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KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells (mRNA microarray)

ABSTRACT: KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells (mRNA microarray)

PROVIDER: PRJNA892964 | ENA |

REPOSITORIES: ENA

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KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells

Project description:Vascular smooth muscle cells (VSMCs) within atherosclerotic lesions undergo a phenotypic switching in a KLF4-dependent manner. Glycolysis plays important roles in transdifferentiation of somatic cells, however, it is unclear whether and how KLF4 mediates the link between glycolytic switch and VSMCs phenotypic transitions. Here, we show that KLF4 upregulation accompanies VSMCs phenotypic switching in atherosclerotic lesions. KLF4 enhances the metabolic switch to glycolysis through increasing PFKFB3 expression. Inhibiting glycolysis suppresses KLF4-induced VSMCs phenotypic switching, demonstrating that glycolytic shift is required for VSMCs phenotypic switching. Mechanistically, KLF4 upregulates expression of circCTDP1 and eEF1A2, both of which cooperatively promote PFKFB3 expression. TMAO induces glycolytic shift and VSMCs phenotypic switching by upregulating KLF4. Our study indicates that KLF4 mediates the link between glycolytic switch and VSMCs phenotypic transitions, suggesting that a previously unrecognized KLF4-eEF1A2/circCTDP1-PFKFB3 axis plays crucial roles in VSMCs phenotypic switching.

2022-11-09 | PXD038057 |

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells (mRNA microarray)

2022-12-14 | GSE216303 | GEO

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells (circRNA microarray)

2022-12-14 | GSE216305 | GEO

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells

Project description:KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells

| PRJNA892956 | ENA

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells (circRNA microarray)

Project description:KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells (circRNA microarray)

| PRJNA892965 | ENA

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells.

| S-EPMC9722670 | biostudies-literature

KLF4-PFKFB3-driven glycolysis is essential for phenotypic switching of vascular smooth muscle cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-14 | GSE216306 | GEO

PFKFB3 inhibits fructose metabolism in pulmonary microvascular endothelial cells

Project description:We hypothesized that PFKFB3 inhibits fructose metabolism in pulmonary microvascular endothelial cells (PMVECs) and found that PFKFB3 knockout cells survive better than wild type cells in fructose-rich media, more so under hypoxia. Our findings indicate that PFKFB3 is a molecular switch that controls glucose versus fructose utilization in glycolysis and help to better understand lung endothelial cell metabolism during respiratory failure.

2023-08-01 | GSE230660 | GEO

Gene expression data of PFKFB3 KD in SMMC7721 cell line

Project description:Overexpression of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a key molecule of glucose metabolism in cytoplasm, was found in various tumors. Emerging evidence suggested that PFKFB3 also located in nucleus and shown regulatory functions other than glycolysis. In this study, we found that PFKFB3 expression is associated with hepatocellular carcinoma (HCC) growth and mainly located in the nucleus of tumor cells. PFKFB3 overexpression was associated with large tumor size, and poor survival of patients with HCC. Knockdown of PFKFB3 inhibited HCC growth, not only by reducing glucose consuming but also damaging DNA repair function leading to G2/M phase arrest and apoptosis. Therefore, we performed a cDNA microarray in PFKFB3 knockdown SMMC7721 cells.

2018-03-01 | GSE106603 | GEO

Tanshinone II A attenuates vascular remodeling through klf4 mediated smooth muscle cell phenotypic switching.

Project description:The aim of this study is to investigate the therapeutic role of Tanshinone II A, a key integrant from salvia miltiorrhiza, against pathological vascular remodeling. Completed ligation of mouse left common carotid arteries animal model and rat smooth muscle cells used to investigate the role of Tanshinone II A in regulating pathological vascular remodeling through hematoxylin and eosin staining, immunohistochemistry staining, immunofluorescence staining, adenovirus infection, real time PCR and western blotting. Our data demonstrated that Tanshinone II A treatment suppresses vascular injury-induced neointima formation. In vitro studies on rat smooth muscle cell indicated that Tanshinone II A treatment attenuates PDGF-BB induced cell growth, and promotes smooth muscle cell differentiated marker genes expression that induced by rapamycin treatment. Tanshinone II A treatment significant inhibits rat smooth muscle cell proliferation and migration. Tanshinone II A promotes KLF4 expression during smooth muscle phenotypic switching. Overexpression of KLF4 exacerbates Tanshinone II A mediated smooth muscle cell growth inhibition. Tanshinone II A plays a pivotal role in regulating pathological vascular remodeling through KLF4 mediated smooth muscle cell phenotypic switching. This study demonstrated that Tanshinone II A is a potential therapeutic agent for vascular diseases.

| S-EPMC7431534 | biostudies-literature

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