Bone marrow mononuclear cells and mannose receptor expression in focal cortical ischemia
| Autor: | Leny A. Cavalcante, Helder Teixeira de Freitas, Hugo Macedo-Ramos, Wagner Baetas-da-Cruz, Arthur Giraldi-Guimarães, Bárbara de Paula Coelho, Rosalia Mendez-Otero |
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| Jazyk: | angličtina |
| Předmět: |
Cell type
Pathology medicine.medical_specialty Neuroscience(all) Ischemia Clinical Neurology Bone Marrow Cells Receptors Cell Surface Inflammation Biology Cell therapy Brain Ischemia Damage-associated molecular patterns (DAMPs) Glial Fibrillary Acidic Protein medicine Animals Lectins C-Type Rats Wistar Receptor Molecular Biology Bone Marrow Transplantation Neurons Stem cell Pattern recognition receptors (PRRs) Microglia General Neuroscience Brain medicine.disease Rats Stroke Mannose-Binding Lectins medicine.anatomical_structure Astrocytes Receptors Mitogen Neurology (clinical) Bone marrow medicine.symptom Mannose Receptor Mannose receptor Repair Developmental Biology |
| Zdroj: | Brain Research. :173-184 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/j.brainres.2012.03.002 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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