Delay modulates the immune response to nerve repair

被引：5

作者：

Golshadi, Masoud ^{[1
]}

Claffey, Elaine F. F. ^{[1
]}

Grenier, Jennifer K. K. ^{[1
]}

Miller, Andrew ^{[1
]}

Willand, Michael ^{[2
]}

Edwards, Michael G. G. ^{[3
]}

Moore, Tim P. P. ^{[1
]}

Sledziona, Michael ^{[1
]}

Gordon, Tessa ^{[4
]}

Borschel, Gregory H. H. ^{[5
]}

Cheetham, Jonathan ^{[1
]}

机构：

[1] Cornell Univ, Coll Vet Med, 930 Campus Rd, Ithaca, NY 14853 USA

[2] Epineuron Technol Inc, 5100 Orbitor Dr, Mississauga, ON L4W 5R8, Canada

[3] Bioinfo Solut LLC, Parker, CO USA

[4] Hosp Sick Children, 555 Univ Ave, Toronto, ON M5G 1X8, Canada

[5] Indiana Univ, 107 S Indiana Ave, Bloomington, IN 47405 USA

来源：

NPJ REGENERATIVE MEDICINE | 2023年 / 8卷 / 01期

基金：

美国国家卫生研究院;

关键词：

MONOCYTE CHEMOATTRACTANT PROTEIN-1; RECOMBINANT HUMAN INTERLEUKIN-10; POOR FUNCTIONAL RECOVERY; SCHWANN-CELL DENERVATION; MACROPHAGE RECRUITMENT; GROWTH-FACTOR; WALLERIAN DEGENERATION; INFLAMMATORY CYTOKINES; ELECTRICAL-STIMULATION; SENSORY AXONS;

D O I：

10.1038/s41536-023-00285-4

中图分类号：

Q813 [细胞工程];

学科分类号：

摘要：

Effective regeneration after peripheral nerve injury requires macrophage recruitment. We investigated the activation of remodeling pathways within the macrophage population when repair is delayed and identified alteration of key upstream regulators of the inflammatory response. We then targeted one of these regulators, using exogenous IL10 to manipulate the response to injury at the repair site. We demonstrate that this approach alters macrophage polarization, promotes macrophage recruitment, axon extension, neuromuscular junction formation, and increases the number of regenerating motor units reaching their target. We also demonstrate that this approach can rescue the effects of delayed nerve graft.

引用

页数：13

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