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Gene therapy with CX3CL1 for murine limb ischemia

Grant number: 16/09547-0
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): September 01, 2016
Effective date (End): August 31, 2018
Field of knowledge:Biological Sciences - Genetics - Human and Medical Genetics
Principal Investigator:Sang Won Han
Grantee:Carlos Alberto Vergani Junior
Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Associated research grant:15/20206-8 - Modulation of monocytes, macrophages and pericytes by the colony stimulating factor genes to treat murine limb ischemia, AP.TEM


Peripheral arterial disease (PAD) is caused by narrowing or obstruction of the arterial blood vessels. One of the main manifestations of PAD is critical limb ischemia (CLI), which is usually caused by atherosclerosis. Macrophages act in the repair of ischemic and damaged tissues or to maintain homeostasis, stimulating the formation of new vessels. Macrophages may have phenotype M1 (pro-inflammatory) or M2 (pro-resolutive). Studies show that M2 macrophages are active in angiogenesis processes, fibrosis, tissue repair and regeneration. The transmembrane protein Fractalkine/CX3CL1 is a chemotactic molecule that participates in the recruitment of monocytes LY6Clow. These monocytes are essential to pro-resolutive process of ischemic tissue because these cells acquire macrophage M2 phenotype after diapedesis. The purpose of this project is to evaluate the LY6Clow monocyte recruitment capacity by transfection of CX3CL1 gene in the ischemic limb, the formation of M2 macrophages and the ischemic muscle repair.

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