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Prenatal cadmium exposure alters proliferation in mouse CD4+ T cells via LncRNA Snhg7

ABSTRACT: Prenatal cadmium (Cd) exposure leads to immunotoxic phenotypes in the offspring. Long non-coding RNAs (lncRNAs) are integral to T cell regulation. Here, we identified genes and pathways altered in CD4+ T cell by prenatal Cd exposure. We investigated the role of long non-coding RNA small nucleolar RNA hostgene 7 (lncSnhg7) in T cell proliferation: LncSnhg7 expression increases in CD4+ T cells following stimulation with anti-CD3/CD28 beads. LngSnhg7 and a downstream protein, GALNT7, are upregulated in T cells from offspring exposed to Cd during gestation. Overexpression of miR-34a, a regulator of lnhcSnhg7 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 in vitro, but Treg suppression and CD4+ T cell apoptosis are not affected by prenatal Cd exposure. In 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 suggesting that the lncSnhg7/miR-34a/GALNT7 is an important pathway in primary CD4+ T cells. These data highlight the need to understand the consequences of environmental exposures on lncRNA functions in non-cancerous cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE175796 | GEO | 2021/12/23

REPOSITORIES: GEO

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Prenatal cadmium exposure alters proliferation in mouse CD4+ T cells via LncRNA Snhg7

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