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Targeting lipid clearance pathways to promote repair after SCI

靶向脂质清除途径促进 SCI 后修复

基本信息

批准号：
10677106
负责人：
Jae K Lee
金额：
$ 45.41万
依托单位：
UNIVERSITY OF MIAMI SCHOOL OF MEDICINE
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-09-01 至 2028-04-30
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10677106
关键词：
AKT inhibition Affect Area Arterial Fatty Streak Autophagocytosis Behavioral Biological Process Blood Vessels Cell Aging Cells Chimera organism Cicatrix Data Disease Environment Failure Fibroblasts Fibrosis Foamy Macrophage Future Gene Expression Profile Gene set enrichment analysis Goals Histopathology IL1R1 gene In Vitro Inflammatory Injury Interleukin-1 Knock-out Knockout Mice Lead Link Lipid-Laden Macrophage Lipids Macrophage Modeling Molecular Myelin PDPK1 gene PIK3CG gene Pathogenesis Pathology Pathway Analysis Pathway interactions Phagocytes Phenotype Process Property Recovery Role Signal Pathway Signal Transduction Site Spinal Cord Spinal cord injury Testing cell transformation central nervous system injury cytokine experimental study in vivo inhibitor monocyte new therapeutic target novel pharmacologic regenerative repaired senescence spinal cord regeneration therapeutic development tissue regeneration uptake

项目摘要

PROJECT SUMMARY/ABSTRACT After spinal cord injury (SCI), the injury site is filled with cellular debris, especially myelin debris that creates a very unique lipid-dense environment. Macrophages are the predominant phagocyte that are responsible for debris-clearance, but this process is not only inefficient, it is also maladaptive. The excessive amount of myelin debris present at the injury site leads to formation lipid-laden macrophages (a.k.a. foamy macrophages) that become pro-inflammatory and contribute to tissue regeneration failure. Therefore, understanding the mechanisms of foamy macrophage formation after SCI may lead to novel therapeutic targets to promote repair after SCI. In this application, we will investigate the molecular mechanisms of lipid accumulation in foamy macrophages and how they contribute to fibrotic scar formation at the spinal cord injury site.

项目摘要/摘要脊髓损伤(SCI)后，损伤部位充满了细胞碎片，特别是髓鞘碎片，产生了非常独特的脂类致密环境。巨噬细胞是主要的吞噬细胞，负责这一进程不仅效率低下，而且适应性差。过量的髓鞘损伤部位存在的碎片导致形成富含脂质的巨噬细胞(又名。泡沫巨噬细胞) 变得容易发炎，并导致组织再生失败。因此，理解脊髓损伤后泡沫巨噬细胞的形成机制可能导致新的促进修复的治疗靶点在SCI之后。在这一应用中，我们将研究泡沫中脂质积累的分子机制。巨噬细胞及其对脊髓损伤部位纤维性瘢痕形成的作用。

项目成果

期刊论文数量（22）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Hematogenous macrophage depletion reduces the fibrotic scar and increases axonal growth after spinal cord injury.

DOI：
10.1016/j.nbd.2014.10.024
发表时间：
2015-02
期刊：
Neurobiology of disease
影响因子：
6.1
作者：
Zhu Y;Soderblom C;Krishnan V;Ashbaugh J;Bethea JR;Lee JK
通讯作者：
Lee JK

Conditional ablation of myeloid TNF increases lesion volume after experimental stroke in mice, possibly via altered ERK1/2 signaling.

DOI：
10.1038/srep29291
发表时间：
2016-07-07
期刊：
Scientific reports
影响因子：
4.6
作者：
Clausen BH;Degn M;Sivasaravanaparan M;Fogtmann T;Andersen MG;Trojanowsky MD;Gao H;Hvidsten S;Baun C;Deierborg T;Finsen B;Kristensen BW;Bak ST;Meyer M;Lee J;Nedospasov SA;Brambilla R;Lambertsen KL
通讯作者：
Lambertsen KL

Animal models of axon regeneration after spinal cord injury.