MicroRNA-668 represses MTP18 to preserve mitochondrial dynamics in ischemic acute kidney injury

Wei, Qingqing; Sun, Haipeng; Song, Shuwei; Liu, Yong; Liu, Pengyuan; Livingston, Man J.; Wang, Jianwen; Liang, Mingyu; Mi, Qing Sheng; Huo, Yuqing; Nahman, N. S.; Mei, Changlin; Dong, Zheng

doi:10.1172/jci121859

Cited by 103 publications

(91 citation statements)

References 69 publications

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“…For PKCδ or CD38 plasmids construction, the coding sequences of human cDNA were amplified and inserted into pcDNA3.1 vector, according to previous studies 40,41 . To construct luciferase reporter plasmids, 50 bp DNA sequences including predicted target sites of miR-26a/b in the 3′UTR fragment of PKCδ or CD38 cDNA were synthesized and subcloned into pRL-TK vector according to published methods 42 . 50 bp sequences as well as mutations were also used.…”

Section: Plasmids Constructionmentioning

confidence: 99%

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MicroRNA-26a/b have protective roles in oral lichen planus

Gao

Wang

et al. 2020

Cell Death Dis

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Oral lichen planus (OLP) is a kind of oral epithelial disorder featured with keratinocyte apoptosis and inflammatory reaction. The pathogenesis of OLP remains an enigma. Herein, we showed that the levels of miR-26a/b were robustly down-regulated in oral mucosal biopsies, serum and saliva in OLP patients compared with healthy control. Moreover, we found the binding sites of vitamin D receptor (VDR) in the promoter regions of miR-26a/b genes and proved that the induction of miR-26a/b was VDR dependent. The reduction of miR-26a/b expression was also detected in the oral epithelium of vitamin D deficient or VDR knockout mice. miR-26a/b inhibitors enhanced apoptosis and Type 1T helper (Th1) cells-related cytokines production in oral keratinocytes, whereas miR-26a/b mimics were protective. Mechanistically, we analyzed miRNA target genes and confirmed that miR-26a/b blocked apoptosis by directly targeting Protein Kinase C δ (PKCδ) which promotes cellular apoptotic processes. Meanwhile, miR-26a/b suppressed Th1-related cytokines secretion through targeting cluster of the differentiation 38 (CD38). In accordant with miR-26a/b decreases, PKCδ and CD38 levels were highly elevated in OLP patients' samples. Taken together, our present investigations suggest that vitamin D/VDR-induced miR-26a/b take protective functions in OLP via both inhibiting apoptosis and impeding inflammatory response in oral keratinocytes.

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Section: Plasmids Constructionmentioning

confidence: 99%

“…ChIP was performed as described previously with some modifications 42,43 . After VDR or control plasmids transfection, HOKs were fixed with 1% formaldehyde and neutralized by glycine.…”

Section: Chromatin Immunoprecipitation (Chip) Assaysmentioning

confidence: 99%

MicroRNA-26a/b have protective roles in oral lichen planus

Gao

Wang

et al. 2020

Cell Death Dis

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“…Interestingly, it was shown that transketolase (TKT) activity correlates with creatinine levels in uremic patients [18], which may possibly partially explain the observation that creatinine levels increased following miR-146a-5p transfection. Remarkably, other reports also demonstrated that creatinine concentrations can be affected by miRNAs [19,20]. Most metabolic genes affected by miR-146a-5p transfection exhibited upregulated gene expression ( Table 2).…”

Section: Discussionmentioning

confidence: 64%

MicroRNA-Mediated Metabolic Reprograming in Renal Cancer

Bogusławska

Popławski

Alseekh

et al. 2019

Cancers

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Metabolic reprogramming is one of the hallmarks of renal cell cancer (RCC). We hypothesized that altered metabolism of RCC cells results from dysregulation of microRNAs targeting metabolically relevant genes. Combined large-scale transcriptomic and metabolic analysis of RCC patients tissue samples revealed a group of microRNAs that contribute to metabolic reprogramming in RCC. miRNAs expressions correlated with their predicted target genes and with gas chromatography-mass spectrometry (GC-MS) metabolome profiles of RCC tumors. Assays performed in RCC-derived cell lines showed that miR-146a-5p and miR-155-5p targeted genes of PPP (the pentose phosphate pathway) (G6PD and TKT), the TCA (tricarboxylic acid cycle) cycle (SUCLG2), and arginine metabolism (GATM), respectively. miR-106b-5p and miR-122-5p regulated the NFAT5 osmoregulatory transcription factor. Altered expressions of G6PD, TKT, SUCLG2, GATM, miR-106b-5p, miR-155-5p, and miR-342-3p correlated with poor survival of RCC patients. miR-106b-5p, miR-146a-5p, and miR-342-3p stimulated proliferation of RCC cells. The analysis involving >6000 patients revealed that miR-34a-5p, miR-106b-5p, miR-146a-5p, and miR-155-5p are PanCancer metabomiRs possibly involved in global regulation of cancer metabolism. In conclusion, we found that microRNAs upregulated in renal cancer contribute to disturbed expression of key genes involved in the regulation of RCC metabolome. miR-146a-5p and miR-155-5p emerge as a key “metabomiRs” that target genes of crucial metabolic pathways (PPP (the pentose phosphate pathway), TCA cycle, and arginine metabolism).

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“…MicroRNAs that affect mitochondrial function have been explored and studied in various disease contexts [38][39][40]. Wherein miR-668 has been shown to affect mitochondrial dynamics during ischemic acute kidney injury [41]. Similarly, Juan Ji et.al.…”

Section: Discussionmentioning

confidence: 99%

MiR-195 regulates mitochondrial function by targeting mitofusin-2 in breast cancer cells

et al. 2019

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Mitochondrial dynamics is a highly dysregulated process in cancer. Apoptosis and mitochondrial fission are two concurrent events wherein increased mitochondrial fragmentation serves as a hallmark of apoptosis. We have shown earlier that miR-195 exerts pro-apoptotic effects in breast cancer cells. Herein, we have demonstrated miR-195 as a modulator of mitochondrial dynamics and function. Imaging experiments upon miR-195 treatment have shown that mitochondria undergo extensive fission. We validated mitofusin2 as a potential target of miR-195. This may provide a molecular explanation for the respiratory defects induced by miR-195 over-expression in breast cancer cells. Active, but not total, mitochondrial mass, was reduced with increasing levels of miR-195. We have further shown that miR-195 enhances mitochondrial SOD-2 expression but does not affect PINK1 levels in breast cancer cells. Collectively, we have revealed that miR-195 is a modulator of mitochondrial dynamics by targeting MFN2 thereby impairing mitochondrial function. Concomitantly, it enhances the scavenger of reactive oxygen species (SOD-2) to maintain moderate levels of oxidative stress. Our findings suggest a therapeutic potential of miR-195 in both ER-positive as well as ER-negative breast cancer cells.

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MicroRNA-668 represses MTP18 to preserve mitochondrial dynamics in ischemic acute kidney injury

Cited by 103 publications

References 69 publications

MicroRNA-26a/b have protective roles in oral lichen planus

MicroRNA-26a/b have protective roles in oral lichen planus

MicroRNA-Mediated Metabolic Reprograming in Renal Cancer

MiR-195 regulates mitochondrial function by targeting mitofusin-2 in breast cancer cells

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