Justin Amakor

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Justin is a rising senior at UCLA majoring in Molecular, Cell, and Developmental Biology. Justin started in the Spencer Lab in the summer of 2022. There, Justin studies the influence of macrophage-specific Spp1 on the dystrophic phenotype and cell-cell interactions in the dystrophic muscle niche. This is all with the aim of better understanding Duchenne Muscular Dystrophy (DMD) and the mechanisms that increase its severity. Duchenne muscular dystrophy (DMD) is an inherited degenerative muscular disorder caused by mutations in the DMD gene. Mutations in the DMD gene cause a loss of function of dystrophin, a protein essential for muscle cell membrane integrity via the dystrophin-glycoprotein complex (DGC). As a result, muscle cells are prone to chronic injury, dysregulated inflammation, and fibrosis. As an Amgen scholar, Justin will study DMD using muscular dystrophy X-linked mice (mdx mice), which are mice with a dystrophic background because of a point mutation in the DMD gene that causes them to express non-function dystrophin. This model will be used alongside the macrophage conditional knockout mouse line (MϕcKO) created by the Spencer Lab. The ablation of macrophage osteopontin has led to the disappearance of two stromal cell subclusters. The two subclusters were transcriptionally characterized and found to be novel stromal cell populations, which the Spencer lab refers to as ApoD(+) and Cxcl13(+) stromal cells. Using immunofluorescence techniques, Justin will find out if macrophage osteopontin is responsible for the viability of these cells and through which mechanism this happens. Justin will also characterize the phenotypic effects of missing ApoD(+) and Cxcl13(+) stromal cells on the mdx mice muscles. The preliminary characterization will involve using intracellular fat staining to uncover any difference in the amount of intracellular fat in MϕcKO compared to the control mice. Justin is exceptionally grateful to everyone at the Spencer Lab for their kindness, patience, and helpfulness. This is especially so for Justin’s graduate student mentor, Raquel Aragón, and his PI, Dr. Melissa Spencer. Justin would also like to thank the Amgen Foundation for this opportunity and their support in his journey to become a physician-scientist.

Justin is a rising senior at UCLA majoring in Molecular, Cell, and Developmental Biology. Justin started in the Spencer Lab in the summer of 2022. There, Justin studies the influence of macrophage-specific Spp1 on the dystrophic phenotype and cell-cell interactions in the dystrophic muscle niche. This is all with the aim of better understanding Duchenne Muscular Dystrophy (DMD) and the mechanisms that increase its severity.

Duchenne muscular dystrophy (DMD) is an inherited degenerative muscular disorder caused by mutations in the DMD gene. Mutations in the DMD gene cause a loss of function of dystrophin, a protein essential for muscle cell membrane integrity via the dystrophin-glycoprotein complex (DGC). As a result, muscle cells are prone to chronic injury, dysregulated inflammation, and fibrosis. As an Amgen scholar, Justin will study DMD using muscular dystrophy X-linked mice (mdx mice), which are mice with a dystrophic background because of a point mutation in the DMD gene that causes them to express non-function dystrophin. This model will be used alongside the macrophage conditional knockout mouse line (MÏ•cKO) created by the Spencer Lab. The ablation of macrophage osteopontin has led to the disappearance of two stromal cell subclusters. The two subclusters were transcriptionally characterized and found to be novel stromal cell populations, which the Spencer lab refers to as ApoD(+) and Cxcl13(+) stromal cells. Using immunofluorescence techniques, Justin will find out if macrophage osteopontin is responsible for the viability of these cells and through which mechanism this happens. Justin will also characterize the phenotypic effects of missing ApoD(+) and Cxcl13(+) stromal cells on the mdx mice muscles. The preliminary characterization will involve using intracellular fat staining to uncover any difference in the amount of intracellular fat in MÏ•cKO compared to the control mice.

Justin is exceptionally grateful to everyone at the Spencer Lab for their kindness, patience, and helpfulness. This is especially so for Justin’s graduate student mentor, Raquel Aragón, and his PI, Dr. Melissa Spencer. Justin would also like to thank the Amgen Foundation for this opportunity and their support in his journey to become a physician-scientist.