Berberine promotes ischemia-induced angiogenesis in mice heart via upregulation of microRNA-29b

Zhu, Mo‐Li; Yin, Yulong; Song, Ping; Hai-ya, YU; G, Wan; Xu, Jian; Li, Peng

doi:10.1080/10641963.2017.1313853

Cited by 40 publications

(29 citation statements)

References 40 publications

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“…In another example, exosomes derived from miR-126-modified MSCs facilitated the angiogenesis and migration of human umbilical venous endothelial cells after spinal cord injury [53]. Besides, upregulation of miR-29b plays a promotive role in ischemiainduced angiogenesis [54], indicating that miR-29b-3p is a promising factor in the treatment of hypoxic-ischemic brain injury. In this study, we revealed that declining cerebral levels of miR-29b-3p in MCAO rat brain was related to decreased angiogenesis, as indicated by the deregulation of VEGFA, VEGFR2 and CD31.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

Hou¹,

Li²,

Zhao³

et al. 2020

J Neuroinflammation

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Background: Mesenchymal stem cells (MSCs) are suspected to exert neuroprotective effects in brain injury, in part through the secretion of extracellular vesicles like exosomes containing bioactive compounds. We now investigate the mechanism by which bone marrow MSCs (BMSCs)-derived exosomes harboring the small non-coding RNA miR-29b-3p protect against hypoxic-ischemic brain injury in rats. Methods:We established a rat model of middle cerebral artery occlusion (MCAO) and primary cortical neuron or brain microvascular endothelial cell (BMEC) models of oxygen and glucose deprivation (OGD). Exosomes were isolated from the culture medium of BMSCs. We treated the MCAO rats with BMSC-derived exosomes in vivo, and likewise the OGD-treated neurons and BMECs in vitro. We then measured apoptosis-and angiogenesis-related features using TUNEL and CD31 immunohistochemical staining and in vitro Matrigel angiogenesis assays. Results: The dual luciferase reporter gene assay showed that miR-29b-3p targeted the protein phosphatase and tensin homolog (PTEN). miR-29b-3p was downregulated and PTEN was upregulated in the brain of MCAO rats and in OGD-treated cultured neurons. MCAO rats and OGD-treated neurons showed promoted apoptosis and decreased angiogenesis, but overexpression of miR-29b-3p or silencing of PTEN could reverse these alterations. Furthermore, miR-29b-3p could negatively regulate PTEN and activate the Akt signaling pathway. BMSCs-derived exosomes also exerted protective effects against apoptosis of OGD neurons and cell apoptosis in the brain samples from MCAO rats, where we also observed promotion of angiogenesis.Conclusion: BMSC-derived exosomal miR-29b-3p ameliorates ischemic brain injury by promoting angiogenesis and suppressing neuronal apoptosis, a finding which may be of great significance in the treatment of hypoxic-ischemic brain injury.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

Hou¹,

Li²,

Zhao³

et al. 2020

J Neuroinflammation

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“…Angiogenesis is critical for re‐establishing the blood supply to the surviving myocardium after MI and, consequently, to the recovery of cardiac function . To test whether this model is suitable for studying angiogenesis, we detected the angiogenesis by analysis of CD31, which is a biomarker for endothelial cells .…”

Section: Resultsmentioning

confidence: 99%

“…Angiogenesis is critical for re-establishing the blood supply to the surviving myocardium after MI and, consequently, to the recovery of cardiac function. 25 To test whether this model is suitable for studying angiogenesis, we detected the angiogenesis by analysis of CD31, which is a biomarker for endothelial cells. 26 As shown in Figure 6A, ischaemia dramatically induced angiogenesis in mice with MI caused by both traditional method and new method, suggesting this new method is suitable for studying in ischaemia-induced angiogenesis.…”

Section: New Methods Of Mim Surgery Induces Angiogenesismentioning

confidence: 99%

A minimally invasive approach to induce myocardial infarction in mice without thoracotomy

Sun

Wang

Pan

et al. 2018

J Cellular Molecular Medi

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Acute myocardial infarction (MI) is a leading cause of morbidity and mortality in the world. Traditional method to induce MI by left coronary artery (LCA) ligation is typically performed by an invasive approach that requires ventilation and thoracotomy, causing serious injuries in animals undergoing this surgery. We attempted to develop a minimally invasive method (MIM) to induce MI in mice. Under the guide of ultrasound, LCA ligation was performed in mice without ventilation and chest‐opening. Compared to sham mice, MIM induced MI in mice as determined by triphenyltetrazolium chloride staining and Masson staining. Mice with MIM surgery revealed the reductions of LVEF, LVFS, E/A and ascending aorta (AAO) blood flow, and the elevations of S‐T segment and serum cTn‐I levels at 24 post‐operative hours. The effects of MI induced by MIM were comparable to the effects of MI produced by traditional method in mice. Importantly, MIM increased the survival rates and caused less inflammation after the surgery of LCA ligation, compared to the surgery of traditional method. Further, MIM induced angiogenesis and apoptosis in ischaemic hearts from mice at postoperative 28 days as similarly as traditional method did. Finally, the MIM model was able to develop into the myocardial ischaemia/reperfusion model by using a balloon catheter with minor modifications. The MI model is able to be efficiently induced by a minimally invasive approach in mice without ventilation and chest‐opening. This new model is potentially to be used in studying ischaemia‐related heart diseases.

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“…Furthermore, the results also demonstrated that the DEGs were correlated with blood vessel morphogenesis and heart development. Previous studies have revealed that angiogenesis plays an essential role in the impaired neovascularization in diabetes (13,14). In addition, effective suppression of the damage of vascular endothelial cells or facilitation of angiogenesis may contribute to the effective treatment of diabetic vascular diseases (15,16).…”

Section: Discussionmentioning

confidence: 99%

Identification and Verification of Candidate Genes Regulating Human Umbilical Vein Endothelial Cells Behavior Under Hyperglycemia

Ma¹,

Zhou²,

Xie³

et al. 2020

Preprint

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Background: Diabetes is a metabolic disease that has been widely demonstrated to be correlated with many microvascular and macrovascular diseases that seriously damage the patient’s life quality. This study intended to investigate the underlying molecular mechanisms of endothelial dysfunction under hyperglycemia. Methods: The gene expression profile of GSE49524 was downloaded and differentially expressed genes (DEGs) in hyperglycemia human umbilical cord endothelial cells (HUVECs) samples compared with normoglycemia HUVECs samples were identified by R software. Afterward, we analyzed the data by applying a combination of the bioinformatics method and used the microRNAs (miRNAs) databases to predict microRNAs that target key genes. The expression of the top 10 differentially expressed genes was validated through quantitative real-time PCR (qRT-PCR). Results: A total of 65 genes were distinguished as DEGs. The dominant GO (gene ontology) terms and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways which were significantly overrepresented in the hyperglycemia HUVECs were identified. The results of the protein-protein interaction networks demonstrated that fibronectin 1 (FN1) is of the highest degree. In addition, several predicted miRNAs that target FN1 were obtained too. The further verification of the top 10 DEGs through qRT-PCR illustrated that nine of the up-regulated DEGs were up-regulated significantly in the hyperglycemia group when compared to the control group. Conclusions:This exploratory study may help to prompt an understanding of the underlying molecular mechanisms of the effect of hyperglycemia on the behavior of HUVECs and contribute to the production of effective therapeutic interventions.

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Berberine promotes ischemia-induced angiogenesis in mice heart via upregulation of microRNA-29b

Abstract: Berberine via upregulation of miR-29b promotes ischemia-induced angiogenesis and improves heart functions.

Cited by 40 publications

References 40 publications

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

A minimally invasive approach to induce myocardial infarction in mice without thoracotomy

Identification and Verification of Candidate Genes Regulating Human Umbilical Vein Endothelial Cells Behavior Under Hyperglycemia

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