Annexin A2 interferes with complement regulation within the glomerulus
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F25%3A00085872" target="_blank" >RIV/00023001:_____/25:00085872 - isvavai.cz</a>
Result on the web
<a href="https://www.sciencedirect.com/science/article/pii/S0021925825025098?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0021925825025098?via%3Dihub</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.jbc.2025.110657" target="_blank" >10.1016/j.jbc.2025.110657</a>
Alternative languages
Result language
angličtina
Original language name
Annexin A2 interferes with complement regulation within the glomerulus
Original language description
The alternative pathway of complement is an important pathogenic driver of a variety of glomerular diseases. Factor H is a soluble complement regulatory protein, and it is known to play a critical role in protecting the kidney from alternative pathway-mediated injury. Other proteins, however, can interfere with complement regulation by Factor H, thereby predisposing the kidney to injury. Annexin A2 was previously shown to bind to Factor H and is expressed by several resident cell types in the kidney. In the current study, we show that extracellular annexin A2 binds to the region of Factor H encompassing short consensus repeats 6 to 8, impairing the ability of Factor H to regulate complement activation on the surface of glomerular endothelial cells and podocytes in vitro and in vivo. Annexin A2 does not, however, impair Factor H function on extracellular matrix or guinea pig erythrocytes. Targeted deletion of annexin A2 in mice attenuates cyclosporine-induced kidney injury in mice and deficiency of annexin A2 expression reduces complement activation on the surface of extracellular vesicles released from endothelial cells in this model. Review of publicly available kidney transcription datasets revealed that annexin A2 is expressed by several cell types in the kidney, and that expression is increased in mulas an intrinsic "positive regulator" of complement activation in the kidney, promoting the inflammatory response after various kidney insults.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10608 - Biochemistry and molecular biology
Result continuities
Project
—
Continuities
N - Vyzkumna aktivita podporovana z neverejnych zdroju
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of biological chemistry
ISSN
0021-9258
e-ISSN
1083-351X
Volume of the periodical
301
Issue of the periodical within the volume
10
Country of publishing house
US - UNITED STATES
Number of pages
15
Pages from-to
"art. no. 110657"
UT code for WoS article
001580252400001
EID of the result in the Scopus database
2-s2.0-105016458807