Downregulation of the Hemoglobin Scavenger Receptor in Individuals With Diabetes and the Hp 2-2 Genotype

Levy, Andrew P.; Purushothaman, K-Raman; Levy, Nina S.; Purushothaman, Meerarani; Strauss, Merav; Asleh, Rabea; Marsh, Stuart; Cohen, Osher; Moestrup, Søren K.; Møller, Holger Jon; Zias, Elias; Benhayon, Daniel; Fuster, Valentín; Moreno, Pedro R.

doi:10.1161/circresaha.107.149435

Cited by 127 publications

(112 citation statements)

References 35 publications

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“…Therefore, oxidative conditions, such as diabetes mellitus, can cause elevated serum sCD163 levels (9 Moreover, sCD163 is found to be increased during wound healing, giving a possible role of CD163 in the pathogenesis of fibrotic diseases and the remodeling of connective tissues (10).…”

Section: Introductionmentioning

confidence: 99%

Serum Soluble CD163 and its association with various disease parameters in patients with systemic sclerosis

et al. 2016

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Objective: Cluster of differentiation 163 (CD163) is a receptor that binds haptoglobin-hemoglobin complexes and is mainly expressed on macrophages and monocytes. As a result of shedding, the extracellular portion of CD163 circulates in the blood as a soluble CD163 (sCD163). This study aimed to measure serum sCD163 levels in patients with systemic sclerosis (SSc) and to assess its association with the clinical, laboratory, and radiological features of the disease. Material and Methods:We measured serum sCD163 levels in 24 patients with SSc and in 30 healthy controls. Complete history of the patients was recorded and thorough clinical, rheumatological, and dermatological examinations were performed. For SSc, the skin thickness score was scored according to the modified Rodnan skin score method and pulmonary involvement was assessed in all patients using high-resolution computed tomography and by performing pulmonary function tests. Results:The mean serum sCD163 levels in patients with diffuse and limited SSc (61.64±19.57 and 60.8±21.43 ng/mL, respectively) demonstrated a highly statistically significant increase compared with the mean serum levels in healthy controls (36.97±16.37 ng/ mL) (p<0.001). Patients with SSc having elevated serum sCD163 levels had significantly higher pulmonary artery systolic pressure (PASP) than those with normal serum sCD163 levels (p<0.05). Furthermore, the serum sCD163 levels were significantly correlated with PASP (r=0.53, p<0.05) in patients with SSc. The mean serum sCD163 level in patients with SSc having digital ulceration (DU) (70.82±18.3 ng/mL) demonstrated a statistically significant increase (p<0.05) compared with that in SSC patients without DU (53.23±18.09 ng/mL). Conclusion:The elevated serum sCD163 levels in patients with SSc and its association with pulmonary hypertension suggest a possible role of macrophages in the pathogenesis and vascular involvement of SSc.

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Section: Introductionmentioning

confidence: 99%

Serum Soluble CD163 and its association with various disease parameters in patients with systemic sclerosis

et al. 2016

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“…Recently it has been shown that TACE is also responsible for the shedding of macrophagespecific soluble CD163 (sCD163) [9]. Plasma sCD163 is regarded as a longer duration circulating marker of TNF-α, and concentrations of sCD163 are increased in obese [10,11] and type 2 diabetic patients [12], consistent with macrophage accumulation in the adipose tissue. Zanni et al, in a study which was published while this manuscript was under review, reported a strong association between sCD163 and insulin resistance in obese individuals and normal-weight controls [11].…”

Section: Introductionmentioning

confidence: 99%

Soluble CD163: a biomarker linking macrophages and insulin resistance

et al. 2012

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Aims/hypothesis Soluble CD163 (sCD163) was recently identified as a strong risk marker for developing type 2 diabetes. We hypothesised that sCD163 independently associates with insulin resistance. Methods This cross-sectional study includes 234 participants: 96 with type 2 diabetes, 34 with impaired glucose tolerance (IGT) and 104 with normal glucose tolerance (NGT), matched for sex and BMI. Glucose-lowering medication was paused for 1 week before plasma samples were obtained for determination of sCD163 and other inflammatory and metabolic variables. Insulin resistance was estimated by homeostasis model assessment of insulin resistance (HOMA-IR).

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“…An approximately 130 kDa soluble form of human CD163 is released from the cell surface by proteolysis after oxidative stress or inflammatory stimuli. Thus, elevated level of circulating soluble CD163 (sCD163) has been reported in diabetes mellitus, which is one of oxidative conditions [12]. However, there have been no studies examining the involvement of sCD163 in SSc patients to our knowledge.…”

Section: Introductionmentioning

confidence: 99%