Accumulating evidence indicates an activated inflammatory response system as a vulnerability factor for schizophrenia (SZ) and bipolar disorder (BD). We aimed to detect a specific inflammatory monocyte gene expression signature in SZ and compare such signature with our recently described inflammatory monocyte gene signature in BD. A quantitative-polymerase chain reaction (Q-PCR) case-control gene expression study was performed on monocytes of 27 SZ patients and compared to outcomes collected in 56 BD patients (all patients naturalistically treated). For Q-PCR we used nine 'SZ specific genes' (found in whole genome analysis), the 19 BD signature genes (previously found by us) and six recently described autoimmune diabetes inflammatory monocyte genes. Monocytes of SZ patients had (similar to those of BD patients) a high inflammatory set point composed of three subsets of strongly correlating genes characterized by different sets of transcription/MAPK regulating factors. Subset 1A, characterized by ATF3 and DUSP2, and subset 1B, characterized by EGR3 and MXD1, were shared between BD and SZ patients (up-regulated in 67% and 51%, and 34% and 41%, respectively). Subset 2, characterized by PTPN7 and NAB2 was up-regulated in the monocytes of 62% BD, but down-regulated in the monocytes of 48% of SZ patients. Our approach shows that monocytes of SZ and BD patients overlap, but also differ in inflammatory gene expression. Our approach opens new avenues for nosological classifications of psychoses based on the inflammatory state of patients, enabling selection of those patients who might benefit from an anti-inflammatory treatment.
cell-type markers indicated that the differential expression between the zones was not caused by an unequal distribution of different cell types. Primary stromal and epithelial prostate cells were used to study cell type expression in the 12 highest differentially expressed zonal-specific genes. RESULTSIn all, 346 genes were identified as preferentially expressed in the TZ or PZ. A few of the TZ-specific genes, including ASPA, FLJ10970 and COCH, were also stromaspecific. Comparisons with other microarray studies showed that gene expression profiles of prostate cancer and BPH correlate with the expression profiles of the PZ and TZ, respectively. CONCLUSIONGene expression differs between the PZ and TZ of the prostate, and stromal-epithelial interactions might be responsible for the distinct zonal localization of prostate diseases.
OBJECTIVE To assess the expression of forkhead transcription factors (FOX) in normal prostate and prostate diseases, as since the first FOX was identified, its family members have been implicated in a variety of cellular processes, including embryonic development and disease. MATERIAL AND METHODS We analysed a set of 12 different FOX genes by quantitative reverse transcription‐polymerase chain reaction in prostate zones, prostate cancer, lymph node metastases, benign prostatic hyperplasia (BPH), xenografts and several prostate cell lines. RESULTS There were striking differences among the expression of various FOX family members; most prominent were the high expression of FOXF1 and FOXF2 in the normal prostate transition zone and BPH, and their decreased expression in prostate cancer. Interestingly, although the FOXF genes are stroma‐specific, some of the androgen‐independent prostate cancer xenografts uniquely express these two genes. FOXD1 and FOXD2 were more highly expressed in prostate cancer and lymph node metastases. FOXA1 and FOXC1 have an opposite expression pattern for androgen‐dependent growth of prostate cancer cell lines and xenografts. CONCLUSIONS Various members of the FOX family are differentially expressed in the zones of the normal prostate and in benign and malignant outgrowths. The expression profiles of FOXF1 and FOXF2 suggest a role in epithelial to mesenchymal transition, while FOXA1 and FOXC1 expression is linked to androgen‐associated growth status of cancer.
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