The expression of long non-coding RNAs is highly enriched in the human nervous system.However, the function of neuronal lncRNAs in the cytoplasm and their potential translation remains poorly understood. Here we performed Poly-Ribo-Seq to understand the interaction of lncRNAs with the translation machinery and the functional consequences during neuronal differentiation of human SH-SY5Y cells. We discovered 237 cytoplasmic lncRNAs upregulated during early neuronal differentiation, 58-70% of which are associated with polysome translation complexes. Amongst these polysome associated lncRNAs, we find 45 small ORFs to be actively translated, 17 specifically upon differentiation. 15/45 of the translated lncRNA-smORFs exhibit sequence conservation within Hominidea suggesting they are under strong selective constraint in this clade. Profiling of publicly available datasets revealed that 8/45 of the translated lncRNAs are dynamically expressed during human brain development and 22/45 are associated with cancers of the central nervous system. One translated lncRNA we discovered is LINC01116, which is induced upon differentiation and contains an 87 codon smORF exhibiting increased ribosome profiling signal upon differentiation. The resulting LINC01116 peptide localises to neurites. Knockdown of LINC01116 results in a significant reduction of neurite length in differentiated cells indicating it contributes to neuronal differentiation. Our findings indicate cytoplasmic lncRNAs interact with translation complexes, are a non-canonical source of novel

The placenta is a temporary organ, which facilitates the exchange of nutrients, waste and gases between the maternal and fetal circulatory systems. To perform its role, the placenta is a villous structure, which branches to cover a large surface area. In gestational diabetes (GDM), a major complication that affects otherwise healthy pregnancies, the placenta displays aberrant vasculature, including altered vascularization, villous immaturity, and endothelial dysfunction. Several contributors including reactive oxygen species (ROS), advanced glycation end products (AGEs) and the dysregulation of key angiogenic factors have been attributed to vascular dysfunction in GDM.

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