Francesca Vacante

All Publications

• CARMN Loss Regulates Smooth Muscle Cells and Accelerates Atherosclerosis in Mice. Circulation research Vacante, F., Rodor, J., Lalwani, M. K., Mahmoud, A. D., Bennett, M., De Pace, A. L., Miller, E., Van Kuijk, K., de Bruijn, J., Gijbels, M., Williams, T. C., Clark, M. B., Scanlon, J. P., Doran, A. C., Montgomery, R., Newby, D. E., Giacca, M., O'Carroll, D., Hadoke, P. W., Denby, L., Sluimer, J. C., Baker, A. H. 2021; 128 (9): 1258-1275

  Abstract

  [Figure: see text].

  View details for DOI 10.1161/CIRCRESAHA.120.318688

  View details for PubMedID 33622045

  View details for PubMedCentralID PMC7610708

• Generation of Marfan syndrome-specific induced pluripotent stem cells harboring FBN1 mutations. Stem cell research Vacante, F., Venkateshappa, R., Htet, M., Yan, C., Wu, J. C. 2024; 80: 103518

  Abstract

  Marfan syndrome (MFS) is a hereditary condition caused by mutations in the FBN1 gene. Genetic mutations in the FBN1 locus impact the function of the encoded protein, Fibrillin 1, a structural molecule forming microfibrils found in the connective tissue. MFS patients develop severe cardiovascular complications including thoracic aortic aneurysm and aortic dissection, which predispose them to an enhanced risk of premature death. Here, we generated two induced pluripotent stem cell (iPSC) lines harboring mutations in the FBN1 gene (p.C1942C>A and c.1954 T>C), directly derived from MFS patients. We have shown that both iPSC lines displayed expression of pluripotency markers, normal karyotype and ability of trilineage differentiation, representing a valuable tool for the identification of new therapeutic strategies for intervening in this disease.

  View details for DOI 10.1016/j.scr.2024.103518

  View details for PubMedID 39096853

• Lnc-ing epicardium-derived cells to cardiac remodelling: lncRNA-TARID as a novel antifibrotic option. European heart journal Wu, X., Vacante, F., Wu, J. C. 2023

  View details for DOI 10.1093/eurheartj/ehad058

  View details for PubMedID 36928295

• The function of miR-143, miR-145 and the MiR-143 host gene in cardiovascular development and disease. Vascular pharmacology Vacante, F., Denby, L., Sluimer, J. C., Baker, A. H. 2019; 112: 24-30

  Abstract

  Noncoding RNAs (long noncoding RNAs and small RNAs) are emerging as critical modulators of phenotypic changes associated with physiological and pathological contexts in a variety of cardiovascular diseases (CVDs). Although it has been well established that hereditable genetic alterations and exposure to risk factors are crucial in the development of CVDs, other critical regulators of cell function impact on disease processes. Here we discuss noncoding RNAs have only recently been identified as key players involved in the progression of disease. In particular, we discuss micro RNA (miR)-143/145 since they represent one of the most characterised microRNA clusters regulating smooth muscle cell (SMC) differentiation and phenotypic switch in response to vascular injury and remodelling. MiR143HG is a well conserved long noncoding RNA (lncRNA), which is the host gene for miR-143/145 and recently implicated in cardiac specification during heart development. Although the lncRNA-miRNA interactions have not been completely characterised, their crosstalk is now beginning to emerge and likely requires further research focus. In this review we give an overview of the biology of the genomic axis that is miR-143/145 and MiR143HG, focusing on their important functional role(s) in the cardiovascular system.

  View details for DOI 10.1016/j.vph.2018.11.006

  View details for PubMedID 30502421

  View details for PubMedCentralID PMC6395947