miR‐217 alleviates high‐glucose‐induced vascular smooth muscle cell dysfunction via regulating ROCK1

Zhou, Wan; Ye, Shandong; Wang, Wei

doi:10.1002/jbt.22668

Cited by 11 publications

(6 citation statements)

References 31 publications

(29 reference statements)

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“…During period of physical inactivity, the increased skeletal muscle miR-148b expression triggered the downregulation of ROCK1 expression and insulin resistance in humans and mice ( 82 ). In contrast to the detrimental effects of miRNA expression fluctuations in the metabolic tissues, up-regulation of miR-217 was found to be beneficial in both VSMCs treated by high glucose and in aorta VSMCs of diabetic rats, miR-217 up-regulation suppressed ROCK1expression in these cases and inhibited excessive proliferation and migration of VSMCs ( 90 ).…”

Section: Growing Research Areas In Rhoa/rock Signaling With Metabolic...mentioning

confidence: 99%

Insight Into Rho Kinase Isoforms in Obesity and Energy Homeostasis

Wei

Shi

2022

Front. Endocrinol.

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Obesity and associated complications increasingly jeopardize global health and contribute to the rapidly rising prevalence of type 2 diabetes mellitus and obesity-related diseases. Developing novel methods for the prevention and treatment of excess body adipose tissue expansion can make a significant contribution to public health. Rho kinase is a Rho-associated coiled-coil-containing protein kinase (Rho kinase or ROCK). The ROCK family including ROCK1 and ROCK2 has recently emerged as a potential therapeutic target for the treatment of metabolic disorders. Up-regulated ROCK activity has been involved in the pathogenesis of all aspects of metabolic syndrome including obesity, insulin resistance, dyslipidemia and hypertension. The RhoA/ROCK-mediated actin cytoskeleton dynamics have been implicated in both white and beige adipogenesis. Studies using ROCK pan-inhibitors in animal models of obesity, diabetes, and associated complications have demonstrated beneficial outcomes. Studies via genetically modified animal models further established isoform-specific roles of ROCK in the pathogenesis of metabolic disorders including obesity. However, most reported studies have been focused on ROCK1 activity during the past decade. Due to the progress in developing ROCK2-selective inhibitors in recent years, a growing body of evidence indicates more attention should be devoted towards understanding ROCK2 isoform function in metabolism. Hence, studying individual ROCK isoforms to reveal their specific roles and principal mechanisms in white and beige adipogenesis, insulin sensitivity, energy balancing regulation, and obesity development will facilitate significant breakthroughs for systemic treatment with isoform-selective inhibitors. In this review, we give an overview of ROCK functions in the pathogenesis of obesity and insulin resistance with a particular focus on the current understanding of ROCK isoform signaling in white and beige adipogenesis, obesity and thermogenesis in adipose tissue and other major metabolic organs involved in energy homeostasis regulation.

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Section: Growing Research Areas In Rhoa/rock Signaling With Metabolic...mentioning

confidence: 99%

Insight Into Rho Kinase Isoforms in Obesity and Energy Homeostasis

Wei

Shi

2022

Front. Endocrinol.

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“…The precise molecular and biochemical function of the majority of circRNAs and miRNAs remains unclear, but their roles in the functional regulation of VSMCs have been widely reported [2,12,13]. Over these years, cir-cRNA LRP6, circRNA-0077930, and circWDR77, as well as miR-217, miR-381-3p, and miR-132 have been found to get involved in the HG-induced proliferation and migration of VSMCs [2,[14][15][16][17][18]. However, it remains unclear whether hsa_circRNA_0008028 and miR-182-5p perform biological functions in diabetes-correlated vasculopathy.…”

Section: Introductionmentioning

confidence: 99%

Hsa_circRNA_0008028 Deficiency Ameliorates High Glucose-Induced Proliferation, Calcification, and Autophagy of Vascular Smooth Muscle Cells via miR-182-5p/TRIB3 Axis

Shi

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. It is well-known that dysfunctions of vascular smooth muscle cells (VSMCs) act an essential part in vascular complications of diabetes. Studies have shown that circular RNAs (circRNAs) and microRNAs (miRNAs) play a crucial role in regulating cell functions. However, their influence on the proliferation, calcification, and autophagy of VSMCs remains to be further explored. Therefore, this study elucidates the role and mechanism of hsa_circRNA_0008028 in high glucose- (HG-, 30 mM) treated VSMCs in vitro. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) was chosen to detect the levels of hsa_circRNA_0008028, miR-182-5p, and tribble 3 (TRIB3). Then, dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to predict and verify the binding relationship between miR-182-5p and hsa_circRNA_0008028 or TRIB3. Cell counting kit-8 assay, 5-ethynyl-2 ′ -deoxyuridine (EdU) staining, corresponding commercial kits, and western blotting were used to measure indexes reflecting cell viability, proliferation, calcification, and autophagy of VSMCs, respectively. Results. In HG-induced VSMCs, hsa_circRNA_0008028 and TRIB3 were highly expressed, whereas miR-182-5p decreased. Meanwhile, cell proliferation, calcification, and autophagy could be repressed by silencing of hsa_circRNA_0008028. However, these effects can be eliminated by miR-182-5p inhibition. Furthermore, it was demonstrated that hsa_circRNA_0008028 could promote the expression of TRIB3, a target of miR-182-5p, by directly sponging miR-182-5p. The expression of TRIB3 was suppressed by hsa_circRNA_0008028 knockout, which was rescued by miR-182-5p inhibition. Conclusion. This study reveals that hsa_circRNA_0008028 can act as a sponge of miR-182-5p and promote HG-induced proliferation, calcification, and autophagy of VSMCs partly by regulating TRIB3.

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“…16 MiR-217, located on chromosome 2P16.1, regulates biological processes in various human diseases, such as cancers, atherosclerosis, diabetes mellitus and nephropathy. [17][18][19] Moreover, miR-217 contributes to osteogenic differentiation as a promoter or a suppressor. For example, miR-217 promotes osteogenic differentiation of bone marrow-derived mesenchymal stem cells during steroid-associated osteonecrosis.…”

Section: Akt3 Is Verified As a Target Of Mir-217mentioning

confidence: 99%

lncRNA MALAT1 promotes osteogenic differentiation through the miR‐217/AKT3 axis: A possible strategy to alleviate osteoporosis

Song

Guo

Chen

et al. 2022

The Journal of Gene Medicine

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Background: Accumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are associated with the development of osteoporosis. The present study aimed to investigate the effect of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on osteogenic differentiation in osteoporosis.Methods: MALAT1 levels were detected by a real-time polymerase chain reaction (RT-qPCR). Moreover, the levels of osteogenic differentiation-related factors (Bmp4, Col1a1 and Spp1) were measured by a RT-qPCR and western blotting. Alkaline phosphatase (ALP) activity was detected using an ALP staining assay.Results: MALAT1 levels were downregulated in hindlimb unloading mice and simulated in microgravity (MG) treated MC3T3-E1 cells. Moreover, MG treatment induced the downregulation of the expression of ALP, BMP4, Col1a1 and Spp1, whereas overexpression of MALAT1 abolished the downregulation. MG also inhibited ALP activity, whereas MALAT1 reversed the effect. Furthermore, miR-217 was identified as a target of MALAT1, and AKT3 was verified as a target of miR-217.Overexpression of miR-217 rescued the promotion of osteogenic differentiation induced by MALAT1 in MG treated cells. Knockdown of AKT3 abolished the facilitation of osteogenic differentiation induced by downregulation of miR-217.Conclusions: MALAT1 promotes osteogenic differentiation through regulating miR-217/AKT3 axis, suggesting that MALAT1 is a potential target with respect to alleviating osteoporosis.

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miR‐217 alleviates high‐glucose‐induced vascular smooth muscle cell dysfunction via regulating ROCK1

Cited by 11 publications

References 31 publications

Insight Into Rho Kinase Isoforms in Obesity and Energy Homeostasis

Insight Into Rho Kinase Isoforms in Obesity and Energy Homeostasis

Hsa_circRNA_0008028 Deficiency Ameliorates High Glucose-Induced Proliferation, Calcification, and Autophagy of Vascular Smooth Muscle Cells via miR-182-5p/TRIB3 Axis

lncRNA MALAT1 promotes osteogenic differentiation through the miR‐217/AKT3 axis: A possible strategy to alleviate osteoporosis

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