Last update 01 Nov 2024

ETV2

Last update 01 Nov 2024

Basic Info

Synonyms

ER71, ETS translocation variant 2, ETS variant transcription factor 2

+ [3]

Introduction

Binds to DNA sequences containing the consensus pentanucleotide 5'-CGGA[AT]-3'.

Drugs associated with ETV2

Targeting ETV2 siRNA (Altamira Therapeutics)

Target

ETV2

Mechanism

ETV2 inhibitors

Active Org.

Altamira Therapeutics Ltd.

Originator Org.

Altamira Therapeutics Ltd.

Active Indication

Lung Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ETV2

100 Translational Medicine associated with ETV2

0 Patents (Medical) associated with ETV2

202

Literatures (Medical) associated with ETV2

14 Oct 2024·Cardiovascular Research

Forward programming of human induced pluripotent stem cells via the ETS variant transcription factor 2: rapid, reproducible, and cost-effective generation of highly enriched, functional endothelial cells

Article

Author: Triantafyllou, Christos ; Hesse, Michael ; Sharma, Kritika ; Rieck, Sarah ; Altringer, Carlotta ; Fleischmann, Bernd K ; Zhang, Yanhui ; Busskamp, Volker

AbstractAimsEndothelial cell (EC) dysfunction plays a key role in the initiation and progression of cardiovascular disease. However, studying these disorders in ECs from patients is challenging; hence, the use of human induced pluripotent stem cells (hiPSCs) and their in vitro differentiation into ECs represents a very promising approach. Still, the generation of hiPSC-derived ECs (hECs) remains demanding as a cocktail of growth factors and an intermediate purification step are required for hEC enrichment. Therefore, we probed the utility of a forward programming approach using transgenic hiPSC lines.Methods and resultsWe have used the transgenic hiPSC line PGP1 ETV2 isoform 2 to explore the in vitro differentiation of hECs via doxycycline-dependent induction of the ETS variant transcription factor 2 (ETV2) and compared these with a standard differentiation protocol for hECs using non-transgenic control hiPSCs. The transgenic hECs were highly enriched without an intermediate purification step and expressed—as non-transgenic hECs and human umbilical vein endothelial cells—characteristic EC markers. The viability and yield of transgenic hECs were strongly improved by applying EC growth medium during differentiation. This protocol was successfully applied in two more transgenic hiPSC lines yielding reproducible results with low line-to-line variability. Transgenic hECs displayed typical functional properties, such as tube formation and LDL uptake, and a more mature phenotype than non-transgenic hECs. Transgenic hiPSCs preferentially differentiated into the arterial lineage; this was further enhanced by adding a high concentration of vascular endothelial growth factor to the medium. We also demonstrate that complexing lentivirus with magnetic nanoparticles and application of a magnetic field enables efficient transduction of transgenic hECs.ConclusionWe have established a highly efficient, cost-effective, and reproducible differentiation protocol for the generation of functional hECs via forward programming. The transgenic hECs can be genetically modified and are a powerful tool for disease modelling, tissue engineering, and translational purposes.

01 Oct 2024·Pulmonary Circulation

PPARγ/ETV2 axis regulates endothelial‐to‐mesenchymal transition in pulmonary hypertension

Article

Author: Passineau, Michael J. ; Kim, Juyoung ; Lee, Raham ; Lee, Dong Hun ; Karmouty‐Quintana, Harry ; Park, Changwon ; Lam, Wilbur A. ; Benza, Raymond L. ; Kim, Minseong ; Jang, Andrew J. ; Sutliff, Roy L. ; Kang, Bum‐Yong ; Hart, C. Michael ; Ma, Jing ; Chang, Sarah S. ; Kopp, Benjamin T.

AbstractEndothelial‐to‐mesenchymal transition (EndoMT) plays an important role in pulmonary hypertension (PH) but the molecular mechanisms regulating EndoMT remain to be defined. We demonstrate that the axis of the transcription factors PPARγ (Peroxisome Proliferator‐Activated Receptor gamma) and ETV2 (ETS variant 2) play important roles in the pathogenesis of PH. Decreased levels of the expression of PPARγ and ETV2 along with reduced endothelial and increased EndoMT markers are consistently observed in lungs and pulmonary artery endothelial cells (PAECs) of idiopathic pulmonary arterial hypertension patients, in hypoxia‐exposed mouse lungs, human PAECs, and in induced‐EndoMT cells. Etv2+/− mice spontaneously developed PH and right ventricular hypertrophy (RVH), associated with increased EndoMT markers and decreased EC markers. Interestingly, chronic hypoxia exacerbated right ventricular systolic pressure and RVH in Etv2+/− mice. PPARγ transcriptionally activates the ETV2 promoter. Consistently, while mice overexpressing endothelial PPARγ increases the expression of ETV2 and endothelial markers with reduced EndoMT markers, endothelial PPARγ KO mice show decreased ETV2 expression and enhanced EndoMT markers. Inducible overexpression of ETV2 under induced‐EndoMT cell model reduces number of cells with mesenchymal morphology and decreases expression of mesenchymal markers with increased EC makers, compared to control. Therefore, our study suggests that PPARγ‐ETV2 signaling regulates PH pathogenesis through EndoMT.

01 Jul 2024·Bioactive Materials

ETV2 regulating PHD2-HIF-1α axis controls metabolism reprogramming promotes vascularized bone regeneration

Article

Author: Lu, Xiaoxuan ; Li, ChengLin ; Wang, YuanYin ; Du, HaoRan ; Xu, Jianguang ; Yang, Fan ; Bao, WeiMin ; Li, Bang ; Zhang, HuiHui ; Yu, Rui ; Zhou, Jian ; Zhao, RongQuan ; Yin, Xuan

The synchronized development of mineralized bone and blood vessels is a fundamental requirement for successful bone tissue regeneration. Adequate energy production forms the cornerstone supporting new bone formation. ETS variant 2 (ETV2) has been identified as a transcription factor that promotes energy metabolism reprogramming and facilitates the coordination between osteogenesis and angiogenesis. In vitro molecular experiments have demonstrated that ETV2 enhances osteogenic differentiation of dental pulp stem cells (DPSCs) by regulating the ETV2- prolyl hydroxylase 2 (PHD2)- hypoxia-inducible factor-1α (HIF-1α)- vascular endothelial growth factor A (VEGFA) axis. Notably, ETV2 achieves the rapid reprogramming of energy metabolism by simultaneously accelerating mitochondrial aerobic respiration and glycolysis, thus fulfilling the energy requirements essential to expedite osteogenic differentiation. Furthermore, decreased α-ketoglutarate release from ETV2-modified DPSCs contributes to microcirculation reconstruction. Additionally, we engineered hydroxyapatite/chitosan microspheres (HA/CS MS) with biomimetic nanostructures to facilitate multiple ETV2-DPSC functions and further enhanced the osteogenic differentiation. Animal experiments have validated the synergistic effect of ETV2-modified DPSCs and HA/CS MS in promoting the critical-size bone defect regeneration. In summary, this study offers a novel treatment approach for vascularized bone tissue regeneration that relies on energy metabolism activation and the maintenance of a stable local hypoxia signaling state.

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ETV2

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