Calreticulin contributes to C1q-dependent recruitment of microglia in the leech Hirudo medicinalis following a CNS injury
| Autor: | Julien Franck, Michel Salzet, Pierre-Eric Sautière, Francesco Drago, Françoise Le Marrec-Croq, Annelise Bocquet-Garcon, Christophe Lefebvre, Maxence Wisztorski, Christelle Vancamp, Jacopo Vizioli |
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| Rok vydání: | 2014 |
| Předmět: |
Central Nervous System
Molecular Sequence Data Central nervous system Leech Context (language use) Biology Hirudo medicinalis Neuroprotection Lab/In Vitro Research Head Injuries Closed medicine Animals Humans Biotinylation Amino Acid Sequence RNA Messenger Phylogeny Base Sequence Microglia Complement C1q Chemotaxis General Medicine biology.organism_classification Cell biology medicine.anatomical_structure Solubility Immunology biology.protein Calreticulin Protein Binding |
| Zdroj: | Medical Science Monitor : International Medical Journal of Experimental and Clinical Research |
| ISSN: | 1643-3750 |
| DOI: | 10.12659/msm.890091 |
| Popis: | BACKGROUND The medicinal leech is considered as a complementary and appropriate model to study immune functions in the central nervous system (CNS). In a context in which an injured leech's CNS can naturally restore normal synaptic connections, the accumulation of microglia (immune cells of the CNS that are exclusively resident in leeches) has been shown to be essential at the lesion to engage the axonal sprouting. HmC1q (Hm for Hirudo medicinalis) possesses chemotactic properties that are important in the microglial cell recruitment by recognizing at least a C1q binding protein (HmC1qBP alias gC1qR). MATERIAL AND METHODS Recombinant forms of C1q were used in affinity purification and in vitro chemotaxis assays. Anti-calreticulin antibodies were used to neutralize C1q-mediated chemotaxis and locate the production of calreticulin in leech CNS. RESULTS A newly characterized leech calreticulin (HmCalR) has been shown to interact with C1q and participate to the HmC1q-dependent microglia accumulation. HmCalR, which has been detected in only some microglial cells, is consequently a second binding protein for HmC1q, allowing the chemoattraction of resident microglia in the nerve repair process. CONCLUSIONS These data give new insight into calreticulin/C1q interaction in an immune function of neuroprotection, suggesting another molecular target to use in investigation of microglia reactivity in a model of CNS injury. |
| Databáze: | OpenAIRE |
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