Intracellular acidosis via activation of Akt-Girdin signaling promotes post ischemic angiogenesis during hyperglycemia

Zhang, Hongming; Liu, Moyan; Lu, Jianrong; Zhu, Mo‐Li; Jin, Qun; Song, Ping; Li, Peng; Xu, Jian; Han, Yaling; Wang, Shuangxi; Li, Xiaoyan

doi:10.1016/j.ijcard.2018.08.028

Cited by 20 publications

(19 citation statements)

References 33 publications

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“…1 In response to MI, myocardial fibrosis is caused by aberrantly activated cardiac fibroblasts, excessive accumulation of collagen fibres in the extracellular matrix of the heart muscle, increased collagen concentration or imbalanced collagen composition. [2][3][4] The extracellular matrix is mainly composed of type I collagen and type III collagen, accounting for more than 90% of the total amount of myocardial interstitial collagen. 5 Maintenance of proper ratio of myocardial interstitial collagen is important for the integrity of cardiac function.…”

Section: Introductionmentioning

confidence: 99%

Up‐regulation of paired‐related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a

Bai

Tang

Shan

et al. 2019

J Cellular Molecular Medi

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Cardiac fibrosis is a key factor to determine the prognosis in patient with myocardial infarction (MI). The aim of this study is to investigate whether the transcriptional factor paired-related homeobox 2 (Prrx2) regulates Wnt5a gene expression and the role in myocardial fibrosis following MI. The MI surgery was performed by ligation of left anterior descending coronary artery. Cardiac remodelling was assessed by measuring interstitial fibrosis performed with Masson staining. Cell differentiation was examined by analysis the expression of alpha-smooth muscle actin (α-SMA). Both Prrx2 and Wnt5a gene expressions were up-regulated in mice following MI, accompanied with increased mRNA and protein levels of α-SMA, collagen I and collagen III, compared to mice with sham surgery. Adenovirus-mediated gene knock down of Prrx2 increased survival rate, alleviated cardiac fibrosis, decreased infarction sizes and improved cardiac functions in mice with MI. Importantly, inhibition of Prrx2 suppressed ischaemia-induced Wnt5a gene expression and Wnt5a signalling. In cultured cardiac fibroblasts, TGF-β increased gene expressions of Prrx2 and Wnt5a, and induced cell differentiations, which were abolished by gene silence of either Prrx2 or Wnt5a. S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Bai W-W, Tang Z-Y, Shan T-C, et al. Up-regulation of paired-related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a.

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Section: Introductionmentioning

confidence: 99%

Up‐regulation of paired‐related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a

Bai

Tang

Shan

et al. 2019

J Cellular Molecular Medi

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“…Hyperglycaemia may cause an imbalance between stimulators and inhibitors of angiogenesis, which further leads to the formation of new blood vessels [18]. These immature blood vessels are more prone to leakage and ultimately result in serious complications [19].…”

Section: Discussionmentioning

confidence: 99%

“…DR is one of the most complex, heterogeneous, and multifactorial clinical disorders. Angiogenesis is one of the critical events in the progression of DR. Hyperglycaemia may cause an imbalance between stimulators and inhibitors of angiogenesis, which further leads to the formation of new blood vessels [ 18 ]. These immature blood vessels are more prone to leakage and ultimately result in serious complications [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of angiogenesis-related genes and pathways in early diabetic retinopathy

Lhamo

Zou

et al. 2020

BMC Med Genomics

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Background Angiogenesis is an important parameter in the development of diabetic retinopathy (DR), and it is indicative of an early stage evolving into a late phase. Therefore, examining the role of angiogenic factors in early DR is crucial to understanding the mechanism of neovascularization. Methods The present study identified hub genes and pathways associated with angiogenesis in early DR using bioinformatics analysis. Genes from published literature and Gene Expression Omnibus (GEO) were collected and analysed. Results We collected 73 genes from 70 published studies in PubMed, which were referred to as DR-related gene set 1 (DRgset1). The gene expression profile of GSE12610 was downloaded, and 578 differentially expressed genes (DEGs) between diabetic and normal samples were identified. DEGs and DRgset1 were further combined to create DR-related gene set 2 (DRgset2). After an enrichment analysis, we identified 12 GO terms and 2 pathways associated with neovascularization in DRgset1, and 8 GO terms and 2 pathways in DRgset2. We found 39 new genes associated with angiogenesis and verified 8 candidate angiogenesis-related genes in DR cells using real-time PCR: PIK3CB, ALDH3A1, ITGA7, FGF23, THBS1, COL1A1, MAPK13, and AIF1. We identified 10 hub genes associated with neovascularization by constructing a protein-protein interaction (PPI) network: TNF, VEGFA, PIK3CB, TGFB1, EDN1, MMP9, TLR4, PDGFB, MMP2, and THBS1. Conclusions The present study analysed angiogenesis-related genes and pathways in early DR in a comprehensive and systematic manner. PIK3CB, ALDH3A1, ITGA7, FGF23, THBS1, COL1A1, MAPK13, and AIF1 may be the candidate genes to further explore the mechanisms of angiogenesis in early DR. TNF, PIK3CB, TGFB1, EDN1, MMP9, TLR4, PDGFB, MMP2, and THBS1 may be new targets for early neovascularization therapy in the future.

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“…Because the growth of collateral vessels offers an alternative route for irrigation when a coronary artery is blocked, angiogenesis may decrease myocardial damage and improve prognosis [149]. HUVEC models have been used to study the molecular and signaling pathways involved in this process [150][151][152][153][154]. Pro-angiogenic factors are known as potential therapeutic agents to treat ischemic heart disease and protect EC in the arteries [108,[150][151][152][153][154][155][156].…”

Section: Angiogenesismentioning

confidence: 99%

Use of Human Umbilical Vein Endothelial Cells (HUVEC) as a Model to Study Cardiovascular Disease: A Review

et al. 2020

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Cardiovascular disease (CVD) is the leading cause of death worldwide, and extensive research has been performed to understand this disease better, using various experimental models. The endothelium plays a crucial role in the development of CVD, since it is an interface between bloodstream components, such as monocytes and platelets, and other arterial wall components. Human umbilical vein endothelial cell (HUVEC) isolation from umbilical cord was first described in 1973. To date, this model is still widely used because of the high HUVEC isolation success rate, and because HUVEC are an excellent model to study a broad array of diseases, including cardiovascular and metabolic diseases. We here review the history of HUVEC isolation, the HUVEC model over time, HUVEC culture characteristics and conditions, advantages and disadvantages of this model and finally, its applications in the area of cardiovascular diseases.

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Intracellular acidosis via activation of Akt-Girdin signaling promotes post ischemic angiogenesis during hyperglycemia

Cited by 20 publications

References 33 publications

Up‐regulation of paired‐related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a

Up‐regulation of paired‐related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a

Comprehensive analysis of angiogenesis-related genes and pathways in early diabetic retinopathy

Use of Human Umbilical Vein Endothelial Cells (HUVEC) as a Model to Study Cardiovascular Disease: A Review

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