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Selected Publication:
SHR Neuro Cancer Cardio Lipid Metab Microb
Díaz-Pérez, FI; Hiden, U; Gauster, M; Lang, I; Konya, V; Heinemann, A; Lögl, J; Saffery, R; Desoye, G; Cvitic, S.
Post-transcriptional down regulation of ICAM-1 in feto-placental endothelium in GDM.
Cell Adh Migr. 2016; 10(1-2):18-27
Doi: 10.1080/19336918.2015.1127467
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- Leading authors Med Uni Graz
- Diaz Perez Francisca Isidora
- Hiden Ursula
- Co-authors Med Uni Graz
- Desoye Gernot
- Gauster Martin
- Heinemann Akos
- Konya Viktoria
- Lang-Olip Ingrid
- Lögl Jelena
- Tokic Silvija
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- Abstract:
- Maternal gestational diabetes (GDM) is associated with hyperglycaemia and hyperinsulinemia in the fetal circulation which consequently may induce endothelial dysfunction in the feto-placental vasculature. In fact, feto-placental vasculature reveals various morphological changes in response to GDM. The cell adhesion molecules (CAMs) ICAM-1, VCAM-1 and E-selectin promote attachment and trans-endothelial migration of leukocytes, and are up regulated in inflammation and endothelial dysfunction. Thus, we hypothesized that the GDM environment upregulates ICAM-1, VCAM-1 and E-selectin in the feto-placental endothelium. We isolated primary feto-placental endothelial cells (fpEC) after normal (n=18) and GDM pregnancy (n=11) and analyzed mRNA (RT-qPCR) and protein expression (Immunoblot) of ICAM-1, VCAM-1 and E-selectin. While other CAMs were unchanged on mRNA and protein levels, ICAM-1 protein was decreased by GDM. Further analysis revealed also a decrease in the release of soluble ICAM-1 (sICAM-1), whose levels correlated negatively with maternal BMI. We conclude that this reduction of ICAM-1 protein species is the result of post-translational regulation, since ICAM-1 mRNA expression was unchanged. In fact, miRNAs targeting ICAM-1 were upregulated in GDM fpEC. Immunohistochemistry showed weaker ICAM-1 staining in the placental endothelium after GDM pregnancies, and demonstrated ICAM-1 binding partners CD11a and CD18 expressed on leukocytes in fetal circulation and on placental tissue macrophages. This study identified reduction of ICAM-1 protein in fpEC in GDM pregnancy, which was regulated post-transcriptionally. Low ICAM-1 protein production may represent a protective, placenta-specific mechanism to avoid leukocyte transmigration into the placenta in response to GDM.
- Find related publications in this database (Keywords)
- E-selectin
- endothelial dysfunction
- feto-placental endothelium
- GDM
- ICAM-1
- VCAM-1