Thymosin β4 is an actin-sequestering peptide that has wound healing and anti-inflammatory activities. It regulates cytoskeletal rearrangement by binding to actin (Kds = 0.7 and 2.1 μM for human platelets and rabbit muscle, respectively) and inhibiting the polymerization of actin monomers. Thymosin β4 increases in vitro migration of human umbilical vein endothelial cells (HUVECs), keratinocytes, and coronary artery endothelial cells, but not fibroblasts, actin smooth muscle cells, neutrophils, monocytes, or HT-1080 fibrosarcoma cells, when used at concentrations ranging from 0.001 to 1 μg/ml. It increases gap closure and reduces wound width in a rat full-thickness cutaneous wound model when administered at a dose of 60 μg. Thymosin β4 (1 μg/ml) inhibits TNF-α-induced NF-ĸB phosphorylation and nuclear translocation in immortalized human corneal epithelial cells and decreases the expression of chemokine (C-X-C motif) ligand 1 (CXCL1), CXCL2, matrix metalloproteinase-9 (MMP-9), and MMP-2 in the cornea in a mouse model of sodium hydroxide-induced corneal injury when administered at a dose of 5 μg.
