Smooth Muscle Cells Move With Mitochondria
Vascular smooth muscle cells (SMCs) are essential components in blood vessel walls and responsible for maintenance of blood vessel structure and function. Normally, SMCs reside in medial layers of blood vessels and do not exhibit migration potential. Under pathological conditions, however, medial SMCs migrate to intimal space where they proliferate and secrete extracellular matrix, contributing to vascular remodeling and repair, the featured characteristics of several cardiovascular diseases including atherosclerosis and restenosis after angioplasty. PDGF (platelet-derived growth factor) is a potent stimulator for SMC migration and has been used widely to examine the underlying molecular mechanisms.1 Although the research on SMC migration has mostly focused on the cellular regulation, recent studies have narrowed down to the subcellular levels, especially mitochondria.2–6 However, the precise mechanisms underlying mitochondrial functions in SMCs remain largely unknown. The new study by Nguyen et al7 in this issue makes the elegant and exciting discovery that mitochondrial Ca2+/CaMKII (calmodulin-dependent kinase II), a serine/threonine-specific protein kinase necessary for cellular Ca2+ homeostasis, promotes mitochondrial motility, serving as an important regulator for PDGF-induced SMC migration.
See accompanying article on page 1333
Mitochondria are double membrane-bound cytoplasmic organelles found in large quantities in most cell types and play a critical role in the generation of metabolic energy. A previous study has demonstrated that the increase in mitochondrial motility because of activation of Ca …