Angiogenin and SDF-1α serum concentration in patients with systemic sclerosis in relation to clinical status

Dziankowska‐Bartkowiak, Bożena; Gerlicz-Kowalczuk, Zofia; Waszczykowska, Elżbieta

doi:10.5114/aoms.2011.20610

Cited by 12 publications

(11 citation statements)

References 20 publications

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“…Systemic sclerosis is a connective tissue disorder characterized by tissue hypoxia due to vascular changes and excessive fibrosis of the skin and internal organs. Damage to blood vessels and endothelium, as well as imbalance of vascular homeostasis, impairment of angiogenesis and vasculogenesis are observed in the course of the disease . In SSc, despite the lack of angiogenesis, the expression of VEGF was shown to be up‐regulated in skin and circulation early in the disease.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of angiogenic homeostasis in systemic sclerosis

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Dysregulation of angiogenic homeostasis in systemic sclerosis

et al. 2013

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“…In the clinical course of SSc, extensive fibrous degeneration develops in various internal organs, including the heart [2]. It was suggested that tissue fibrosis observed in SSc is partially related to matrix metalloproteinases (MMP) inhibition by tissue inhibitors of metalloproteinases (TIMP) [3].…”

Section: Introductionmentioning

confidence: 99%

Heart diastolic dysfunction in patients with systemic sclerosis

Ciurzyński¹,

Bienias²,

Irzyk³

et al. 2014

aoms

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IntroductionThere are limited data on left (LV) and right ventricular (RV) diastolic function in systemic sclerosis (SSc) patients especially in relation to biomarkers of matrix remodeling. The aim of the study was to analyze LV and RV myocardial diastolic function in SSc patients at baseline and after at least 1 year of follow-up and its relation to serum tissue inhibitors of metalloproteinase 1 (TIMP-1) level.Material and methodsWe prospectively studied 111 SSc patients (101 female, 10 male, age 54.2 ±13.8 years) and 21 age-matched controls (18 female, 3 male, age 49.3 ±10.5 years). After at least 1 year of observation (3.0 ±1.1 years) we reevaluated 69 of the SSc patients. Transthoracic echocardiography (Philips, iE33) for assessment of LV and RV diastolic function was performed and TIMP-1 serum level was measured.ResultsImpaired LV relaxation was observed in 38 (34%) SSc patients and in 1 (5%) of the controls (p < 0.001). The mean E/A ratio was lower in patients with SSc than in controls (p = 0.002) and significantly decreased after the follow-up period (p = 0.02). Impaired RV relaxation was detected in 25 (22.5%) SSc patients and in 1 (5%) control subject (p < 0.001) but did not deteriorate after follow-up. Mean serum level of TIMP-1 was significantly elevated in the follow-up group compared to baseline examination (p = 0.0001). Serum TIMP-1 level correlated positively with E/E’, both septal and lateral (r = 0.4, p = 0.002 and r = 0.32, p = 0.01).ConclusionsThe LV and RV relaxation is impaired in SSc patients. Moreover, left ventricular diastolic function deteriorated after the follow-up period. The TIMP-1 serum levels correlate with echocardiographic parameters, providing a potent link for LV diastolic function and matrix remodeling in patients with SSc.

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“…Pathogenesis of the disease remains unknown. It is postulated that, as in SSc, the primary phenomenon involves injury of endothelial cells, which is followed by a cascade of immune events, including autoaggression and, finally, leads to a disturbed turnover of extracellular matrix [2, 3, 6–9]. Interestingly, interleukin (IL)-17, the significance of which has been postulated recently in several autoimmune diseases, including SSc [10–14], may potentially play a role in all of the above listed processes which are supposed to participate in pathogenesis of morphea.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-17A and interleukin-23 in morphea

Dańczak‐Pazdrowska¹,

Kowalczyk²,

Szramka-Pawlak³

et al. 2012

aoms

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IntroductionMorphea is a disease included in the group of scleroderma type autoimmune diseases. Interleukin (IL)-17A may play a role at every stage of its pathogenesis. The study aimed at evaluation of IL-17A and IL-23 (as the main cytokine which is supposed to stimulate and maintain synthesis of IL-17) in pathogenesis of morphea.Material and methodsThe studies were performed on 41 blood samples from patients with morphea. Skin was sampled from 29 patients. The evaluation included: (1) expression of IL-17A and IL-23 genes in peripheral blood mononuclear cells (PBMC) using real-time polymerase chain reaction (PCR), (2) plasma concentrations of IL-17A and IL-23 using ELISA, (3) expression of IL-17A and IL-23 genes in skin using real-time PCR.ResultsThe results of gene expression are expressed as median number of copies per million copies of GAPDH. Higher expression of IL-17A has been demonstrated in PBMC of morphea vs. control group (2630 and 1906 respectively; p = 0.004), accompanied by absence of significant differences in its plasma concentration (10 pg/ml in both groups) and by lowered expression in affected skin (9119 and 19113 respectively; p = 0.036). The results failed to demonstrate elevated IL-23 plasma concentration in morphea vs. control group (5 pg/ml and 6 pg/ml respectively; p = 0.335) or its increased expression in the skin (292 vs. 427; p = 0.383), although we noted its increased expression in PBMC (4419 vs. 808; p < 0.001).ConclusionsBased on the observed correlations we suggest that: (1) IL-17A does not represent a factor which promotes tissue injury in morphea, (2) IL-23 may playa role in pathogenesis of morphea.

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Angiogenin and SDF-1α serum concentration in patients with systemic sclerosis in relation to clinical status

Cited by 12 publications

References 20 publications

Dysregulation of angiogenic homeostasis in systemic sclerosis

Dysregulation of angiogenic homeostasis in systemic sclerosis

Heart diastolic dysfunction in patients with systemic sclerosis

Interleukin-17A and interleukin-23 in morphea

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