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探索凝血因子 XIII 游离 B 亚基的功能：与补体因子的相互作用及一种识别潜在结合伴侣的新方法。

Exploring the function of factor XIII free B subunit: Interactions with complement factors and a novel approach to identify potential binding partners.

作者信息

Li Bojun, Bechtler Clément, Jenny Lorenz, Ricklin Daniel, Schroeder Verena

机构信息

Experimental Haemostasis Group, Department for BioMedical Research DBMR University of Bern Bern Switzerland.

Molecular Pharmacy Group, Department of Pharmaceutical Sciences University of Basel Basel Switzerland.

出版信息

Res Pract Thromb Haemost. 2022 Jul 21;6(5):e12766. doi: 10.1002/rth2.12766. eCollection 2022 Jul.

DOI:10.1002/rth2.12766
PMID:35873217
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9301527/
Abstract

BACKGROUND

The factor XIII (FXIII)-B subunit has a critical function as a carrier protein to stabilize FXIII-A in plasma and supply it to its main substrate, fibrinogen. However, the function of the excess free FXIII-B circulating in plasma is still elusive.

OBJECTIVES

In the present study, we explored potential interactions of free FXIII-B with complement factors and searched for novel binding partners.

METHODS

We tested for cofactor activity in the degradation of complement C3b and C4b and used ELISA- and surface plasmon resonance-based binding assays to investigate interactions between FXIII-B and complement components. We performed immunoprecipitation and mass spectrometry analysis to identify potential binding partners of free FXIII-B in freshly drawn plasma samples.

RESULTS

FXIII-B did not exhibit cofactor activity in the degradation of C3b and C4b similar to factor H and C4b-binding protein, nor did it bind to complement factors to a relevant extent. Identification of proteins potentially binding to free FXIII-B revealed high interindividual variation. We confirmed α-macroglobulin (α2MG) as a candidate, although direct interactions or functional effects remain to be validated.

CONCLUSIONS

Our study reveals that free FXIII-B has no direct role in regulating the complement system, despite a structural similarity to major complement regulators. Further studies are needed to validate α2MG as a binding partner and explore potential functional consequences of this binding.

摘要

背景

凝血因子 XIII（FXIII）-B 亚基作为一种载体蛋白具有关键功能，可在血浆中稳定 FXIII-A 并将其提供给主要底物纤维蛋白原。然而，血浆中循环的过量游离 FXIII-B 的功能仍不清楚。

目的

在本研究中，我们探索了游离 FXIII-B 与补体因子之间的潜在相互作用，并寻找新的结合伴侣。

方法

我们检测了补体 C3b 和 C4b 降解中的辅因子活性，并使用基于酶联免疫吸附测定（ELISA）和表面等离子体共振的结合试验来研究 FXIII-B 与补体成分之间的相互作用。我们进行了免疫沉淀和质谱分析，以鉴定新鲜采集的血浆样本中游离 FXIII-B 的潜在结合伴侣。

结果

FXIII-B 在 C3b 和 C4b 的降解中未表现出类似于因子 H 和 C4b 结合蛋白的辅因子活性，也未在相关程度上与补体因子结合。对可能与游离 FXIII-B 结合的蛋白质的鉴定显示个体间差异很大。我们证实α-巨球蛋白（α2MG）为候选蛋白，尽管直接相互作用或功能效应仍有待验证。

结论

我们的研究表明，尽管游离 FXIII-B 与主要补体调节因子在结构上相似，但在调节补体系统方面没有直接作用。需要进一步研究来验证α2MG 作为结合伴侣，并探索这种结合的潜在功能后果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/5fd3e893edf4/RTH2-6-e12766-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/bdea46d05315/RTH2-6-e12766-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/1264941e8907/RTH2-6-e12766-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/f16b80a98ee2/RTH2-6-e12766-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/5ee0a732fccc/RTH2-6-e12766-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/199caca5e106/RTH2-6-e12766-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/5fd3e893edf4/RTH2-6-e12766-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/bdea46d05315/RTH2-6-e12766-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/1264941e8907/RTH2-6-e12766-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/f16b80a98ee2/RTH2-6-e12766-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/5ee0a732fccc/RTH2-6-e12766-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/199caca5e106/RTH2-6-e12766-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90c8/9301527/5fd3e893edf4/RTH2-6-e12766-g003.jpg

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