ArticleFrontiers in immunology2021
Prenatal Cadmium Exposure Alters Proliferation in Mouse CD4
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Dietary influence on lung injury and immune modulation in cadmium-exposed mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Epigenetics of maternal-fetal interface immune microenvironment and placental related pregnancy complications.Frontiers in immunology · 2025Review
- Cadmium-induced lung injury disrupts immune cell homeostasis in the secondary lymphoid organs in mice.Toxicology · 2024Article
- Exercise Attenuates Doxorubicin-Induced Myocardial Injury by Inhibiting TSHR and Regulating Macrophage Polarization Through miR-30d-5p/GALNT7.Journal of immunology research · 2024Article
- Non-coding RNAs in immunoregulation and autoimmunity: Technological advances and critical limitations.Journal of autoimmunity · 2023Review
- SnoRNA and lncSNHG: Advances of nucleolar small RNA host gene transcripts in anti-tumor immunity.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Objective: Prenatal cadmium (Cd) exposure leads to immunotoxic phenotypes in the offspring affecting coding and non-coding genes. Recent studies have shown that long non-coding RNAs (lncRNAs) are integral to T cell regulation. Here, we investigated the role of long non-coding RNA small nucleolar RNA host gene 7 (lncSnhg7) in T cell proliferation. Methods: RNA sequencing was used to analyze the expression of lncRNAs in splenic CD4 Results: We identified 23 lncRNAs that were differentially expressed in stimulated versus unstimulated T cells, including lncSnhg7. LncSnhg7 and a downstream protein, GALNT7, are upregulated in T cells from offspring exposed to Cd during gestation. Overexpression of miR-34a, a regulator of lncSnhg7 and GALNT7, suppresses GALNT7 protein levels in primary T cells, but not in a mouse T lymphocyte cell line. The T cells isolated from Cd-exposed offspring exhibit increased proliferation after activation Conclusion: Prenatal Cd exposure alters the expression of lncRNAs during T cell activation. The induction of lncSnhg7 is enhanced in splenic T cells from Cd offspring resulting in the upregulation of GALNT7 protein and increased proliferation following activation. miR-34a overexpression decreased GALNT7 expression and knockdown of lncSnhg7 inhibited proliferation suggesting that the lncSnhg7/miR-34a/GALNT7 is an important pathway in primary CD4
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.