TGF-b1 and hardening of the arteries
A study in which participated the National Research Council (CSIC) has identified a new target potentially involved in this process. The work has been published in the journal Molecular and Cellular Biology.
The extracellular matrix, the organic component exists between the cells in multicellular organisms, determines the properties of hardness and elasticity of the tissues, an important aspect in the cardiovascular system. The lysyl oxidases are a family of enzymes responsible for establishing covalent bonds in collagen and elastin fibers, a key step in the maturation and stabilization of the extracellular matrix.
"The increased expression of these enzymes results in a more rigid matrix, less elastic, so that the lysyl oxidase largely determine the biomechanical properties of tissues," says researcher Fernando Rodriguez Pascual CISC, Center for Molecular Biology "Severo Ochoa", CSIC joint center and the Autonomous University of Madrid.
The synthesis and deposition of extracellular matrix components are governed by a set of hormones, and cellular factors, including transforming growth factor-B1 (TGF-b1) plays an important role, directly related to the development of cardiovascular diseases which cause loss of elasticity of blood vessels.
This study relates directly the action of TGF-b1 with a remarkable increase of the expression of a form of vascular lysyl oxidase isoform 4 (in English "lysyl oxidase-like 4" LOXL4). "Through this effect on LOXL4 expression could explain the ability of TGF-b1 to promote arterial stiffness and, therefore, its contribution to the development of these diseases," adds the researcher.
- Oscar Busnadiego, José González-Santamaría, David Lagares, Juan Guinea-Viniegra, Cathy Pichol-Thievend, Laurent Muller, Fernando Rodríguez-Pascual. LOXL4 Is Induced by Transforming Growth Factor β1 through Smad and JunB/Fra2 and Contributes to Vascular Matrix Remodeling. Molecular and Cellular Biology. DOI: 10.1128/MCB.00036-13.
Fotografía By Rhcastilhos (Own work) [Public domain], via Wikimedia Commons.