What question did this study set out to answer?

To investigate whether estrogen prevents senescence of human endothelial progenitor cells and to elucidate the underlying molecular mechanisms.

August 8, 2005Journal of Hypertension

Estrogen reduces endothelial progenitor cell senescence through augmentation of telomerase activity

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Authors

TIToshio ImanishiInterventional / Structural Cardiology THTakuzo HanoWakayama Medical University INIchiro NishioWakayama Medical University

Discussion

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Overview

In vitro study demonstrates that 17beta-estradiol prevents senescence in human endothelial progenitor cells via PI3-K/Akt-dependent telomerase activation, suggesting benefits for cell therapy.

Key Points

To investigate whether estrogen prevents senescence of human endothelial progenitor cells and to elucidate the underlying molecular mechanisms.
Isolated human endothelial progenitor cells (EPCs) from peripheral blood, evaluated senescence through acidic beta-galactosidase staining, and tested 17beta-estradiol interventions.
Measured telomerase activity via PCR-ELISA and quantified telomerase reverse transcriptase (TERT) expression with RT-PCR alongside pharmacological PI3-K inhibitors (wortmannin and LY294002).
Analyzed Akt phosphorylation by immunoblotting, assessed EPC mitogenic activity with an MTS assay, quantified VEGF secretion, and evaluated vascular network integration in Matrigel.
17beta-estradiol dose-dependently reduced senescence and elevated telomerase activity in EPCs by upregulating TERT through PI3-K/Akt activation.
Treatment with 17beta-estradiol significantly increased EPC mitogenic activity compared to untreated controls (P < 0.01), enhanced VEGF release, and improved network formation in Matrigel.

Cite This Study

Imanishi et al. (2005) studied this question.

synapsesocial.com/papers/6a722d92f44fa9f079dfbf45 https://doi.org/10.1097/01.hjh.0000176788.12376.20

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August 8, 2005Journal of Hypertension

Estrogen reduces endothelial progenitor cell senescence through augmentation of telomerase activity

View Full Paper

Ask AI

Bookmark

Authors

TIToshio ImanishiInterventional / Structural Cardiology THTakuzo HanoWakayama Medical University INIchiro NishioWakayama Medical University

Discussion

Member takes

Overview

In vitro study demonstrates that 17beta-estradiol prevents senescence in human endothelial progenitor cells via PI3-K/Akt-dependent telomerase activation, suggesting benefits for cell therapy.

Key Points

To investigate whether estrogen prevents senescence of human endothelial progenitor cells and to elucidate the underlying molecular mechanisms.
Isolated human endothelial progenitor cells (EPCs) from peripheral blood, evaluated senescence through acidic beta-galactosidase staining, and tested 17beta-estradiol interventions.
Measured telomerase activity via PCR-ELISA and quantified telomerase reverse transcriptase (TERT) expression with RT-PCR alongside pharmacological PI3-K inhibitors (wortmannin and LY294002).
Analyzed Akt phosphorylation by immunoblotting, assessed EPC mitogenic activity with an MTS assay, quantified VEGF secretion, and evaluated vascular network integration in Matrigel.
17beta-estradiol dose-dependently reduced senescence and elevated telomerase activity in EPCs by upregulating TERT through PI3-K/Akt activation.
Treatment with 17beta-estradiol significantly increased EPC mitogenic activity compared to untreated controls (P < 0.01), enhanced VEGF release, and improved network formation in Matrigel.

Cite This Study

Imanishi et al. (2005) studied this question.

synapsesocial.com/papers/6a722d92f44fa9f079dfbf45 https://doi.org/10.1097/01.hjh.0000176788.12376.20

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