---
title: "Prenatal Alcohol Exposure Reduces Tensin 1 and Tensin 2 in Brain Endothelial Cells, Impairing Angi"
id: "biorxiv-5-prenatal-alcohol-exposure-downregulates-focal-adhesion-molecules-tensin-1-and"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-5-prenatal-alcohol-exposure-downregulates-focal-adhesion-molecules-tensin-1-and"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1?rss=1"
published_at: "2026-10-07T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Prenatal Alcohol Exposure Reduces Tensin 1 and Tensin 2 in Brain Endothelial Cells, Impairing Angi
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-5-prenatal-alcohol-exposure-downregulates-focal-adhesion-molecules-tensin-1-and
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1?rss=1)
- **Published At:** 2026-10-07T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Prenatal alcohol exposure (PAE) contributes to fetal alcohol spectrum disorders (FASD) and disrupts developmental processes including **angiogenesis**. - In brain microvascular endothelial cells (BMVECs), expression of the focal adhesion proteins **Tensin 1 (Tns1)** and **Tensin 2 (Tns2)** was significantly reduced after alcohol exposure. - The microRNA **miR-150-5p**, previously reported to be increased by PAE, negatively regulates Tns1 and Tns2 expression in BMVECs. - Dual-luciferase reporter assays demonstrated direct binding of **miR-150-5p** to the 3′ untranslated regions (3′UTRs) of both Tns1 and Tns2, supporting a post-transcriptional regulatory mechanism. - Functional sprouting angiogenesis bead assays showed that ethanol (EtOH) impaired endothelial cell sprouting; overexpression of Tns1 and/or Tns2 rescued sprouting deficits caused by EtOH and by miR-150-5p modulation. - The data indicate that augmenting Tns1 and Tns2 expression can reverse EtOH- and miR-150-5p–mediated angiogenic deficits in BMVECs, suggesting a mechanistic link between PAE, miRNA changes, focal adhesion dynamics, and cerebrovascular dysfunction. - The study was funded by the National Institutes of Health (R01AA031486) and is posted as a bioRxiv preprint; authors declared no competing interests. - Details such as exact experimental conditions, quantitative effect sizes, and in vivo validation were not reported in the source abstract and would require consultation of the full preprint for complete methods and data.
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Richard J Justice University of New Mexico * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Richard%2BJ%2BJustice%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Justice%20RJ&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ARichard%2BJ%2BJustice%2B) Amy S Gardiner University of New Mexico * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Amy%2BS%2BGardiner%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Gardiner%20AS&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAmy%2BS%2BGardiner%2B) * [ORCID record for Amy S Gardiner](http://orcid.org/0000-0002-8179-4919 "Open in new tab") * For correspondence: agardiner@salud.unm.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5846125/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5846125/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5846125/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5846125/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.06.757079v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5846125/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Fetal alcohol spectrum disorders (FASD) are caused by prenatal alcohol exposure (PAE), which leads to developmental defects during embryogenesis. Angiogenesis is one facet of development that is heavily dysregulated during PAE and where such impairment is poorly understood. Here we found that expression levels of focal adhesion molecules Tensin 1 (Tns1) and Tensin 2 (Tns2) were significantly reduced by alcohol exposure in brain microvascular endothelial cells (BMVECs). We also found that miR-150-5p, which we previously found was increased by PAE, regulates the expression of Tns1 and Tns2. Dual-luciferase assays demonstrated direct binding of miR-150-5p to the 3UTRs of Tns1 and Tns2. Additionally, we utilized sprouting angiogenesis bead assays to evaluate endothelial cell sprouting in response to ethanol (EtOH) treatment and following Tns1 and/or Tns2 overexpression as well as miR-150-5p modulation. Tns1 and Tns2 rescued both EtOH- and miR-150-5p-mediated deficits in sprouting angiogenesis. Overall, we found that miR-150-5p negatively regulates Tns1 and Tns2 in BMVECs and that augmenting Tns1 and Tns2 expression may reverse the negative effects of EtOH, and subsequent miR-150-5p elevation, thus improving endothelial cell sprouting during cerebrovascular development. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared National Institutes of Health, R01AA031486 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. 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