Literature DB >> 31984663

Contact activation-induced complex formation between complement factor H and coagulation factor XIIa.

Sai Sindhu Thangaraj1,2, Stig Hill Christiansen2, Jonas Heilskov Graversen2, Johannes Jakobsen Sidelmann1,3, Søren Werner Karlskov Hansen2, Anette Bygum4, Jørgen Brodersen Gram1,3, Yaseelan Palarasah1,2,3.   

Abstract

BACKGROUND: The complement and coagulation systems share an evolutionary origin with many components showing structural homology. Certain components, including complement factor H (FH) and coagulation factor XII (FXII), have separately been shown to have auxiliary activities across the two systems.
OBJECTIVES: The interaction between FXII and FH was investigated.
METHODS: Using enzyme-linked immunosorbent assay (ELISA) and surface plasmon resonance (SPR) complex formation between different FXII forms and FH was investigated. The presence of α-FXIIa:FH complexes upon contact activation in plasma was evaluated by ELISA and immunoprecipitation.
RESULTS: We identified and characterized a direct interaction between the components and demonstrated that among different forms of FXII, only the activated α-FXIIa formed complexes with FH, with an apparent binding strength Kd of 34 ± 9 nmol/L. The complex formation involved the kringle domain of the heavy chain of FXII. C1-inhibitor induced inhibition of α-FXIIa did not alter the binding of α-FXIIa toward FH. We further demonstrated the presence of α-FXIIa:FH complexes in normal human plasma upon contact activation, indicating formation of α-FXIIa:FH complexes as a consequence of α-FXIIa generation. Complex formation between α-FXIIa and FH was also assessed in hereditary angioedema (HAE) patients with C1-inhibitor deficiency as well as rheumatoid arthritis (RA) patients with high levels of anti-cyclic citrullinated peptide (anti-CCP) upon contact activation. We observed elevated levels of α-FXIIa:FH complexes in HAE patients, and equal levels of complexes in RA patients and healthy individuals upon contact activation.
CONCLUSION: A direct interaction between α-FXIIa and FH is demonstrated. Our findings represent a new crosstalk between these systems, potentially important in the onset and pathology of inflammatory vascular diseases.
© 2020 International Society on Thrombosis and Haemostasis.

Entities:  

Keywords:  C1 inhibitor deficiency; coagulation; complement; factor H; factor XII

Mesh:

Substances:

Year:  2020        PMID: 31984663     DOI: 10.1111/jth.14742

Source DB:  PubMed          Journal:  J Thromb Haemost        ISSN: 1538-7836            Impact factor:   5.824


  3 in total

1.  Cross-Talk between the Complement Pathway and the Contact Activation System of Coagulation: Activated Factor XI Neutralizes Complement Factor H.

Authors:  Cristina Puy; Jiaqing Pang; Stéphanie E Reitsma; Christina U Lorentz; Erik I Tucker; David Gailani; András Gruber; Florea Lupu; Owen J T McCarty
Journal:  J Immunol       Date:  2021-04-15       Impact factor: 5.422

2.  Exercise plasma boosts memory and dampens brain inflammation via clusterin.

Authors:  Nathalie Khoury; Michael J Betley; Zurine De Miguel; Benoit Lehallier; Drew Willoughby; Niclas Olsson; Andrew C Yang; Oliver Hahn; Nannan Lu; Ryan T Vest; Liana N Bonanno; Lakshmi Yerra; Lichao Zhang; Nay Lui Saw; J Kaci Fairchild; Davis Lee; Hui Zhang; Patrick L McAlpine; Kévin Contrepois; Mehrdad Shamloo; Joshua E Elias; Thomas A Rando; Tony Wyss-Coray
Journal:  Nature       Date:  2021-12-08       Impact factor: 69.504

Review 3.  Coagulation and complement: Key innate defense participants in a seamless web.

Authors:  Edward L G Pryzdial; Alexander Leatherdale; Edward M Conway
Journal:  Front Immunol       Date:  2022-08-09       Impact factor: 8.786

  3 in total

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