TY  - JOUR
A1  - McLaughlin, Katie-May
A1  - Bechtel, Marco
A1  - Bojkova, Denisa
A1  - Münch, Christian
A1  - Ciesek, Sandra
A1  - Wass, Mark N.
A1  - Michaelis, Martin
A1  - Cinatl, Jindrich
T1  - COVID-19-related coagulopathy - is transferrin a missing link?
T2  - Diagnostics
N2  - SARS-CoV-2 is the causative agent of COVID-19. Severe COVID-19 disease has been associated with disseminated intravascular coagulation and thrombosis, but the mechanisms underlying COVID-19-related coagulopathy remain unknown. The risk of severe COVID-19 disease is higher in males than in females and increases with age. To identify gene products that may contribute to COVID-19-related coagulopathy, we analyzed the expression of genes associated with the Gene Ontology (GO) term “blood coagulation” in the Genotype-Tissue Expression (GTEx) database and identified four procoagulants, whose expression is higher in males and increases with age (ADAMTS13, F11, HGFAC, KLKB1), and two anticoagulants, whose expression is higher in females and decreases with age (C1QTNF1, SERPINA5). However, the expression of none of these genes was regulated in a proteomics dataset of SARS-CoV-2-infected cells and none of the proteins have been identified as a binding partner of SARS-CoV-2 proteins. Hence, they may rather generally predispose individuals to thrombosis without directly contributing to COVID-19-related coagulopathy. In contrast, the expression of the procoagulant transferrin (not associated to the GO term “blood coagulation”) was higher in males, increased with age, and was upregulated upon SARS-CoV-2 infection. Hence, transferrin warrants further examination in ongoing clinic-pathological investigations.
KW  - SARS-CoV-2
KW  - COVID-19
KW  - thrombosis
KW  - coagulation
KW  - coagulopathy
KW  - transferrin
Y1  - 2020
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/55498
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-554983
SN  - 2075-4418
N1  - SARS-CoV-2 is the causative agent of COVID-19. Severe COVID-19 disease has been
associated with disseminated intravascular coagulation and thrombosis, but the mechanisms
underlying COVID-19-related coagulopathy remain unknown. The risk of severe COVID-19 disease
is higher in males than in females and increases with age. To identify gene products that may
contribute to COVID-19-related coagulopathy, we analyzed the expression of genes associated
with the Gene Ontology (GO) term “blood coagulation” in the Genotype-Tissue Expression (GTEx)
database and identified four procoagulants, whose expression is higher in males and increases with age
(ADAMTS13, F11, HGFAC, KLKB1), and two anticoagulants, whose expression is higher in females
and decreases with age (C1QTNF1, SERPINA5). However, the expression of none of these genes was
regulated in a proteomics dataset of SARS-CoV-2-infected cells and none of the proteins have been
identified as a binding partner of SARS-CoV-2 proteins. Hence, they may rather generally predispose
individuals to thrombosis without directly contributing to COVID-19-related coagulopathy. In contrast,
the expression of the procoagulant transferrin (not associated to the GO term “blood coagulation”)
was higher in males, increased with age, and was upregulated upon SARS-CoV-2 infection. Hence,
transferrin warrants further examination in ongoing clinic-pathological investigations.
VL  - 10
IS  - 8, art. 539
SP  - 1
EP  - 8
PB  - MDPI
CY  - Basel
ER  -