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Item No. 28605

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Explore how neutrophils shape the immune response in health and disease. This poster highlights neutrophil pathogen defense mechanisms, including phagocytosis, degranulation, and NETosis, as well as neutrophil roles in inflammation and NET-associated pathologies.
DOWNLOAD NOWThymosin β4 is an actin-sequestering peptide that has wound healing and anti-inflammatory activities.1,2,3 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.1 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.2,4 It increases gap closure and reduces wound width in a rat full-thickness cutaneous wound model when administered at a dose of 60 µg.2 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.3
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1. Interaction of thymosin β4 with muscle and platelet actin: Implications for actin sequestration in resting platelets. Biochemistry 31(27), 6179-6185 (1992).
2. Thymosin β4 accelerates wound healing. J. Invest. Dermatol. 113(3), 364-368 (1999).
3. Thymosin beta 4 suppression of corneal NFκB: A potential anti-
4. Thymosin β4 stimulates directional migration of human umbilical vein endothelial cells. The FASEB Journal 11(6), 474-481 (1997).