymorphisms were not associated with lung function or decline, suggesting that the CRP–lung function relationship is due to reverse causality, an unmeasured confounding factor or only has a modest causal effect.

Impaired lung function after liver transplantation: Role of themembrane factor and reduced function of respiratory muscles

2000 ◽  
Vol 32 ◽  
pp. 58 ◽  
Author(s):  
K. Walldorf ◽  
R. Ewert ◽  
C. Witt ◽  
M. Böhm ◽  
P. Rogalla ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Lung Function ◽  
Respiratory Muscles ◽  
Impaired Lung Function

scholarly journals Galectin‑3 in patients with left ventricular hypertrophy and metabolic syndrome

2018 ◽  
Vol 24 (3) ◽  
pp. 272-280
Author(s):  
O. M. Drapkina ◽  
R. N. Shepel ◽  
T. A. Deeva ◽  
A. N. Kaburova
Keyword(s):  
Metabolic Syndrome ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Serum Levels ◽  
Mean Value ◽  
Left Ventricular ◽  
Galectin 3 ◽  
The Mean ◽  
Design And Methods

Objective. To investigate the serum levels of galectin‑3 in patients with metabolic syndrome (MS) and in patients with combination of MS and left ventricular hypertrophy (LVH), as well as to define the role of this marker of fibrosis in MS.Design and methods. The study included 43 patients with MS (33 patients had LVH), and 33 patients of comparable age without MS (LVH was diagnosed in 10). The level of serum galectin‑3 was determined by enzyme immunoassay kits Platinum ELISA.Results. The average level of galectin‑3 in the MS group was significantly higher (1,89 ± 1,71 ng/ml), compared to the group without MS (1,03 ± 0,22 ng/ml, p = 0,006). The study showed a positive correlation between the level of galectin‑3 and LVH (r = 0,323, p = 0,004). The mean value of galectin‑3 in patients with no evidence of LVH was 1,2 ± 0,76 ng/ml, in patients with LVH — 2,1 ± 2,02 ng/ml.Conclusions. In patients with MS the level of galectin‑3 was higher than in patients without MS, and in patients with MS and concomitant LVH it was higher than in patients without LVH. In patients with MS and LVH increased galectin‑3 levels may indicate the severity of myocardial fibrosis and help for prognosis evaluation. 

Acute chest syndrome in sickle cell anaemia: higher serum levels of interleukin-8 and highly sensitive C-reactive proteins are associated with impaired lung function

2018 ◽  
Vol 38 (4) ◽  
pp. 244-250 ◽  
Author(s):  
Samuel Ademola Adegoke ◽  
Bankole Peter Kuti ◽  
Kehinde Oluyori Omole ◽  
Olufemi Samuel Smith ◽  
Oyeku Akibu Oyelami ◽  
...  
Keyword(s):  
Lung Function ◽  
Sickle Cell ◽  
Sickle Cell Anaemia ◽  
Serum Levels ◽  
Interleukin 8 ◽  
Acute Chest Syndrome ◽  
Highly Sensitive ◽  
Impaired Lung Function

scholarly journals FSTL1 aggravates Cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy

2020 ◽  
Author(s):  
Ying Liu ◽  
Jiawei Xu ◽  
Tian Liu ◽  
Jinxiang Wu ◽  
Jiping Zhao ◽  
...  
Keyword(s):  
Lung Function ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Airway Remodeling ◽  
Critical Factor ◽  
Lavage Fluid ◽  
Copd Patients ◽  
Tnf Α ◽  
Impaired Lung Function

Abstract Background Cigarette smoke (CS) is a major risk factor for COPD. Follistatin-like protein 1(FSTL1), a critical factor during embryogenesis particularly in respiratory lung development, is a novel mediator related to inflammation and tissue remodeling. We tried to investigate the role of FSTL1 in CS-induced autophagy dysregulaton, airway inflammation and remodeling. Methods Serum and lung specimens were obtained from COPD patients and controls. Adult female wild-type (WT) mice, FSTL1+/- mice and FSTL1flox/+ mice were exposed to room air or chronic CS. Additionally, 3-methyladenine (3-MA) ,an inhibitor of autophagy, were applied in CS exposed WT mice. The lung tissue and serum from patients and murine models were tested for FSTL1 and autophagy associated protein expression by ELISA, western blotting and immunohistochemical. Autophagosome were observed by Electron Microscope Technology(EMT). LTB4, IL-8 and TNF-α in bronchoalveolar lavage fluid of mice were examined by ELISA. Airway remodeling and lung function were also assessed. Results Both FSTL1 and autophagy biomarkers increased in COPD patients and CS exposed WT mice. Autophagy activation was upregulated in CS exposed mice accompanied by airway remodeling and airway inflammation. FSTL1+/- mice showed a lower level of CS-induced autophagy compared with control mice. FSTL1+/- mice can also resist CS-induced inflammatory response, airway remodeling and impaired lung function. CS exposed WT mice with 3-MA pretreatment have a similar manifestation with CS exposed FSTL1+/- mice. Conclusions FSTL1 promotes CS-induced COPD by modulating autophagy, therefore targeting FSTL1 and autophagy may shed light on treating cigarette smoke induced COPD.

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

Galectin-3 in Heart Failure – Linking Fibrosis, Remodelling and Progression

2010 ◽  
Vol 6 (2) ◽  
pp. 33 ◽  
Author(s):  
Christopher R deFilippi ◽  
G Michael Felker ◽  
◽  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Risk Stratification ◽  
Cardiac Fibrosis ◽  
The Elderly ◽  
Preserved Ejection Fraction ◽  
Heart Failure Patients ◽  
Large Populations ◽  
Galectin 3

For many with heart failure, including the elderly and those with a preserved ejection fraction, both risk stratification and treatment are challenging. For these large populations and others there is increasing recognition of the role of cardiac fibrosis in the pathophysiology of heart failure. Galectin-3 is a novel biomarker of fibrosis and cardiac remodelling that represents an intriguing link between inflammation and fibrosis. In this article we review the biology of galectin-3, recent clinical research and its application in the management of heart failure patients.

Sign in / Sign up

Export Citation Format

Share Document