| First Author | Lin YT | Year | 2015 |
| Journal | J Invest Dermatol | Volume | 135 |
| Issue | 1 | Pages | 258-268 |
| PubMed ID | 25007042 | Mgi Jnum | J:216201 |
| Mgi Id | MGI:5607857 | Doi | 10.1038/jid.2014.288 |
| Citation | Lin YT, et al. (2015) Galectin-1 Accelerates Wound Healing by Regulating the Neuropilin-1/Smad3/NOX4 Pathway and ROS Production in Myofibroblasts. J Invest Dermatol 135(1):258-68 |
| abstractText | Myofibroblasts have a key role in wound healing by secreting growth factors and chemoattractants to create new substrates and proteins in the extracellular matrix. We have found that galectin-1, a beta-galactose-binding lectin involved in many physiological functions, induces myofibroblast activation; however, the mechanism remains unclear. Here, we reveal that galectin-1-null (Lgals1(-/-)) mice exhibited a delayed cutaneous wound healing response. Galectin-1 induced myofibroblast activation, migration, and proliferation by triggering intracellular reactive oxygen species (ROS) production. A ROS-producing protein, NADPH oxidase 4 (NOX4), was upregulated by galectin-1 through the neuropilin-1/Smad3 signaling pathway in myofibroblasts. Subcutaneous injection of galectin-1 into wound areas accelerated the healing of general and pathological (streptozotocin-induced diabetes mellitus) wounds and decreased the mortality of diabetic mice with skin wounds. These findings indicate that galectin-1 is a key regulator of wound repair that has therapeutic potential for pathological or imperfect wound healing. |
