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Downregulation of miR-185 is a common pathogenic event in 22q11.2 deletion syndrome-related and idiopathic schizophrenia

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Abstract

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 find 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 miR-185 expression profile 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 difference within the expression profile 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 significant difference 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 first research to highlight the expression of the miR-185 and CKAMP59 genes in the PB from subjects with idiopathic SCZ. Our findings 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-miR-185-5p, 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 significant. Further research with greater sample sizes and particular leukocyte subsets can greatly make these results stronger.

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Data availability

The analyzed data sets generated during the study are available from the corresponding author on reasonable request.

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Acknowledgements

The research protocol was approved & supported by Student Research Committee, Tabriz University of Medical Sciences (grant number: 64802).

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Authors and Affiliations

  1. Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran

    Hani Sabaie & Mohammad Reza Asadi

  2. Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

    Hani Sabaie, Jalal Gharesouran, Mohammad Reza Asadi & Maryam Rezazadeh

  3. Research Center of Psychiatry and Behavioral Sciences, Tabriz University of Medical Sciences, Tabriz, Iran

    Sara Farhang

  4. Rob Giel Research Center, University Medical Center Groningen, University Center for Psychiatry, University of Groningen, Groningen, Netherlands

    Sara Farhang

  5. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

    Noora Karim Ahangar

  6. Psychiatric Clinics, Center for Affective, Stress and Sleep Disorders, University of Basel, Basel, Switzerland

    Serge Brand

  7. Cancer Gene Therapy Research Center, Zanjan University of Medical Science, Zanjan, Iran

    Shahram Arsang-Jang

  8. Division of Cancer Genetics, Department of Basic Oncology, Oncology Institute, Istanbul University, Fatih, Istanbul, Turkey

    Saba Dastar

  9. Men’s Health and Reproductive Health Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Mohammad Taheri

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Contributions

HS, MR, MT, SB, and SD wrote the manuscript and revised it. MRA, HS and JG supervised the study and performed the experiment. SAJ analyzed the data. SF and NKA was the clinical consultant and assessed patients for inclusion in the study. All authors read and approved the final version of manuscript.

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Correspondence to Mohammad Taheri or Maryam Rezazadeh.

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All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent forms were obtained from all study participants. The study protocol was approved by the ethical committee of Tabriz University of Medical Sciences. All methods were performed in accordance with the relevant guidelines and regulations.

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Sabaie, H., Gharesouran, J., Asadi, M.R. et al. Downregulation of miR-185 is a common pathogenic event in 22q11.2 deletion syndrome-related and idiopathic schizophrenia. Metab Brain Dis 37, 1175–1184 (2022). https://doi.org/10.1007/s11011-022-00918-5

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