Levels of 17β-Hydroxysteroid Dehydrogenase Type 10 in CSF are not a Valuable Biomarker For Multiple Sclerosis

Abstract

Aim: We aimed to characterize the role of mitochondrial 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) overexpression in multiple sclerosis (MS) and to evaluate its use as a biomarker. Materials & methods: We estimated levels of 17β-HSD10, amyloid β 1–42, cyclophilin D, 17β-HSD10-cyclophilin D complexes or 17β-HSD10-parkin complexes in cerebrospinal fluid (CSF) samples. Results: The increase in 17β-HSD10 levels or in 17β-HSD10-parkin complexes and links to leukocytes were found only in relapsing–remitting MS. The sensitivity of the biomarker was 64%, the specificity equaled 60–63% compared with controls. Conclusion: Increased CSF levels of 17β-HSD10 in later stages of MS could be interpreted via its upregulation in demyelinated neuronal axons. CSF levels of 17β-HSD10 are not the valuable biomarker for the early diagnosis or for the progression of MS.

Correlation between auto/mitophagic processes and magnetic resonance imaging activity in multiple sclerosis patients

“…Parkin is a ubiquitin ligase, with an amino-terminal ubiquitin-like domain and a carboxyl-terminal ubiquitin ligase domain [34], that is recruited from the cytosol to depolarized mitochondria to promote the selective removal of the damaged organelle [35]. The presence of augmented levels of Parkin in CSF levels was recently confirmed by Kristofikova and colleagues, who found increased levels of the kinase bound to the mitochondrial protein 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) in CSF of MS-affected patients [36]. Interestingly, no difference was found when 17β-HSD10 was dissociated with Parkin, confirming the importance of the kinase during MS.…”

Friend or enemy? Review of 17β‐HSD10 and its role in human health or disease

“…17β‐HSD10‐CypD binding prevents CypD translocation to the inner mitochondrial membrane and mPTP formation. However, in the presence of elevated levels of the Aβ peptide, the 17β‐HSD10‐CypD complex is disrupted and CypD can form the mPTP pore, which subsequently leads to the cell death (Carlson et al., 2015; Kristofikova et al., 2018). It might be that in cancer, cells might also use over‐expression of 17β‐HSD10 as a tool to prevent mPTP opening, thus preventing themselves from cell death (Carlson et al., 2015).…”