| Schizophrenia (SCZ) is known as a complicated mental disease with an unknown etiology. The microdeletion of 22q11.2
is the most potent genetic risk factor. Researchers are still trying to fnd which genes in the deletion region are linked to
SCZ. MIR185, encoding microRNA (miR)-185, is present in the minimal 1.5 megabase deletion. Nonetheless, the miR185 expression profle and its corresponding target genes in animal models and patients with 22q11.2 deletion syndrome
(22q11.2DS) imply that more study is required about miR-185 and its corresponding downstream pathways within idiopathic
SCZ. The expression of hsa-miR-185-5p and its corresponding target gene, shisa family member 7 (SHISA7), sometimes
called CKAMP59, were evaluated in the peripheral blood (PB) samples of Iranian Azeri patients with idiopathic SCZ and
healthy subjects, matched by gender and age as control groups by quantitative polymerase chain reaction (qPCR). Fifty
SCZ patients (male/female: 22/28, age (mean±standard deviation (SD)): 35.9±5.6) and 50 matched healthy controls
(male/female: 23/27, age (mean±SD): 34.7±5.4) were enrolled. The expression of hsa-miR-185-5p in the PB samples
from subjects with idiopathic SCZ was substantially lower than in that of control groups (posterior beta=-0.985, adjusted
P-value<0.0001). There was also a diference within the expression profle between female and male subgroups (posterior
beta=-0.86, adjusted P-value=0.046 and posterior beta=-1.015, adjusted P-value=0.004, in turn). Nevertheless, no signifcant diference was present in the expression level of CKAMP59 between PB samples from patients and control groups
(adjusted P-value>0.999). The analysis of the receiver operating characteristic (ROC) curve suggested that hsa-miR-185-5p
may correctly distinguish subjects with idiopathic SCZ from healthy people (the area under curve (AUC) value: 0.722).
Furthermore, there was a strong positive correlation between the expression pattern of the abovementioned genes in patients
with SCZ and healthy subjects (r=0.870, P<0.001 and r=0.812, P<0.001, respectively), indicating that this miR works as
an enhancer. More research is needed to determine if the hsa-miR-185-5p has an enhancer activity. In summary, this is the
frst research to highlight the expression of the miR-185 and CKAMP59 genes in the PB from subjects with idiopathic SCZ.
Our fndings suggest that gene expression alterations mediated by miR-185 may play a role in the pathogenesis of idiopathic
and 22q11.2DS SCZ. It is worth noting that, despite a substantial and clear relationship between CKAMP59 and hsa-miR185-5p, indicating an interactive network, their involvement in the development of SCZ should be reconsidered based on
the whole blood sample since the changed expression level of CKAMP59 was not signifcant. Further research with greater
sample sizes and particular leukocyte subsets can greatly make these results stronger. |