ArticleAmerican journal of translational research2016
Dihydrotestosterone modulates endothelial progenitor cell function via RhoA/ROCK pathway.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Dihydrotestosterone Augments the Angiogenic and Migratory Potential of Human Endothelial Progenitor Cells by an Androgen Receptor-Dependent Mechanism.International journal of molecular sciences · 2024Article
- Sex, hormones and cerebrovascular function: from development to disorder.Fluids and barriers of the CNS · 2024Review
- Low androgen levels induce ferroptosis of rat penile cavernous endothelial cells.Sexual medicine · 2023Article
- Sexual dimorphism in cardiac remodeling: the molecular mechanisms ruled by sex hormones in the heart.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Androgens' effects on cerebrovascular function in health and disease.Biology of sex differences · 2020Review
- The Protective Effect of Total Flavones fromEvidence-based complementary and alternative medicine : eCAM · 2018Article
- Genomic and non-genomic effects of androgens in the cardiovascular system: clinical implications.Clinical science (London, England : 1979) · 2017Review
- Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels.Endocrine reviews · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious findings indicate that testosterone level is negatively correlated with the incidence and mortality of cardiovascular diseases in men. Endothelial progenitor cells (EPCs) play a critical role in endothelial healing and vascular integrity. This study aimed to examine the effects of dihydrotestosterone (DHT), an active metabolite of testosterone, on human EPC function and investigate the underlying mechanism.
methodsEPCs were isolated from peripheral blood of healthy adult males and incubated with a series of concentrations (1, 10, and 100 nmol/L in dimethyl sulfoxide) of DHT for 24 h or with 10 nmol/L DHT for different periods (6, 12, 24, 36, and 48 h). EPC proliferation, migration, and adhesion were determined by MTT assay, modified Boyden chamber assay, and cell counting, respectively. Furthermore, vascular endothelial growth factor (VEGF) production was examined by ELISA, RhoA activity was determined through pull-down assay. The protein level of RhoA was quantified by Western blot analysis.
resultsDHT significantly increased the proliferative, migratory, and adhesive abilities of EPCs in a dose- and time-dependent manner and upregulated the levels of VEGF and activated RhoA. However, RhoA inhibitor C3 exoenzyme or ROCK inhibitor Y-27632 significantly inhibited DHT-induced proliferation, migration, and adhesion, as well as VEGF production. Moreover, C3 exoenzyme inhibited the activation of RhoA stimulated by DHT.
conclusionsDHT promotes EPC proliferation, migration, and adhesion activities via RhoA/ROCK pathway.
Indexed as
Identifiers
27830013PMC5095322W2589927331What OpenQuestion holds
Registered trials
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