| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Maugeri, Norma Rigamonti, Elena Bianchi, Marco E. Manfredi, Angelo A. Campana, Lara Esposito, Antonio Monno, Antonella Del Maschio, Alessandro Rovere-Querini, Patrizia Santarella, Francesco Canu, Tamara |
| Description |
Author Affiliation: Campana L ( Innate Immunity and Tissue Remodeling Unit, San Raffaele Scientific Institute, 20132 Milan, Italy); Santarella F ( Innate Immunity and Tissue Remodeling Unit, San Raffaele Scientific Institute, 20132 Milan, Italy); Esposito A ( Vita-Salute, San Raffaele University, 20132 Milan, Italy); Maugeri N ( Autoimmunity and Vascular Inflammation Unit, San Raffaele Scientific Institute, 20132 Milan, Italy); Rigamonti E ( Innate Immunity and Tissue Remodeling Unit, San Raffaele Scientific Institute, 20132 Milan, Italy); Monno A ( Innate Immunity and Tissue Remodeling Unit, San Raffaele Scientific Institute, 20132 Milan, Italy); Canu T ( Radiology Department, Centre for Experimental Imaging, San Raffaele Scientific Institute, 20132 Milan, Italy); Del Maschio A ( Vita-Salute, San Raffaele University, 20132 Milan, Italy); Bianchi ME ( Radiology Department, Centre for Experimental Imaging, San Raffaele Scientific Institute, 20132 Milan, Italy); Manfredi AA ( Vita-Salute, San Raffaele University, 20132 Milan, Italy); Rovere-Querini P ( Innate Immunity and Tissue Remodeling Unit, San Raffaele Scientific Institute, 20132 Milan, Italy) |
| Abstract |
Signals of tissue necrosis, damage-associated molecular patterns (DAMPs), cause inflammation. Leukocytes migrating into injured tissues tonically release DAMPs, including the high mobility group box 1 protein (HMGB1). In the absence of suitable models, the relative role of DAMPs released because of necrosis or leukocyte activation has not, so far, been dissected. We have generated a mouse model lacking Hmgb1 in the hematopoietic system and studied the response to acute sterile injury of the skeletal muscle. Regenerating fibers are significantly less numerous at earlier time points and smaller at the end of the process. Leukocyte Hmgb1 licenses the skeletal muscle to react to hypoxia, to express angiopoietin-2, and to initiate angiogenesis in response to injury. Vascularization of the regenerating tissue is selectively jeopardized in the absence of leukocyte Hmgb1, revealing that it controls the nutrient and oxygen supply to the regenerating tissue. Altogether, our results reveal a novel nonredundant role for leukocyte Hmgb1 in the repair of injured skeletal muscle. |
| ISSN |
00221767 |
| e-ISSN |
15506606 |
| Journal |
The Journal of Immunology |
| Issue Number |
11 |
| Volume Number |
192 |
| Language |
English |
| Publisher |
The American Association of Immunologists |
| Publisher Date |
2014-06-01 |
| Publisher Place |
United States |
| Access Restriction |
Open |
| Subject Keyword |
Angiopoietin-2 Immunology Hmgb1 Protein Muscle, Skeletal Blood Supply Neovascularization, Physiologic Regeneration Genetics Animals Leukocytes Mice Mice, Knockout Injuries Research Support, Non-u.s. Gov't Discipline Immunology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Immunology and Allergy Immunology |
