Long non-coding RNA DLX6-AS1 is the key mediator of glomerular podocyte injury and albuminuria in diabetic nephropathy by targeting the miR-346/GSK-3β signaling pathway

Guo, Jia; Wen, Zheng; Liu, Yong; Zhou, Mengwen; Shi, Yan; Lei, M.; Zhang, Chaojie; Liu, Zhangsuo

doi:10.1038/s41419-023-05695-2

Cited by 11 publications

(8 citation statements)

References 73 publications

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“…Our results showed a low miR‐346 expression in DN patients and HG‐stimulated HRMCs. A recent paper reported that miR‐346 promoted cellular damage and inflammatory response of podocytes in DN through the lncRNA DLX6‐AS1/miR‐346/GSK‐3β pathway 18 . Our work showed the involvement of miR‐346 in Alisol A‐induced effects on HG‐stimulated HRMC injury.…”

Section: Discussionsupporting

confidence: 62%

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Alisol A inhibits the circ_0001831/miR‐346/LIN28B pathway to ameliorate high glucose‐induced injury of human renal mesangial cells

Yue,

Dai,

Song

et al. 2023

Nephrology

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BackgroundAlisol A can ameliorate glucose metabolism disorders, however, there is no data regarding its role in diabetic nephropathy (DN). The present work evaluates the role of Alisol A in DN and the underlying mechanism.MethodsRNA expression of circ_0001831, miR‐346, and lin‐28 homolog B (LIN28B) was detected by qRT‐PCR. Cell viability and proliferation were investigated by MTT assay and EdU assay, respectively. The inflammatory cytokines were examined by ELISAs. Oxidative stress was evaluated by the commercial kits. Protein expression was detected by western blotting. The interactions among circ_0001831, miR‐346, and LIN28B were identified by dual‐luciferase reporter assay and RIP assay. DN mouse model assay was used to analyse the effect of Alisol A on renal injury of diabetic mice.ResultsHG treatment promoted HRMC proliferation, fibrosis, inflammation, and oxidative stress; however, these effects were reversed after Alisol A treatment. Alisol A treatment ameliorated STZ‐induced renal injury of diabetic mice. Additionally, circ_0001831 or LIN28B overexpression or miR‐346 downregulation relieved Alisol A‐induced effects under HG conditions. Mechanistically, circ_0001831 acted as a miR‐346 sponge, and LIN28B was identified as a target gene of miR‐346. Further, the regulation of circ_0001831 in HG‐induced HRMC dysfunction involved LIN28B.ConclusionAlisol A ameliorated HG‐induced HRMC fibrosis, inflammation, and oxidative stress and STZ‐induced renal injury of diabetic mice by regulating the circ_0001831/miR‐346/LIN28B pathway.image

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Section: Discussionsupporting

confidence: 62%

“…17 pathway. 18 Our work showed the involvement of miR-346 in Alisol A-induced effects on HG-stimulated HRMC injury.…”

Section: Discussionmentioning

confidence: 56%

Alisol A inhibits the circ_0001831/miR‐346/LIN28B pathway to ameliorate high glucose‐induced injury of human renal mesangial cells

Yue,

Dai,

Song

et al. 2023

Nephrology

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“…It was needed to research how lncRNA SNHG1 regulating SERPINA3 mRNA. Combining with our result that lncRNA SNHG1 located mainly in the cytoplasm, we sought much evidence in literatures that lncRNAs locating in cytoplasm often depend on sponging miRNAs [41,42]. But it is limited of just focusing on this sponging mechanism, because more and more scientists have proven that lncRNAs also could interact with proteins to in uence target genes [3].…”

Section: Discussionmentioning

confidence: 87%

LncRNA SNHG1 promotes colorectal cancer cells invasion and migration by upregulating SERPINA3

Xiao

Yang

Gong

et al. 2023

Preprint

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Colorectal cancer metastasis (CRC) is the main reason for patients’ death and remains a crucial clinical challenge. LncRNAs play kinds of important roles in the progression of CRC metastasis, but the implied mechanisms are still unclear. In our research, we studied the lncRNA small nucleolus host gene 1 (SNHG1) which was up-regulated in CRC tissues, and the high expression of lncRNA SNHG1 was correlated with poor prognosis of patients. Functionally, lncRNA SNHG1 acted as an oncogene and promoted CRC cells invasion and migration. Mechanistically, lncRNA SNHG1 mainly located in cell cytoplasm, in which it recruited heterogeneous nuclear ribonucleoprotein D (HNRNPD) and increased the mRNA stability of serpin family A member 3 (SERPINA3), and then subsequently upregulated SERPINA3 expression to facilitated CRC cells invasion and migration. Our finding demonstrated a different role of lncRNA SNHG1 in the cytoplasm and lncRNA SNHG1/HNRNPD-SERPINA3 might serve as a potential therapy for CRC.

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“…A plethora of research has highlighted the role of podocyte injury, characterized by a reduction in podocyte count/density and foot process fusion/effacement, in DN progression. This injury is viewed as a significant contributor to the development of albuminuria [28][29][30]. Nevertheless, the mechanisms through which basement membrane thickening leads to albuminuria are not yet fully understood.…”

Section: Discussionmentioning

confidence: 99%

ITGAM-mediated macrophages contribute to basement membrane damage in diabetic nephropathy and atherosclerosis

Lou,

Li,

Liu

et al. 2024

BMC Nephrol

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Background Diabetic nephropathy (DN) and atherosclerosis (AS) are prevalent and severe complications associated with diabetes, exhibiting lesions in the basement membrane, an essential component found within the glomerulus, tubules, and arteries. These lesions contribute significantly to the progression of both diseases, however, the precise underlying mechanisms, as well as any potential shared pathogenic processes between them, remain elusive. Methods Our study analyzed transcriptomic profiles from DN and AS patients, sourced from the Gene Expression Omnibus database. A combination of integrated bioinformatics approaches and machine learning models were deployed to identify crucial genes connected to basement membrane lesions in both conditions. The role of integrin subunit alpha M (ITGAM) was further explored using immune infiltration analysis and genetic correlation studies. Single-cell sequencing analysis was employed to delineate the expression of ITGAM across different cell types within DN and AS tissues. Results Our analyses identified ITGAM as a key gene involved in basement membrane alterations and revealed its primary expression within macrophages in both DN and AS. ITGAM was significantly correlated with tissue immune infiltration within these diseases. Furthermore, the expression of genes encoding core components of the basement membrane was influenced by the expression level of ITGAM. Conclusion Our findings suggest that macrophages may contribute to basement membrane lesions in DN and AS through the action of ITGAM. Moreover, therapeutic strategies that target ITGAM may offer potential avenues to mitigate basement membrane lesions in these two diabetes-related complications.

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Long non-coding RNA DLX6-AS1 is the key mediator of glomerular podocyte injury and albuminuria in diabetic nephropathy by targeting the miR-346/GSK-3β signaling pathway

Cited by 11 publications

References 73 publications

Alisol A inhibits the circ_0001831/miR‐346/LIN28B pathway to ameliorate high glucose‐induced injury of human renal mesangial cells

Alisol A inhibits the circ_0001831/miR‐346/LIN28B pathway to ameliorate high glucose‐induced injury of human renal mesangial cells

LncRNA SNHG1 promotes colorectal cancer cells invasion and migration by upregulating SERPINA3

ITGAM-mediated macrophages contribute to basement membrane damage in diabetic nephropathy and atherosclerosis

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