多发性硬化症患者血浆中转化到总α - 2巨球蛋白浓度显著增加。

IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2004-11-05 DOI:10.1016/j.bbadis.2004.06.010
Poul Erik H. Jensen, Signe Humle Jørgensen, Pameli Datta, Per Soelberg Sørensen
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引用次数: 0

摘要

我们检测了多发性硬化症(MS)患者血浆中的蛋白酶抑制剂alpha2-巨球蛋白(alpha2M);中枢神经系统的一种神经系统疾病。测定了90例临床明确的MS患者、73例复发缓解型MS患者、17例继发性进展型MS患者和132名健康个体的血浆天然和转化alpha2M浓度。MS患者体内天然alpha2M浓度显著降低,转化alpha2M浓度显著升高。结果发现,天然α - 2和转化α - 2的浓度之间存在显著的相关性。MS患者转化的alpha2M占总alpha2M的比例比健康人高36%。结果表明,在MS疾病中发生的蛋白水解活性增加的调节中,alpha2M的重要参与。
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Significantly increased fractions of transformed to total α2-macroglobulin concentrations in plasma from patients with multiple sclerosis
We examined the proteinase inhibitor α2-macroglobulin (α2M) in plasma from patients with multiple sclerosis (MS); a neurological disease of the central nervous system. The plasma concentrations of native and transformed α2M were measured in 90 patients with clinically definite MS, 73 with relapsing–remitting and 17 with secondary progressive MS, and 132 healthy individuals. Significantly lower concentrations of native α2M and significantly higher concentrations of transformed α2M were found in MS patients. A significant correlation between the concentrations of native and transformed α2M was found. The fraction of transformed to total α2M in the MS patients was 36% higher than in the healthy individuals. The results suggest an important involvement of α2M in regulation of increased proteolytic activity occurring in MS disease.
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来源期刊
CiteScore
12.30
自引率
0.00%
发文量
218
审稿时长
32 days
期刊介绍: BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.
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