Transcriptional and postranslational regulation of the cell cycle has been widely studied. However, there is scarce knowledge concerning translational control of this process. Several mammalian eukaryotic initiation factors (eIFs) seem to be implicated in controlling cell proliferation. In this work, we investigated if the human eIF3f expression and function is cell cycle related.

EIF3f is a multifunctional protein capable of interacting with proteins involved in different cellular processes, such as protein synthesis, DNA repair, and viral mRNA edition. In human cells, eIF3f is related to cell cycle and proliferation, and its deregulation compromises cell viability. We here report that, in native conditions, eIF3f physically interacts with the alpha 1B-adrenergic receptor, a plasma membrane protein considered as a proto-oncogene, and involved in vasoconstriction and cell proliferation. The complex formed by eIF3f and alpha 1B-ADR was found in human and mouse cell lines. Upon catecholamine stimulation, eIF3f promotes adrenoceptor activity in vitro, independently of the eIF3f proline- and alanine-rich N-terminal region. The eIF3f/alpha adrenergic receptor interaction opens new insights regarding adrenoceptor-related transduction pathways and proliferation control in human cells. The eIf3f/alpha 1B-ADR complex is found in mammals and is not tissue specific.

COVID-19 has been associated with an active immunothrombotic process. The involvement of endothelial cells (ECs) in the feedback loop of the inflammatory and thrombotic process characteristic of COVID-19, as well as its differences with other infectious inflammatory conditions, remains an area requiring further elucidation. This study aimed to assess the immunothrombotic phenotype induced by the SARS-CoV-2 Spike (S) protein and its receptor-binding domain (RBD) in endothelial-derived cell lines. HUVEC and EA.hy926 cell lines were exposed to S protein and to its RBD. Inflammatory, thrombotic, and fibrinolytic mediators were quantified. Molecular docking assays were conducted to identify potential EC receptors for S protein. EC activation was dependent on both protein concentration and stimulation time. An increased release of immunothrombotic biomarkers were observed in endothelial-derived cells exposed to the S protein and to its RBD. The RBD induced a stronger endothelial response. Molecular docking demonstrated high affinity and a possible interaction between the S protein and endothelial receptors: CD-141, CD-147, IL-6R, TLR 2, 4, and 7. These findings confirm that the S protein and its RBD can induce an immunothrombotic phenotype in EC-derived cell lines, potentially exacerbating the disease pathology. We propose possible endothelial receptors mediating this response.

Bone tissue engineering is an excellent alternative to reduce bone disorders and conditions, by inducing new functional bone regeneration starting from the synthesis of the biomaterials and then the combination of cell and factor therapy. In the present contribution, the scaffolds were made with a ratio of 80 wt.% of β-TCP and 20 wt. % of phosphate-based bioglass, in addition the phosphate-based bioglass was reinforced with zirconia in different amounts (0, 0.5 and 1.0 mol%) with the aim to reduce the dissolution rate, improve the osteoconduction and the osteogenesis of the bone tissue. The results obtained by μCT of the scaffolds containing zirconia showed a wide pore size distribution between 1.5 and 303 μm. AlamarBlue assays showed that the cell proliferation of MC3T3-E1 preosteoblasts scaffolds were sixfold increase in relation to the number of the initial cells. FE-SEM helped to observe the cauliflower structure of HA and DRX showed that crystalline phases formed after heat treatment were (NaCaPO4 and NaZr5PO4) owing both to the crystallization and combination of the bioglass and β-TCP .