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PMID |
Sentence |
1 |
24086574
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We and others have previously shown that podocyte-selective genetic deletion of the microRNA (miR)-processing enzyme, Dicer, caused glomerulosclerosis that was associated with podocyte apoptosis, and the miR-30 family was implicated in the process.
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2 |
24086574
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Here, we report that apoptosis-associated genes were highly enriched among the predicted targets of miR-30 when compared with randomly selected miRs (26% vs. 4.5 ± 2.1%) or with the known TGF-β-regulated miR-192 (6%), miR-216a (5.1%), and miR-217 (0%). miR-30 family members were abundantly expressed in podocytes in normal mice but were downregulated in albumin/TGF-β transgenic mice with podocyte apoptosis and glomerulosclerosis.
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3 |
24086574
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In vitro, TGF-β downregulated miR-30s in wildtype and Smad3-deficient, but not Smad2- or Smad2/Smad3-deficient, podocytes.
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4 |
24086574
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In contrast, miR-30d had no effect on the phosphorylation of pro-apoptotic p38 MAP kinase induced by TGF-β.
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5 |
24086574
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Thus, we report that Smad2-dependent inhibition of miR-30s in podocytes is required for the activation of p53 and the induction of apoptosis by TGF-β.
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6 |
28017719
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Repression of miR-217 protects against high glucose-induced podocyte injury and insulin resistance by restoring PTEN-mediated autophagy pathway.
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7 |
28017719
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Simultaneously, miR-217 repression restored HG-disrupted insulin resistance by elevating glucose uptake and nephrin expression, an essential component for insulin-induced glucose uptake.
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8 |
28017719
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Importantly, suppressing autophagy pathway with 3-MA alleviated the protective roles of miR-217 down-regulation in podocyte injury and insulin resistance.
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9 |
28017719
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Furthermore, PTEN down-regulation attenuated the beneficial role of miR-217 suppression in HG-induced injury and insulin resistance.
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10 |
28017719
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Repression of miR-217 protects against high glucose-induced podocyte injury and insulin resistance by restoring PTEN-mediated autophagy pathway.
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11 |
28017719
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Simultaneously, miR-217 repression restored HG-disrupted insulin resistance by elevating glucose uptake and nephrin expression, an essential component for insulin-induced glucose uptake.
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12 |
28017719
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Importantly, suppressing autophagy pathway with 3-MA alleviated the protective roles of miR-217 down-regulation in podocyte injury and insulin resistance.
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13 |
28017719
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Furthermore, PTEN down-regulation attenuated the beneficial role of miR-217 suppression in HG-induced injury and insulin resistance.
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14 |
28017719
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Repression of miR-217 protects against high glucose-induced podocyte injury and insulin resistance by restoring PTEN-mediated autophagy pathway.
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15 |
28017719
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Simultaneously, miR-217 repression restored HG-disrupted insulin resistance by elevating glucose uptake and nephrin expression, an essential component for insulin-induced glucose uptake.
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16 |
28017719
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Importantly, suppressing autophagy pathway with 3-MA alleviated the protective roles of miR-217 down-regulation in podocyte injury and insulin resistance.
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17 |
28017719
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Furthermore, PTEN down-regulation attenuated the beneficial role of miR-217 suppression in HG-induced injury and insulin resistance.
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18 |
28017719
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Repression of miR-217 protects against high glucose-induced podocyte injury and insulin resistance by restoring PTEN-mediated autophagy pathway.
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19 |
28017719
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Simultaneously, miR-217 repression restored HG-disrupted insulin resistance by elevating glucose uptake and nephrin expression, an essential component for insulin-induced glucose uptake.
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20 |
28017719
|
Importantly, suppressing autophagy pathway with 3-MA alleviated the protective roles of miR-217 down-regulation in podocyte injury and insulin resistance.
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21 |
28017719
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Furthermore, PTEN down-regulation attenuated the beneficial role of miR-217 suppression in HG-induced injury and insulin resistance.
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22 |
29214160
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miR-217 Is a Useful Diagnostic Biomarker and Regulates Human Podocyte Cells Apoptosis via Targeting TNFSF11 in Membranous Nephropathy.
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23 |
32412691
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Dicer and Drosha expression in patients with nephrotic syndrome.
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24 |
32412691
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Some in vivo studies in Dicer/Drosha knockout mice indicate the importance of Dicer, Drosha, and microRNAs (miRNAs) in the pathogenesis of NS.
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25 |
32412691
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In the present study, the expression levels of Dicer and Drosha along with miR-30 family, miR-186, miR-193, and miR-217 were evaluated in peripheral blood mononuclear cell samples of patients with NS (N = 60) using real-time PCR.
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26 |
32412691
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In conclusion, dysregulation in expression level of Dicer and Drosha and consequently, alteration in miRNA levels are involved in the pathophysiology of NS.
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