Transcription Profiling of Authophagy Genes and Preeclampsia
Tamar Cesla, Yoav Smith*, Caryn Greenfield, Simcha Yagel, Ronit Haimov-Kochman and Debra Goldman-Wohl
Center for Human Placental Research, Department of Obstetrics and Gynecology Hadassah University Hospital Mt. Scopus, Jerusalem and *Bioinformatics Unit, Faculty of Medicine
Macroautophagy, a lysosomal pathway of cellular component degradation, is known to play an essential role in diverse cellular processes, including survival under stress and nutrient deprivation, development, immunity and clearance of defective macromolecules. In addition to its role in normal cellular homeostasis, autophagy is implicated in processes of inflammation, aging and numerous pathologies. Human placental function is subject to variations in maternal nutrition, which impacts the resources accessible to support the developing fetus. We hypothesized that defective autophagy may be involved in the etiology of preeclampsia where placental insufficiency is implicated in the initiation of the maternal syndrome.
We used the microarray data publicly available through the NCBI Gene Expression Omnibus (Geo) platform to analyze if over 50 autophagy pathway associated genes display differential expression in normal as compared to preeclamptic placental samples. Five data sets were examined for a total of 59 preeclampsia and 87 control samples. Analysis of whole genome expression transcriptional profiling with RMA (quantile based) normalization using the PARTEK GENOMIC SUITE 6.6. PCA (principal component analysis) was performed to remove outlier samples. a t-test performed on the data did not reveal a statistical difference between autophagy associated gene expression of normal and preeclamptic placental samples.
We conclude that although preeclampsia displays many of the features that would suggest altered autophagy, including premature aging and placental insufficiency, defective autophagy as a cause of preeclampsia is not supported by whole placental microarray differential expression profiling.