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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: 3' Untranslated Regions, Animals, Binding Sites, Cell Line, Disease Models, Animal, Down-Regulation, Kidney, Male, MicroRNAs, RNA Interference, RNA Processing, Post-Transcriptional, RNA, Messenger, Rats, Sprague-Dawley, Renal Insufficiency, Chronic, Transfection, Up-Regulation, Uremia, Vitamin D Deficiency, Vitamin D3 24-Hydroxylase.
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Does loss of miR-125b contribute to upregulation of CYP24 in uraemic rats? Context: Abnormal upregulation of CYP24 contributes to vitamin D insufficiency and resistance to vitamin D therapy in chronic kidney disease (CKD), because human CYP24 is a key enzyme involved in the inactivation of 1a,25-dihydroxyvitamin D3 (1a,25(OH)2D3; calcitriol) and 1,25(OH)2D3. There are multiple mechanisms regulating CYP24 in a variety of types of tissues and diseases. An increasing body of evidence suggests that microRNA-125b (miR-125b) plays an important role in post-transcriptional regulation of CYP24 mRNA. We sought to test hypothesis that abnormal elevation of CYP24 in CKD is a consequence of loss of miR-125b in CKD in a uraemia rat model. We found that expression of miR-125b was significantly inhibited in uraemic rats coupled with increased CYP24 at both protein and mRNA levels compared with normal controls. In NRK-52 kidney cells, we further found that miR-125b antagomirs increased CYP24 but miR-125b mimics decreased CYP24, and luciferase assay confirmed that CYP24 is a direct target of miR-125b. Vitamin D status exerted no significant effects on expression of both miR-125b and CYP24 in uraemic rats.
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These results suggest that modulation of miR-125b may be used for treatment of Vitamin D insufficiency in CKD. Final Decision: yes