CD44 Is Critically Involved in Infarct Healing by Regulating the Inflammatory and Fibrotic Response

• DOI: 10.4049/jimmunol.180.4.2625
• Publication Date: 2014-04-18T23:26:28Z
• Authors: Peter Huebener; Tareq Abou-Khamis; Pawel Zymek; Marcin Bujak; Xia Ying; Khaled Chatila; Sandra Haudek; Geeta Thakker; Nikolaos G Frango...
• Keywords: Proinflammatory cytokine; Myofibroblast; Infiltration (HVAC)

Abstract Infarct healing is dependent on an inflammatory reaction that results in leukocyte infiltration and clearance of the wound from dead cells matrix debris. However, optimal infarct requires timely activation “stop signals” suppress mediator synthesis mediate resolution infiltrate, promoting formation a scar. A growing body evidence suggests interactions involving transmembrane receptor CD44 may play important role inflammation migration fibroblasts injured tissues. We examined signaling cardiac remodeling using mouse model reperfused infarction. expression was markedly induced infarcted myocardium localized infiltrating leukocytes, myofibroblasts, vascular cells. In comparison with wild-type mice, CD44−/− animals showed enhanced prolonged neutrophil macrophage increased proinflammatory cytokines following myocardial CD44null infarcts, phase followed by decreased fibroblast infiltration, reduced collagen deposition, diminished proliferative activity. Isolated had proliferation upon stimulation serum response to TGF-β fibroblasts. The defects mice were associated dilative ventricle, without affecting size infarct. Our findings suggest CD44-mediated are critically involved healing. for postinfarction regulates function.