Mark Hamer
Research Interest:
Skeletal muscle’s remarkable capacity to regenerate is dependent on precisely coordinated biochemical and physical cues. Satellite cells, fibroadipogenic progenitors, and endothelial cells must carefully orchestrate with inflammatory cells to properly repair muscle after injury. Severely damaged muscle, where the physical and geometric properties of the tissue have been disrupted by traumatic damage, are incapable of properly regenerating, which leads to severe functional deficiencies. The root cause of this failure is the lack of proper physical support normally provided by the structural scaffolding composed of muscular extracellular matrix proteins. As such, even if the cells required for regeneration are re-introduced to the site of injury, they fail to effectively respond to the damage. Thus, therapeutics designed to treat traumatic muscle injuries must consider not just the cellular elements of the regenerative paradigm, but also the biophysical properties of the tissue that we know to be critical to normal muscle physiology and recovery. My research interests lie in designing humanized models of traumatic skeletal muscle injury and biotherapeutics aimed at targeting the underlying structural damage and modulating the cellular responses to it. Critical to this will be the design of improved synthetic biocompatible scaffolds that imitate the spatial/temporal tissue dynamics that support healthy tissue regeneration. Another is the utilization of iPSCs and/or hESCs to improve the reliability and scalability of cell transplantations. The engineering of cells and their environments represent the future of therapeutics aimed at treating traumatic muscle injuries.
Personal Summary:
I am a graduate of the California State University system, where I double majored with a BSc in Cellular and Molecular Biology and a BA in French. I attended California Polytechnic State University as a Master’s student and completed my thesis work studying proteomic signatures of hormonally regulated growth in 2015. I spent two and half years training as a LSRA in Dr. Thomas Rando’s lab at Stanford under supervision of Marco Quarta PhD where I was introduced to the wonderful field of MuSC biology and bioengineering. In 2017, I moved to Vancouver and began working with Dr. Fabio at the University of British Columbia as a research technician, where I oversaw operation of the CyTOF2 mass cytometer. In 2020, I entered into the School of Biomedical Engineering’s PhD program at UBC, where I will study barrier function in intercellular communication networks during tissue regeneration.
Selected Publications:
Bosiljcic M, Cederberg RA, Hamilton, MJ, Harbourne BT, LePard NE, Franks ES, Halvorsen EC, Kim AY, Banath, JP, Collier JL, Hamer M, Rossi FM, Bennewith KL. Targeting MDSCs in combination with primary mammary tumor resection reduces metastatic growth in the lungs. Breast Cancer Research (2019) DOI: 10.1186/s13058-019-1189
Judson RN, Quarta M, Oudhoff M, Soliman H, Yi L, Chang CK, Lou G, Vander Werff R, Hamer M, Blonigan J, Paine P, Doan L Grippa E, He W, Zhang R, Xu P, Eisner C, Low M, Barta A, Lewis C, Zaph C, Karimi MM, Rando T, Rossi F. Inhibition of methyltransferase Setd7 allows the in vitro expansion of myogenic stem cells with improved therapeutic potential. Cell Stem Cell (2018) DOI: 10.1016/j.stem.2017.12.010
Quarta M, Cromie M, Chacon R, Blonigan J, Garcia V, Akimenko I, Hamer M, Paine P, Stok M., Shrager JB, Rando TA. Bioengineered constructs combined with exercise enhance stem cell-mediated treatment of volumetric muscle loss. Nature Communications (2017) DOI: 10.1038/ncomms15613
Skeletal muscle’s remarkable capacity to regenerate is dependent on precisely coordinated biochemical and physical cues. Satellite cells, fibroadipogenic progenitors, and endothelial cells must carefully orchestrate with inflammatory cells to properly repair muscle after injury. Severely damaged muscle, where the physical and geometric properties of the tissue have been disrupted by traumatic damage, are incapable of properly regenerating, which leads to severe functional deficiencies. The root cause of this failure is the lack of proper physical support normally provided by the structural scaffolding composed of muscular extracellular matrix proteins. As such, even if the cells required for regeneration are re-introduced to the site of injury, they fail to effectively respond to the damage. Thus, therapeutics designed to treat traumatic muscle injuries must consider not just the cellular elements of the regenerative paradigm, but also the biophysical properties of the tissue that we know to be critical to normal muscle physiology and recovery. My research interests lie in designing humanized models of traumatic skeletal muscle injury and biotherapeutics aimed at targeting the underlying structural damage and modulating the cellular responses to it. Critical to this will be the design of improved synthetic biocompatible scaffolds that imitate the spatial/temporal tissue dynamics that support healthy tissue regeneration. Another is the utilization of iPSCs and/or hESCs to improve the reliability and scalability of cell transplantations. The engineering of cells and their environments represent the future of therapeutics aimed at treating traumatic muscle injuries.
Personal Summary:
I am a graduate of the California State University system, where I double majored with a BSc in Cellular and Molecular Biology and a BA in French. I attended California Polytechnic State University as a Master’s student and completed my thesis work studying proteomic signatures of hormonally regulated growth in 2015. I spent two and half years training as a LSRA in Dr. Thomas Rando’s lab at Stanford under supervision of Marco Quarta PhD where I was introduced to the wonderful field of MuSC biology and bioengineering. In 2017, I moved to Vancouver and began working with Dr. Fabio at the University of British Columbia as a research technician, where I oversaw operation of the CyTOF2 mass cytometer. In 2020, I entered into the School of Biomedical Engineering’s PhD program at UBC, where I will study barrier function in intercellular communication networks during tissue regeneration.
Selected Publications:
Bosiljcic M, Cederberg RA, Hamilton, MJ, Harbourne BT, LePard NE, Franks ES, Halvorsen EC, Kim AY, Banath, JP, Collier JL, Hamer M, Rossi FM, Bennewith KL. Targeting MDSCs in combination with primary mammary tumor resection reduces metastatic growth in the lungs. Breast Cancer Research (2019) DOI: 10.1186/s13058-019-1189
Judson RN, Quarta M, Oudhoff M, Soliman H, Yi L, Chang CK, Lou G, Vander Werff R, Hamer M, Blonigan J, Paine P, Doan L Grippa E, He W, Zhang R, Xu P, Eisner C, Low M, Barta A, Lewis C, Zaph C, Karimi MM, Rando T, Rossi F. Inhibition of methyltransferase Setd7 allows the in vitro expansion of myogenic stem cells with improved therapeutic potential. Cell Stem Cell (2018) DOI: 10.1016/j.stem.2017.12.010
Quarta M, Cromie M, Chacon R, Blonigan J, Garcia V, Akimenko I, Hamer M, Paine P, Stok M., Shrager JB, Rando TA. Bioengineered constructs combined with exercise enhance stem cell-mediated treatment of volumetric muscle loss. Nature Communications (2017) DOI: 10.1038/ncomms15613