Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Varga, Lilian; Laki, Judit; Dósa, Edit; Rugonfalvi-Kiss, Szabolcs; Madsen, Hans O.; Prohászka, Zoltán; Kocsis, Andrea; Gál, Péter; Szabó, Attila; Acsády, György; Karádi, István; Selmeci, L.; Garred, Peter; Füst, George; Entz, László

doi:10.1161/atvbaha.107.146860

Cited by 9 publications

(5 citation statements)

References 36 publications

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“…However, in our earlier work, we had similar findings; for example, while C1-INH levels were predicted, CRP levels did not predict inflammation-associated restenosis of the carotid artery after eversion endarterectomy (Szeplaki et al 2007). …”

Section: Discussionsupporting

confidence: 71%

“…Serum concentration of the highly sensitive CRP was determined with the particleenhanced immunoturbidimetric assay (Roche Cobas Integra 4000). Serum levels of C1 inhibitor, C3, and C9 were measured by radial immunodiffusion, as described in detail previously (Biro et al 2000;Derzsy et al 2010;Szeplaki et al 2007). Serum concentration of MASP-2 was determined using the method described in Varga et al (2008).…”

Section: Laboratory Methodsmentioning

confidence: 99%

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High levels of acute phase proteins and soluble 70 kDa heat shock proteins are independent and additive risk factors for mortality in colorectal cancer

Kocsis

Mészáros

Madaras

et al. 2011

Cell Stress and Chaperones

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Recently, we reported that high soluble Hsp70 (sHsp70) level was a significant predictor of mortality during an almost 3-year-long follow-up period in patients with colorectal cancer. This association was the strongest in the group of <70-year-old female patients as well as in those who were in a less advanced stage of the disease at baseline. According to these observations, measurement of the serum level of sHsp70 is a useful, stage-independent prognostic marker in colorectal cancer, especially in patients without distant metastasis. Since many literature data indicated that measurement of C-reactive protein (CRP) and other acute phase proteins (APPs) may also be suitable for predicting the mortality of patients with colorectal cancer, it seemed reasonable to study whether the effect of sHsp70 and other APPs are related or independent. In order to answer this question, we measured the concentrations of CRP as well as of other complement-related APPs (C1 inhibitor, C3, and C9) along with that of the MASP-2 complement component in the sera of 175 patients with colorectal cancer and known levels of sHsp70, which have been used in our previous study. High (above median) levels of CRP, C1 esterase inhibitor (C1-INH), and sHsp70 were found to be independently associated with poor patient survival, whereas no such association was observed with the other proteins tested. According to the adjusted Cox proportional hazards analysis, the additive effect of high sHsp70, CRP, and C1-INH levels on the survival of patients exceeded that of high sHsp70 alone, with a hazard ratio (HR) of 2.83 (1.13-70.9). In some subgroups of patients, such as in females )] or in ≤70-year-old patients )], even greater differences were obtained. These findings indicate that the clinical mortality-prediction value of combined measurements of sHsp70, CRP, and C1-INH with inexpensive methods can be very high, especially in specific subgroups of patients with colorectal cancer.

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Section: Discussionsupporting

confidence: 71%

Section: Laboratory Methodsmentioning

confidence: 99%

High levels of acute phase proteins and soluble 70 kDa heat shock proteins are independent and additive risk factors for mortality in colorectal cancer

Kocsis

Mészáros

Madaras

et al. 2011

Cell Stress and Chaperones

Self Cite

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“…More interestingly, the scFv-QuVHVL or its derivative when fully humanized may become a useful therapeutic tool, especially when used together with exogenously supplied recombinant C1-inhibitor (Padilla et al, 2007;Széplaki et al, 2007) and C4b-and C3b-scavenging (nonspecific) intravenous immunoglobulin preparations (Boackle et al,. 2006;Arumugam et al 2007), designed to control complement-mediated assaults on host tissues in circumstances such as organ transplants, antibody-mediated autoimmune diseases, extended cardiac damage following myocardial infarctions and neuronal cell death following stroke.…”

Section: Discussionmentioning

confidence: 99%

Highly specific inhibition of C1q globular-head binding to human IgG: A novel approach to control and regulate the classical complement pathway using an engineered single chain antibody variable fragment

Duvall

Tomlinson

Boackle

2008

Molecular Immunology

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We sought to specifically regulate the binding of human C1q, and thus the activation of the first complement component, via the construction of a single chain antibody variable binding region fragment (scFv) targeting the C1q globular heads. Here we describe details of the construction, expression and evaluation of this scFv, which was derived from a high affinity hybridoma (Qu) specific for the C1q globular heads. The scFv was comprised of the Qu variable-heavy chain domain (VH) linked to the Qu variable-light chain domain (VL) and was termed scFv-QuVHVL. When mixed with either purified C1q or with human serum as a source of C1, scFv-QuVHVL bound to C1q and competitively restricted the interaction of C1q or C1 with immobilized IgG or with IgG1 antibody-coated cells, and prevented the activation of native C1 in human serum as determined by analyses of C1-mediated C4 deposition and fluid phase C4 conversion. However scFv-QuVHVL could be manipulated to become a C1 activator when it was irreversibly immobilized onto microtiter ELISA plates, prior to contact with human serum complement. This functional dichotomy can be a useful tool in selectively elucidating, differentiating, inducing or inhibiting specific roles of human C1q and the classical complement pathway in complement-mediated physiological processes. We project that once fully humanized, fluid phase scFv-QuVHVL could become a useful therapeutic in limiting inadvertent host tissue damage elicited by the classical complement pathway.

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“…Considering the impact of MBL2 genotype on the occurrence of early restenosis after CEA, the role of C1-inhibitor (C1-INH), known as an inhibitor of the lectin pathway, has been also studied [ 67 ]. The aim of the study was to determine whether the C1-INH levels have predictive value for restenosis after CEA.…”

Section: Clinical Features Of the Restenosismentioning

confidence: 99%

Restenosis and Therapy

Dénès

Entz

Jancsik

2012

International Journal of Vascular Medicine

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The vascular disease involves imbalanced function of the blood vessels. Risk factors playing a role in development of impaired vessel functions will be briefly discussed. In ischemia/reperfusion (I/R), ischemic hypoxia is one of the cardinal risk factors of restenosis. Various insults are shown to initiate the phenotype switch of VSMCs. The pathological process, leading to activated inflammatory process, complement activation, and release of growth factors, initiate the proliferation of VSMCs in the media and cause luminal narrowing and impaired vascular function. The review summarizes the alteration process and demonstrates some of the clinical genetic background showing the role of complement and the genotypes of mannose-binding lectin (MBL2). Those could be useful markers of carotid restenosis after stent implantation. Gene therapy and therapeutic angiogenesis is proposed for therapy in restenosis. We suggest a drug candidate (iroxanadine), which ensures a noninvasive treatment by reverse regulation of the highly proliferating VSMCs and the disturbed function of ECs.

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Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Cited by 9 publications

References 36 publications

High levels of acute phase proteins and soluble 70 kDa heat shock proteins are independent and additive risk factors for mortality in colorectal cancer

High levels of acute phase proteins and soluble 70 kDa heat shock proteins are independent and additive risk factors for mortality in colorectal cancer

Highly specific inhibition of C1q globular-head binding to human IgG: A novel approach to control and regulate the classical complement pathway using an engineered single chain antibody variable fragment

Restenosis and Therapy

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