MicroRNA‐1 facilitates hypoxia‐induced injury by targeting NOTCH3

Xu, Jinjin; Cao, Dandan; Zhang, Daping; Zhang, Yuan; Yue, Yuxia

doi:10.1002/jcb.29663

Cited by 17 publications

(13 citation statements)

References 24 publications

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“…The relationship between aggregation and cellular toxicity remains controversial, and the uncoupling of aggregation and toxicity is observed in various disease models. Mammalian studies suggest context-dependent mir-1 effects, where mir-1 either promotes or inhibits autophagy ( Ejlerskov et al, 2020 ; Hua et al, 2018 ; Xu et al, 2020 ). Whether miR-1 is proteoprotective or limits proteoprotection in C. elegans could hinge on many factors.…”

Section: Discussionmentioning

confidence: 99%

miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact proteotoxicity and muscle function during aging

Schiffer

Gerisch

Kawamura

et al. 2021

eLife

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Muscle function relies on the precise architecture of dynamic contractile elements, which must be fine-tuned to maintain motility throughout life. Muscle is also plastic, and remodeled in response to stress, growth, neural and metabolic inputs. The conserved muscle-enriched microRNA, miR-1, regulates distinct aspects of muscle development, but whether it plays a role during aging is unknown. Here we investigated Caenorhabditis elegans miR-1 in muscle function in response to proteostatic stress. mir-1 deletion improved mid-life muscle motility, pharyngeal pumping, and organismal longevity upon polyQ35 proteotoxic challenge. We identified multiple vacuolar ATPase subunits as subject to miR-1 control, and the regulatory subunit vha-13/ATP6V1A as a direct target downregulated via its 3′UTR to mediate miR-1 physiology. miR-1 further regulates nuclear localization of lysosomal biogenesis factor HLH-30/TFEB and lysosomal acidification. Our studies reveal that miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact muscle function and health during aging.

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Section: Discussionmentioning

confidence: 99%

miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact proteotoxicity and muscle function during aging

Schiffer

Gerisch

Kawamura

et al. 2021

eLife

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“…Studies have demonstrated that miRNAs can negatively regulate gene expression via the translational suppression of target mRNAs, playing critical roles in regulating cell proliferation, apoptosis and autophagy ( 46 , 47 ). Various disease-specific miRNAs, such as miR-155, miR-194 and miR-182 have been identified to exert their biological functions in renal tubular epithelial cells subjected to H/R via suppressing their downstream molecules ( 20 , 24 , 48 ).…”

Section: Discussionmentioning

confidence: 99%

Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4

Wang

et al. 2021

Int J Mol Med

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Acute renal injury (ARI) is a life-threatening condition and a main contributor to end-stage renal disease, which is mainly caused by ischemia-reperfusion (I/R). miR-106b-5p is a kidney function-related miRNA; however, whether miR-106b-5p regulates the progression of ARI remains unclear. The present study thus aimed to examine the effects of miR-106b-5p antagonist on the regulation of ARI progression. It was found that miR-106b-5p expression was upregulated in the renal tissue of rats with I/R-induced ARI and in NRK-52E rat renal proximal tubular epithelial cells subjected to hypoxia-reoxygenation (H/R). In vitro, H/R induction suppressed the proliferation, and promoted the apoptosis and autophagy of NRK-52E cells, whereas miR-106b-5p antagonist (inhibition of miR-106b-5p) promoted the proliferation, and attenuated the apoptosis and autophagy of NRK-52E cells under the H/R condition. dual luciferase reporter gene assay validated that transcription factor 4 (TcF4) was a target of miR-106b-5p. It was further found that TcF4 overexpression promoted the proliferation, and inhibited the apoptosis and autophagy of NRK-52E cells subjected to H/R. Moreover, the effects of miR-106b-5p antagonist on NRK-52E cell proliferation, apoptosis and autophagy were mediated through the regulation of TcF4. In vivo, miR-106b-5p antagonist reduced the severity of renal injury, decreased cell proliferation in renal tissues and lowered the serum creatinine (Scr) and blood urea nitrogen (BUN) levels in the blood samples from rats with I/R-induced ARI. On the whole, the findings presented herein demonstrate that miR-106b-5p antagonist attenuates ARI by promoting the proliferation, and suppressing the apoptosis and autophagy of renal cells via upregulating TcF4.

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“…Three miRNAs are interesting-miR-1, miR-155 and miR-204. These miRNAs are connected with proliferation, apoptosis, and cardiac injury [25] as well as transforming growth factor-β1 (TGF-β1) and glial cell line-derived neurotrophic factor (GDNF) regulation during glaucoma, asthma and obesity [26][27][28][29]. However, what is even more interesting is that it has been also shown that these miRNAs regulate brain-derived neurotrophic factor (BDNF) [30][31][32].…”

Section: Discussionmentioning

confidence: 99%

“…The level of this miRNA was lower in the serum of control groups of NET-KO and SWR/J, and it decreased in WT mice upon RS, while it did not change in other two genotypes. The miR-1 has been associated with cardiac dysfunction, immunology (allergy), skeletal muscle changes (amyotrophic lateral sclerosis), but also as a regulator of glucose metabolism in the liver [25,[43][44][45]. It was also detected during stress studies, such as temperature changes, exercise (longer running), and stress connected with elevated platforms [38,[46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

Solich

Kuśmider

Faron-Górecka

et al. 2020

Cells

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In the present study, we used three strains of mice with various susceptibility to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype, as well as two strains of mice displaying two different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and SWR/J. The procedure of restraint stress (RS, 4 h) was applied, and the following behavioral experiments (the forced swim test and sucrose preference test) indicated that NET-KO and SWR/J mice were less sensitive to RS than WT mice. Then, we aimed to find the miRNAs which changed in similar ways in the serum of NET-KO and SWR/J mice subjected to RS, being at the same time different from the miRNAs found in the serum of WT mice. Using Custom TaqMan Array MicroRNA Cards, with primers for majority of miRNAs expressed in the serum (based on a preliminary experiment using the TaqMan Array Rodent MicroRNA A + B Cards Set v3.0, Thermo Fisher Scientific, Waltham, MA, USA) allowed the identification of 21 such miRNAs. Our further analysis focused on miR-1 and miR-155 and their targets-these two miRNAs are involved in the regulation of BDNF expression and can be regarded as biomarkers of stress-resilience.Cells 2020, 9, 917 2 of 17 are regarded as endogenous "hubs" (as Issler and Chen have put it) for the fine tuning of target gene expression or an "expression switch", and can provide deeper insight into complex biological processes underlying stress response.In the present study, we used three strains of mice differentially reacting to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype [7-9], as well as two other strains of mice displaying different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and swiss SWR/J, described extensively by Szklarczyk and co-workers [10]. The different reaction to stress of these strains of mice has been confirmed by measuring corticosterone level. The NET-KO mice display a slower increase in corticosterone level after stress compared with WT animals, while corticosterone level was not changed at 2 h after restraint stress in the blood of SWR/J mice [8,10]. We applied the procedure of restraint stress (RS), which has been shown to induce an uncontrollable aversive situation that produces both physical and psychological consequences leading to neuronal and behavioral alterations [11]. The aim of following molecular studies was to find biomarkers for different behavioral responses to RS among miRNAs expressed in the serum of three genotypes under study. This goal was achieved, as we were able to identify a group of miRNAs differentiating the stress response of NET-KO and SWR/J mice from WT animals. The most interesting were the alterations in the miR-1 and miR-155 levels, which are involved in regulation of BDNF expression, which in turn affects important biochemical processes. Materials and Methods AnimalsH...

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MicroRNA‐1 facilitates hypoxia‐induced injury by targeting NOTCH3

Cited by 17 publications

References 24 publications

miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact proteotoxicity and muscle function during aging

miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact proteotoxicity and muscle function during aging

Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

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