Vesa M. Kaartinen

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University of Michigan - Ann Arbor
Biologic and Materials Sciences
Short bio: 

Ph.D. University of Eastern Finland (Kuopio), Finland. Biochemistry. 1991.

M.Sc. University of Kuopio, Finland. Biochemistry. 1986.

B.S. University of Kuopio, Finland. Biochemistry. 1984.

Research summary: 

Dr. Kaartinen’s laboratory is interested in underlying molecular reasons that lead to a formation of  common craniofacial and cardiac birth defects in human newborn babies. Their particular interest is in TGF-beta/BMP superfamily signaling. They have a long history of using gene targeting in mouse ES cells and subsequent generation of knockout, knockin and conditional/tissue-specific knockout mice, which form a primary research model in their research laboratory.

Dr. Kaartinen’s laboratory is currently investigating a role TGF-beta superfamily signaling in lip fusion, and differentiation and anterior-posterior patterning of the palatal epithelium, regulation of TGF-beta3 expression in the palatal epithelium and the role of TGF-beta3 signaling in the palatal mesenchyme. Moreover, they currently study the role of a novel negative regulator of TGF-beta signaling (Trim33) in craniofacial development, and they have a project to identify micro-RNAs that regulate gene expression in the prefusion palatal epithelium.

Studies on cardiac development include investigations on a role of TGF-beta signaling via the Alk5 receptor in the epicardium, the role of Alk2 mediated signaling in outflowt tract and aortic valve development, and BMP type I receptor signaling interactions in atrio-ventricular canal transformation.

Recent publications: 
  1. Xi, Q., Wang, Z., Zaromytidou, A.I., Zhang, X.H., Chow-Tsang, L.F., Liu, J.X., Kim, H., Barlas, A., Manova-Todorova, K., Kaartinen, V., Studer, L., Mark, W., Patel, D.J., Massagué, J. A Poised Chromatin Platform for TGF-β Access to Master Regulators. Cell, 148, 1511-1524, 2011. PubMed PMCID: PMC3582033
  2. Thomas, P.S., Sridurongrit, S., Ruiz-Lozano, P., Kaartinen, V.  Deficient signaling via Alk2 (Acvr1) leads to bicuspid aortic valve development. PloS One. 7(4):e35539, 2012. PubMed PMCID:PMC3334911
  3. Yumoto, K., Thomas, P.S., Lane, J., Matsuzaki, K., Inagaki, M., Ninomiya-Tsuji, J., Scott, G.J., Ray, M.K., Ishii, M., Maxson, R., Mishina, Y., Kaartinen, V. TGF-β-activated Kinase 1 (Tak1) Mediates Agonist-induced Smad Activation and Linker Region Phosphorylation in Embryonic Craniofacial Neural Crest-derived Cells. J. Biol. Chem. 288, 13467-13480, 2013. PubMed PMCID:PMC3650384
  4. Thomas, P.S., Rajderkar, S., Lane, J., Mishina, Y., Kaartinen, V. AcvR1-mediated BMP signaling in second heart field is required for arterial pole development: Implications for myocardial differentiation and regional identity. Dev Biol. 2014 Mar 26. doi:pii: S0012-1606(14)00152-3. 10.1016/j.ydbio.2014.03.008. PubMed PMID: 24680892.
  5. Lane, J., Yumoto, K., Pisano, J., Azhar, M., Thomas, P.S., Kaartinen, V. Control elements targeting Tgfb3 expression to the palatal epithelium are located intergenically and in intron of the upstream Ift43 gene. Front Physiol. 5, 258, 2014. PubMed PMCID:PMC4083190
  6. Lane, J., Yumoto, K., Azhar, M., Ninomiya-Tsuji, J., Inagaki, M., Hu, Y., Deng, CX., Kim, J., Mishina, Y., Kaartinen, V. Tak1, Smad4 and Trim33 redundantly mediate TGF-β3 signaling during palate development. Dev Biol. 2015 Feb 15;398(2):231-41. PubMed PMCID:PMC431444