ArticleMolecular and cellular biochemistry2024
LINC01232 targeting miR-1250-3p/MSH2 axis attenuates mesangial cell proliferation and fibrosis in diabetic nephropathy.
Article in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The significance of long non-coding RNA (ncRNAs) in the initiation and progression of diabetic nephropathy (DN) has attracted much interest. The purpose of this work was to ascertain the role of LINC01232 in cell models and animal models of DN. C57BL/6 J mice were administered with streptozotocin (STZ) to develop animal models of DN, and mouse glomerular mesangial cells (MCs) were exposed to high glucose (HG) to establish cell models of DN. Expression levels of LINC01232, miR-1250-3p and MSH2 were identified by quantitative real-time PCR (qPCR) or western blotting. Fibrosis-related proteins were quantified by western blotting. MC proliferative capacity was checked by EdU assay. DN progression and fibrosis level in animal models were assessed by hematoxylin and eosin (HE) and Masson staining. The potential binding sites between miR-1250-3p and LINC01232 or MSH2 were examined by dual-luciferase reporter assay. LINC01232 expression was heightened in kidney tissues of DN patients. Its overexpression in HG-treated MCs alleviated MC proliferation and fibrosis. Overexpression of LINC01232 alleviated the pathological state of glomerular hypertrophy, MC hyperplasia, basement membrane thickening, and fibrosis in the DN models. LINC01232 bound to miR-1250-3p and competed for miR-1250-3p binding sites with MSH2. LINC01232 overexpression decoyed miR-1250-3p to increase MSH2 expression, and MSH2 depletion restored LINC01232 overexpression-inhibited MC proliferation and fibrosis. LINC01232 alleviated the mesangial cell proliferation and fibrosis in the progression of DN by targeting miR-1250-3p/MSH2 pathway.
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