Inhibition of LINC00707/miR-223-3p/FKBP5 axis has a protective effect on diabetic kidney disease
Hongzhen Ye1, Yiting Chen2, Hong Xia3
1Department of Laboratory Medicine, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China.
Objective:
Research indicates that LINC00707 is abnormally expressed in patients suffering from diabetic kidney disease (DKD). Nevertheless, the precise role of LINC00707 in the context of DKD remains enigmatic and warrants further investigation.
Methods:
Initially, RT-qPCR was employed to assess the expression levels of LINC00707 in patients with DKD. Subsequently, we cultured glomerular podocytes under high-glucose conditions. The effects of LINC00707 on cell proliferation, apoptosis, podocyte functionality (Podocin, Nephrin, and CD2AP), oxidative stress (MDA and SOD), and inflammatory responses (IL-1β, IL-6, and TNF-α) were evaluated using CCK-8, flow cytometry, RT-qPCR, and ELISA assays. Finally, we co-regulated LINC00707 alongside its downstream targets to elucidate the molecular mechanisms by which LINC00707 influences podocyte injury.
Results:
LINC00707 is abnormally upregulated in DKD patients. Furthermore, a notable inverse correlation has been observed between LINC00707 levels and renal function in these patients. Upon downregulating LINC00707, we observed an increase in cellular proliferative activity, alongside elevated levels of Podocin, Nephrin, and CD2AP. Concurrently, the reduction of LINC00707 was associated with decreased levels of MDA, as well as proinflammatory cytokines. Significantly, the inhibition of miR-223-3p was found to reverse these observed effects. Further investigation revealed that miR-223-3p directly targets FK506-binding protein 5 (FKBP5).
Conclusions:
Inhibition of LINC00707 may reduce podocyte damage during hyperglycemia by targeting miR-223-3p/FKBP5.
Insights
Inhibition of LINC00707 reduces diabetic kidney disease (DKD) podocyte damage by targeting miR-223-3p and FKBP5. This finding offers a potential therapeutic strategy for DKD patients.
Area of Science:
- Nephrology
- Molecular Biology
- Biochemistry
Background:
- Diabetic kidney disease (DKD) is a major complication of diabetes.
- LINC00707 is abnormally expressed in DKD patients, but its role is unclear.
Purpose of the Study:
- To investigate the role of LINC00707 in DKD.
- To elucidate the molecular mechanisms of LINC00707 in podocyte injury.
Main Methods:
- Assessed LINC00707 expression in DKD patients using RT-qPCR.
- Evaluated LINC00707 effects on high-glucose cultured podocytes (proliferation, apoptosis, function, oxidative stress, inflammation).
- Investigated LINC00707 downstream targets and molecular mechanisms.
Main Results:
- LINC00707 was upregulated in DKD patients and inversely correlated with renal function.
- Downregulating LINC00707 improved podocyte proliferation, function, and reduced oxidative stress and inflammation.
- LINC00707 targeted miR-223-3p, which targets FKBP5, mediating podocyte injury.
Conclusions:
- LINC00707 inhibition ameliorates hyperglycemia-induced podocyte damage.
- The miR-223-3p/FKBP5 pathway is a key mechanism in LINC00707-mediated podocyte injury.
- Targeting LINC00707 may be a therapeutic strategy for DKD.
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