Bone marrow mononuclear cells and mannose receptor expression in focal cortical ischemia

被引:26
作者
Giraldi-Guimaraes, Arthur [1 ]
de Freitas, Helder Teixeira [1 ]
Coelho, Barbara de Paula [1 ]
Macedo-Ramos, Hugo [2 ]
Mendez-Otero, Rosalia
Cavalcante, Leny A. [2 ]
Baetas-da-Cruz, Wagner [2 ,3 ]
机构
[1] Univ Estadual Norte Fluminense Darcy Ribeiro UENF, Ctr Biociencias & Biotecnol, Lab Biol Celular & Tecidual, BR-28013602 Campos Dos Goytacazes, RJ, Brazil
[2] Univ Fed Rio de Janeiro UFRJ, Inst Biofis Carlos Chagas Filho, Programa Terapia Celular & Bioengn, Lab Neurobiol Celular & Mol,CCS, BR-21941902 Rio De Janeiro, RJ, Brazil
[3] Univ Fed Rio de Janeiro UFRJ, BR-27930560 Macae, RJ, Brazil
关键词
Stroke; Cell therapy; Stem cell; Repair; Pattern recognition receptors (PRRs); Damage-associated molecular patterns (DAMPs); PATTERN-RECOGNITION RECEPTORS; ENDOTHELIAL PROGENITOR CELLS; STEM-CELLS; THERAPEUTIC WINDOW; STROKE; TRANSPLANTATION; INJURY; INFLAMMATION; MACROPHAGES; IMMUNITY;
D O I
10.1016/j.brainres.2012.03.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The use of bone marrow mononuclear cells (BMMCs) has been shown as a putative efficient therapy for stroke. However, the mechanisms of therapeutic action are not yet completely known. Mannose receptor (MR) is a subgroup of the C-type lectin receptor superfamily involved in innate immune response in several tissues. Although known primarily for its immune function, MR also has important roles in cell migration, cell debris clearance and tissue remodeling during inflammation and wound healing. Here we analyzed MR expression in brains of rats one week after induction of unilateral focal cortical ischemia by thermocoagulation in blood vessels of sensorimotor cortex. Additionally, we evaluated possible changes in such expression in cortices of rats subjected to ischemia plus treatment with BMMCs. Our results showed high expression of MR in an unknown GFAP(+) cell type and in phagocytic macrophages/microglia within the lesion boundary zone whereas in the non-injured (contralateral) cortical parenchyma, low levels of MR expression were observed. Moreover, therapy with BMMCs induced overexpression of MR in ipsilateral (injured) cortex. Previous studies from our group have shown functional recovery and decreased neurodegeneration in BMMC-treated rats in the same model of focal cortical ischemia. Thus, we suggest that ischemic injury induces large increase in MR expression as part of a mechanism for clearance of damage-associated molecular patterns (DAMPs). In addition, induction of MR overexpression by BMMCs might increase the efficiency of clearance, being one of the protective mechanisms of these cells. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:173 / 184
页数:12
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