Osteopontin expression and its possible functions in the aortic disorders and coronary artery disease

Yuan, Shi‐Min; Wang, Jun; Huang, Hairong; Hua, Jing

doi:10.1590/s0102-76382011000200006

Cited by 16 publications

(10 citation statements)

References 27 publications

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“…We used the protocol provided by the manufacturer of the Reverse Transcriptase IMPROM-II™ Kit (Promega ® , Madison, Wisconsin, USA). From the cDNAs obtained, we amplified the target fragment using PCR [19,20]. The primers used in this technique were ET-3 (Endothelin 3), ETr-A (receptor type A) and ETr-B (Receptor Type B) ( Table 2).…”

Section: Molecular Analysismentioning

confidence: 99%

Gene expression of endothelin receptors in replaced rheumatic mitral stenotic valves

Leão

Souto

Costa

et al. 2012

Revista Brasileira De Cirurgia Cardiovascular

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Objectives: Rheumatic fever is a highly prevalent disease in Brazil, and it poses a major public health problem. It is the leading cause of acquired heart disease in childhood and adolescence. The aim of this study was to evaluate the gene expression of ET-3 and its receptors, in replaced rheumatic mitral valves.Methods: We studied the gene expression of endothelin-3 (ET-3) and its receptors, endothelin receptor A and endothelin receptor B (ETr-A and ETr-B), in the rheumatic mitral valves of 17 patients who underwent valve replacement surgery. The samples also underwent a histological analysis.Results: Our data showed that almost all patients, regardless of individual characteristics such as gender or age, expressed the endothelin receptor genes, but did not express the genes for ET-3. In quantitative analysis, the ETr-A/GAPDH mean ratio was 33.04 ± 18.09%; while the ETr-B/GAPDH mean ratio was 114.58 ± 42.30%. Regarding histopathological individual features, the frequency of fibrosis is 100%, 88.23% of mononuclear infiltrate, 52.94% of neovascularization, 58.82% of calcification and absence of ossification.Conclusion: The presence of receptors ETr-A and ETr-B in rheumatic mitral valves suggests its interaction with the system of circulating endothelins, particularly ETr-B (known for acting in the removal of excess endothelin) detected in a greater proportion, which could explain the lack of expression of endothelin in rheumatic mitral valve, process to be elucidated.Descriptors: Rheumatic fever. Mitral valve stenosis. Endothelins.

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Section: Molecular Analysismentioning

confidence: 99%

Gene expression of endothelin receptors in replaced rheumatic mitral stenotic valves

Leão

Souto

Costa

et al. 2012

Revista Brasileira De Cirurgia Cardiovascular

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“…OPN in human atherosclerotic plaques is reportedly closely associated with the severity of atherosclerosis 28–31 . More importantly, OPN is recognized as a critical angiogenic factor in the regulation of proliferation and migration of vascular endothelial cells associated with neointima formation 32, 33 .…”

Section: Resultsmentioning

confidence: 99%

“…VEGF is also known to play a central role in inflammation and wound healing by controlling both angiogenesis and vascular permeability 54 , and OPN is recognized as a significant participant in the atherosclerotic inflammatory milieu 28 . Many studies have shown that OPN mRNA expression in human atherosclerotic plaques was closely associated with the severity of atherosclerosis 28–31 . Beyond its role in the regulation of intraplaque angiogenesis, previous works also showed that OPN plays an important role in inflammation regulation, such as the migration of macrophages 55 .…”

Section: Discussionmentioning

confidence: 99%

Hairy/enhancer of Split Homologue-1 Suppresses Vascular Endothelial Growth Factor-induced Angiogenesis via Downregulation of Osteopontin Expression

Yao

et al. 2017

Sci Rep

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Atherosclerosis is the principal contributing factor to the pathology of cardiovascular disease 1 . The clinical complications of atherosclerosis are mainly caused by thrombus formation, which result from rupture of a vulnerable atherosclerotic plaque 2 . Importantly, angiogenesis is a key feature of atherosclerosis 3 . The formation of microvessels (angiogenesis) in an atherosclerotic plaque contributes to the development of vulnerable plaques, thereby increasing the risk of rupture 4 . Although the regulation of angiogenesis in atherosclerotic plaques is still under investigation, suppression of angiogenesis is considered a promising therapeutic strategy for the treatment of atherosclerosis.Hairy/enhancer of split homologue-1 (Hes-1) is a transcriptional repressor of members of the basic helix-loop-helix family of transcription factors. It has been shown that Hes-1 plays a critical role in the regulation of various physiological processes, including cellular differentiation, cycling, apoptosis, and self-renewal 5,6 . Hes-1-regulated transcription is essential to cardiovascular development and its function has been linked to smooth muscle differentiation, angiogenic processes, arterial-venous cell fate determination, and vascular morphogenesis 7 . In addition, increasing evidence has shown that Hes-1 is involved in the regulation of endothelial cell (EC) proliferation, differentiation, and apoptosis, which are fundamental processes necessary for angiogenesis 8 . Curry et al. 9

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“…In early vascular development, synthetic phenotypic SMCs are required to migrate around lumens, proliferate and secrete extracellular matrix to promote intercellular connections. Osteopontin (OPN), a multifunctional protein which highly expressed in synthetic SMCs, is often used as a marker for synthetic SMCs [52]. α-SMA , a contractile-associated protein [53], was also tested in this study.…”

Section: Discussionmentioning

confidence: 99%

AKT/FOXO1 axis links cross-talking of endothelial cell and pericyte in TIE2-mutated venous malformations

Jiang

Si²,

Huang

et al. 2020

Preprint

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Background: Venous malformations (VMs), most of which associated with activating mutations in the endothelial cells (ECs) tyrosine kinase receptor TIE2, are characterized by dilated and immature veins with scarce smooth muscle cells (SMCs) coverage. However, the underlying mechanism of interaction between ECs and SMCs responsible for VMs has not been fully understood.Methods: Here, we screened 5 patients with TIE2-L914F mutation who were diagnosed with VMs by SNP sequencing, and we compared the expression of platelet-derived growth factor beta (PDGFB) and α-SMA in TIE2 mutant veins and normal veins by immunohistochemistry. In vitro, we generated TIE2-L914F-expressing human umbilical vein endothelial cells (HUVECs) and performed BrdU, CCK-8, transwell and tube formation experiments on none-transfected and transfected ECs. Then we investigated the effects of rapamycin (RAPA) on cellular characteristics. Next we established a co-culture system and investigated the role of AKT/FOXO1/PDGFB in regulating cross-talking of mutant ECs and SMCs.Results: VMs with TIE2-L914F mutation showed lower expression of PDGFB and α-SMA than normal veins. TIE2 mutant ECs revealed enhanced cell viability and motility, and decreased tube formation, whereas these phenotypes could be reversed by rapamycin. Mechanically, RAPA ameliorated the physiological function of mutant ECs by inhibiting AKT-mTOR pathway, but also facilitated the nuclear location of FOXO1 and the expression of PDGFB in mutant ECs, and then improved paracrine interactions between ECs and SMCs. Moreover, TIE2 mutant ECs strongly accelerated the transition of SMCs from contractile phenotype to synthetic phenotype, whereas RAPA could prevent the phenotype transition of SMCs.Conclusions: Our data demonstrate a previously unknown mechanistic linkage of AKT-mTOR/FOXO1 pathway between mutant ECs and SMCs in modulating venous dysmorphogenesis, and AKT/FOXO1 axis might be a potential therapeutic target for the recovery of TIE2-mutation causing VMs.

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Osteopontin expression and its possible functions in the aortic disorders and coronary artery disease

Cited by 16 publications

References 27 publications

Gene expression of endothelin receptors in replaced rheumatic mitral stenotic valves

Gene expression of endothelin receptors in replaced rheumatic mitral stenotic valves

Hairy/enhancer of Split Homologue-1 Suppresses Vascular Endothelial Growth Factor-induced Angiogenesis via Downregulation of Osteopontin Expression

AKT/FOXO1 axis links cross-talking of endothelial cell and pericyte in TIE2-mutated venous malformations

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