Gewählte Publikation:
SHR
Neuro
Krebs
Kardio
Lipid
Stoffw
Microb
Sedlmayr, P; Blaschitz, A; Stocker, R.
The role of placental tryptophan catabolism.
Front Immunol. 2014; 5(7):230-230
Doi: 10.3389/fimmu.2014.00230
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
-
Sedlmayr Peter
- Co-Autor*innen der Med Uni Graz
-
Blaschitz Astrid
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
-
This review discusses the mechanisms and consequences of degradation of tryptophan (Trp) in the placenta, focusing mainly on the role of indoleamine 2,3-dioxygenase-1 (IDO1), one of three enzymes catalyzing the first step of the kynurenine pathway of Trp degradation. IDO1 has been implicated in regulation of feto-maternal tolerance in the mouse. Local depletion of Trp and/or the presence of metabolites of the kynurenine pathway mediate immunoregulation and exert antimicrobial functions. In addition to the decidual glandular epithelium, IDO1 is localized in the vascular endothelium of the villous chorion and also in the endothelium of spiral arteries of the decidua. Possible consequences of IDO1-mediated catabolism of Trp in the endothelium encompass antimicrobial activity and immunosuppression, as well as relaxation of the placental vasotonus, thereby contributing to placental perfusion and growth of both placenta and fetus. It remains to be evaluated whether other enzymes mediating Trp oxidation, such as indoleamine 2,3-dioxygenase-2, Trp 2,3-dioxygenase, and Trp hydroxylase-1 are of relevance to the biology of the placenta.
- Find related publications in this database (Keywords)
-
pregnancy
-
placenta
-
intrauterine growth restriction
-
fetal growth restriction
-
preeclampsia
-
vasotonus
-
feto-maternal tolerance
-
immunoregulation