&lt;p&gt;miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the &lt;em&gt;ANGPT2&lt;/em&gt; Gene and Involving the NFκB Signaling Pathway&lt;/p&gt;

Zhang, Wen; Tang, Xiaoning; Zhang, Jinjuan; He, Quan

doi:10.2147/dmso.s273451

Cited by 6 publications

(4 citation statements)

References 19 publications

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“…Moreover, as reported in previous studies, a continuous presence of inflammatory responses and oxidative stress increases apoptosis, which is similar to the findings of our current results 37 . While endothelial cells maintain vascular endothelial function by secreting a variety of cytokines, 38 hyperglycaemia induces death or apoptosis in these endothelial cells, directly leading to vascular endothelial dysfunction 39 . An accumulation of ROS also affects several intracellular pathways associated with vascular endothelial function, such as decreased eNOS expression or activity, resulting in poor endothelium‐dependent vasorelaxation and ED 40 .…”

Section: Discussionsupporting

confidence: 93%

“… 37 While endothelial cells maintain vascular endothelial function by secreting a variety of cytokines, 38 hyperglycaemia induces death or apoptosis in these endothelial cells, directly leading to vascular endothelial dysfunction. 39 An accumulation of ROS also affects several intracellular pathways associated with vascular endothelial function, such as decreased eNOS expression or activity, resulting in poor endothelium‐dependent vasorelaxation and ED. 40 Additional mechanisms may also represent significant components contributing to ED.…”

Section: Discussionmentioning

confidence: 99%

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N‐acetylcysteine improves diabetic associated erectile dysfunction in streptozotocin‐induced diabetic mice by inhibiting oxidative stress

Wang

Pan

et al. 2022

J Cellular Molecular Medi

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Oxidative stress appears to play a role in the pathogenesis of diabetes mellitus erectile dysfunction (DMED). This study aimed to investigate the effect of N‐acetylcysteine (NAC) on DMED in streptozotocin‐induced diabetic mice and to explore potential mechanisms. In the present study, we show that an erectile dysfunction is present in the streptozotocin‐induced mouse model of diabetes as indicated by decreases in intracavernous pressure responses to electro‐stimulation as well as from results of the apomorphine test of erectile function. After treatment of NAC, the intracavernous pressure was increased. In these DMED mice, oxidative stress and inflammatory responses were significantly reduced within the cavernous microenvironment, while activity of antioxidant enzymes in this cavernous tissue was enhanced after NAC treatment. These changes protected mitochondrial stress damage and a significant decreased in apoptosis within the cavernous tissue of DMED mice. This appears to involve activation of the nuclear factor erythroid 2‐like‐2 (Nrf2) signalling pathway, as well as suppression of the mitogen‐activated protein kinase (MAPK) p38/ NF‐κB pathway within cavernous tissue. In conclusion, NAC can improve erectile function through inhibiting oxidative stress via activating Nrf2 pathways and reducing apoptosis in streptozotocin‐induced diabetic mice. NAC might provide a promising therapeutic strategy for individuals with DMED.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

N‐acetylcysteine improves diabetic associated erectile dysfunction in streptozotocin‐induced diabetic mice by inhibiting oxidative stress

Wang

Pan

et al. 2022

J Cellular Molecular Medi

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“…Inflammation, oxidative stress, endoplasmic reticulum stress, and vascular dysfunction occur during diabetes 20 , and sustained glycotoxicity and lipotoxicity will promote islet cell damage and cell insensitivity to insulin, and jointly aggravate diabetic ischemia, hypoxia, and tissue damage 21 . The researchers used rat, mouse or human aortic endothelial cells (HAECs), and human umbilical vein endothelial cells (HUVECs) to establish a diabetes model to mimic the high sugar and high fat, inflammation, oxidative stress, and the state of metabolic disorders, in order to carry out diabetes‐related research 22 , 23 , 24 .…”

Section: Discussionmentioning

confidence: 99%

miR‐31 ameliorates type 2 diabetic vascular damage through up‐regulation of hypoxia‐inducible factor‐1α/vascular endothelial growth factor‐A

Fang

Wang

et al. 2023

J of Diabetes Invest

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AimsmicroRNA may be a new therapeutic direction for diabetes. As a typical tumor marker, miR‐31 is involved in a variety of metabolic diseases, but the specific role is still unclear. This study aimed to investigate the effect of miR‐31 on type 2 diabetes mellitus and its accompanying vascular injury, as well as on the effects of hypoxia‐inducible factor‐1α inhibitor (HIF1AN), hypoxia‐inducible factor (HIF)‐1α, and vascular endothelial growth factor (VEGF)‐A expression in vitro and in vivo.Materials and MethodsIn vitro, a model of high‐fat and high‐glucose‐induced human aortic endothelial cell (HAEC) injury was established to simulate diabetes mellitus (DM). Cell functions were compared between the control group, the DM damage group, and the group transfected with miR‐31 after DM damage. In vivo, overexpressing miR‐31 FVB mice and FVB mice were divided into the control and induced type 2 diabetes mellitus groups. Type 2 diabetes mellitus models were induced by a high‐fat diet combined with streptozotocin. The lipid metabolism levels, viscera, and vascular damage were compared between the control and type 2 diabetes mellitus groups.ResultsIn vitro, miR‐31 improved the proliferation ability of damaged cells by targeting HIF1AN and up‐regulating the expression of HIF‐1α and VEGF‐A. In vivo, miR‐31 ameliorated the development of type 2 diabetes mellitus, disturbance of glucose and lipid metabolism, and damage to some organs. Meanwhile, miR‐31 had a protective effect on vascular damage complicated by type 2 diabetes mellitus by increasing the levels of HIF‐1α and VEGF‐A.ConclusionOur experiments show that miR‐31 can delay the progression of type 2 diabetes mellitus and ameliorate diabetic vascular injury.

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“…Bta-miR-145 has been identified to be a major immune-related miRNA involved in immune response by NF-κB signaling pathway (Zhang et al. 2020 ), Li found that miR-145 was involved in the regulation of BMECs function by detecting transcriptome microRNAs in S. aureus induced BMECs (Li et al. 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs

Sun,

Zhao,

et al. 2023

Veterinary Quarterly

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Bovine mastitis is one of the most serious and costly disease affecting dairy cattle production. The present study explored the inflammatory response and autoprotective mechanism of a novel specific high expression BMNCR (bovine mastitis related long non-coding RNA) in S. aureus induced mastitis by miR-145/CBFB axis in dairy cows from the perspective of molecular genetics. In bovine mammary epithelial cells, we preformed loss of function experiments to detect changes in cytokine, proliferation and apoptosis by qRT-PCR, western blot, flow cytometry and EdU staining. The results demonstrated that BMNCR significantly increased cell apoptosis, and inhibited cell proliferation. However, the secretion of IL-1α, IL-2, IL-6, IL-8 and IL-12 were enhanced after knock-down BMNCR. Bioinformatics analysis demonstrated that BMNCR could target 8 miRNAs, in-depth analyses indicated that BMNCR acts as a molecular sponge for bta-miR-145 and CBFB was one of 23 target gene of bta-miR-145 . The results of the present study demonstrated that the role of BMNCR in S. aureus induced mastitis can be mediated by sponge bta-miR-145 activating CBFB expression. BMNCR could be a potential target for mastitis diagnosis and therapy, which may enrich the theoretical research of therapeutic intervention, and further increase milk yield and improve milk quality.

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<p>miR145 Regulates the Proliferation and Apoptosis of Rat Vascular Endothelial Cells under Hyperglycemia by Targeting the <em>ANGPT2</em> Gene and Involving the NFκB Signaling Pathway</p>

Cited by 6 publications

References 19 publications

N‐acetylcysteine improves diabetic associated erectile dysfunction in streptozotocin‐induced diabetic mice by inhibiting oxidative stress

N‐acetylcysteine improves diabetic associated erectile dysfunction in streptozotocin‐induced diabetic mice by inhibiting oxidative stress

miR‐31 ameliorates type 2 diabetic vascular damage through up‐regulation of hypoxia‐inducible factor‐1α/vascular endothelial growth factor‐A

Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs

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