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Introduction: The trefoil factor family (TFF) comprises a group of small peptides (TFF1, TFF2 and TFF3), with their mRNA found in the brain, lungs, trachea, thyroid gland, salivary glands, prostate, uterus and other organs. Hereby, we aimed to investigate the role of Tff3 in cardiovascular system and vascular reactivity. Methods: PUBMED search by keywords: cardiovascular, microcirculation, Tff3 peptide, oxidative stress, high salt diet was performed, retrieving, depending on combination, from 2 to >780 papers. Results: According to studies, TFFs may have important roles in processes related to differentiation of airways (1, 2). Tff3 protein is present in the cartilage of mice fetuses which indicates its role in morphogenesis of organs (3, 4). The regeneration of the mucous membrane of the gastrointestinal tract of the Tff3-/-mice is hampered (5). Tff3-/- mice lacking Tff3 peptide in their liver lack the protective effect of the Tff3 in the serum after myocardial and brain ischemia, suffering greater tissue damage (6, 7). In addition, the Tff3 protein is related to angiogenesis (8). Discussion: Transgenic Tff3-/- mice were introduced as a new model for cardiovascular studies, due to altered ratio of ω-6/ω-3 free fatty acids and modified metabolism of arachidonic acid (AA) compared to wild type controls, which could affect vascular reactivity. Our results demonstrated that high-salt diet (HS) causes endothelial dysfunction and impairs vascular reactivity to various stimuli due to increased oxidative stress. As observed, the impact of acute HS intake on FIR (flow-induced response) in Tff3-/- mice is much smaller than in the wild type (WT) (9). HS intake decreases flow- induced vascular NO production in WT mice probably due to increased oxidative stress. Study showed that HS intake does not affect NO production in Tff3-/- mice even though superoxide levels are increased in basal levels and in flow conditions, suggesting protective role of this phenotype on NO bioavailability (10). Conclusion: All together, Tff3-/- mice may give valuable information on the impact of HS diet on vascular function. Acknowledgements: The work is supported by institutional project VIF-2018-MEFOS-09-1509 (PI Ines Drenjančević) and Croatian Science Fund grant # IP-2014-09-6380/V-ELI Athero. Thank to Cedars - Sinai Medical Center’s International Research and Innovation in Medicine Program, the Association for Regional Cooperation in the Fields of Health, Science and Technology (RECOOP HST Association) for their support of our organization as participating Cedars – Sinai Medical Center - RECOOP Research Centers (CRRC). |
