Evaluation of CXCL9 and CXCL10 as circulating biomarkers of human cardiac allograft rejection

Karason, Kristjan; Jernås, Margareta; Hägg, Daniel; Svensson, Per‐Arne

doi:10.1186/1471-2261-6-29

Cited by 28 publications

(18 citation statements)

References 23 publications

(25 reference statements)

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“…These subjects all had angiography-verified absence of coronary artery disease in any major myocardial coronary artery branch. Nonischemic left ventricle myocardial biopsies were obtained from 19 subjects 4 months after orthotopic heart transplantation as a routine check for graft rejection (49). Only biopsies without signs of rejection were used.…”

Section: Figurementioning

confidence: 99%

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Perman¹,

Boström²,

Lindbom³

et al. 2011

J. Clin. Invest.

140

139

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Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr -/-mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr -/-mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis.

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Section: Figurementioning

confidence: 99%

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Perman¹,

Boström²,

Lindbom³

et al. 2011

J. Clin. Invest.

140

139

View full text Add to dashboard Cite

show abstract

“…DNA microarrays were scanned with a confocal laser scanner (GeneArray scanner36 G2500A Hewlett Packard, Palo Alto, CA, USA). In the diet study, the scanned output files were analyzed with Affymetrix Microarray Suite Version 5.0 (MAS 5.0) software as previously described [27]. The raw data was globally scaled to an arbitrary target intensity value of 100.…”

Section: Dna Microarray Analysismentioning

confidence: 99%

Regulation of human aldoketoreductase 1C3 (AKR1C3) gene expression in the adipose tissue

Svensson

Gabrielsson

Jernås

et al. 2008

Cellular and Molecular Biology Letters

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Aldoketoreductase 1C3 (AKR1C3) is a functional prostaglandin F synthase and a negative modulator of the availability of ligands for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARγ). AKR1C3 expression is known to be associated with adiposity, one of the components of the metabolic syndrome. The aim of this study was to characterize the expression of AKR1C3 in the adipose tissue and adipocytes and to investigate its potential role in the metabolic syndrome. Using microarray analysis and realtime PCR, we studied the expression of AKR1C3 in adipose tissue samples from obese subjects with or without metabolic complications, during very low calorie diet-induced weight loss, and its expression in isolated human adipocytes of different sizes. The adipose tissue AKR1C3 expression levels were marginally lower in obese subjects with the metabolic syndrome compared with the levels in healthy obese subjects when analyzed using microarray (p = 0.078) and realtime PCR (p < 0.05), suggesting a secondary or compensatory effect. The adipose tissue mRNA levels of AKR1C3 were reduced during and after dietinduced weight-loss compared to the levels before the start of the diet (p < 0.001 at all time-points). The gene expression of AKR1C3 correlated with both adipose tissue mRNA levels and serum levels of leptin before the start of the diet (p < 0.05 and p < 0.01, respectively). Furthermore, large adipocytes displayed a higher expression of AKR1C3 than small adipocytes (1.5-fold, p < 0.01). In conclusion, adipose tissue AKR1C3 expression may be affected by metabolic disease, and its levels are significantly reduced in response to dietinduced weight loss and correlate with leptin levels.

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“…As from those evidences, this chemokine seems by different aspects to be an optimal candidate to predict acute kidney and heart organ rejection before transplantation; conversely, post-transplant serum measurement showed no changes in CXCL10 associated with heart rejection [98]. Of note, CXCL10 does not relate with general systemic inflammation but with early critical response to the antigen [98].…”

Section: Cxcl10-cxcr3 Axis and Outcomementioning

confidence: 93%

“…Of note, CXCL10 does not relate with general systemic inflammation but with early critical response to the antigen [98]. Accordingly, C reactive protein, index of general inflammatory status, and N-terminal natriuretic peptide, marker of ventricular function, are unable to predict rejection and, indeed, are associated with later occurring complications, such as allograft vasculopathy development and all causes of mortality [96].…”

Section: Cxcl10-cxcr3 Axis and Outcomementioning

confidence: 99%

Chemokines and transplant outcome

Crescioli

2016

Clinical Biochemistry

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Evaluation of CXCL9 and CXCL10 as circulating biomarkers of human cardiac allograft rejection

Cited by 28 publications

References 23 publications

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction

Regulation of human aldoketoreductase 1C3 (AKR1C3) gene expression in the adipose tissue

Chemokines and transplant outcome

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