TY  - JOUR
A1  - Wilmes, Verena
A1  - Lux, Constantin Peter
A1  - Niess, Constanze
A1  - Gradhand, Elise
A1  - Verhoff, Marcel A.
A1  - Kauferstein, Silke
T1  - Changes in gene expression patterns in postmortem human myocardial infarction
T2  - International journal of legal medicine
N2  - In murine models, the expression of inducible nitric oxide synthase (iNOS) in myocardial infarction (MI) has been reported to be the result of tissue injury and inflammation. In the present study, mRNA expression of iNOS, hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) was investigated in postmortem human infarction hearts. Since HIF-1α is the inducible subunit of the transcription factor HIF-1, which regulates transcription of iNOS and VEGF, the interrelation between the three genes was observed, to examine the molecular processes during the emergence of MI. iNOS and VEGF mRNAs were found to be significantly upregulated in the affected regions of MI hearts in comparison to healthy controls. Upregulation of HIF-1α was also present but not significant. Correlation analysis of the three genes indicated a stronger and significant correlation between HIF-1α and iNOS mRNAs than between HIF-1α and VEGF. The results of the study revealed differences in the expression patterns of HIF-1 downstream targets. The stronger transcription of iNOS by HIF-1 in the affected regions of MI hearts may represent a pathological process, since no correlation of iNOS and HIF-1α mRNA was found in non-affected areas of MI hearts. Oxidative stress is considered to cause molecular changes in MI, leading to increased iNOS expression. Therefore, it may also represent a forensic marker for detection of early changes in heart tissue.
KW  - Inducible nitric oxide synthase (iNOS)
KW  - Hypoxia-inducible factor-1α (HIF-1α)
KW  - Vascular endothelial growth factor (VEGF)
KW  - Myocardial infarction (MI)
KW  - Hypoxia
KW  - Transcription regulation
Y1  - 2020
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/63789
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-637893
SN  - 1437-1596
N1  - Open Access funding provided by Projekt DEAL.
N1  - This work is supported by the German Heart Foundation/German Foundation of Heart Research.
VL  - 134.2020
IS  - 5
SP  - 1753
EP  - 1763
PB  - Springer
CY  - Berlin ; Heidelberg
ER  -