Peripheral artery disease (PAD) is characterized by the development of atherosclerotic plaques on arterial walls, leading to the narrowing of blood vessels, resulting in ischemia in the downstream tissue. In the United States, 12% of the adult population is affected by PAD and its related symptoms. Current surgical revascularization techniques can be effective in part of the patient population, but there is a need for other options. Alternatively, collateral blood vessels, or natural bypass arteries, enlarge to increase blood flow to the ischemic tissue in a process called arteriogenesis, which has been studied as a therapeutic option. Cell-based therapies, such as BM-MNCs, have been investigated as means to enhance arteriogenesis, but have largely failed in clinical trials. An alternative cell-based therapy candidate are myoblasts, or muscle progenitor cells. Myoblasts increase arteriogenesis in murine models and are known to interact with macrophages, which are immune cells that are primary regulators of arteriogenesis. Macrophages can polarize to inflammatory (M1) and regenerative (M2) phenotypes, with the M2 phenotype promoting enhanced arteriogenesis. This interaction suggests that myoblasts may be signaling macrophage polarization to enhance arteriogenesis. The purpose of this study was to determine if myoblasts in vitro can affect macrophage polarization into inflammatory (M1) or regenerative (M2) phenotypes. Protocols for macrophage culture and polarization were implemented, and then macrophages were co-cultured with myoblasts for 24 hours to assess the effects in vitro. Concentrations of known inflammatory (TNF-a) and regenerative (IL-10) cytokines released by macrophages were measured after co-culture with myoblasts. Surprisingly, macrophages co-cultured with myoblasts showed a decrease in both TNF-a and IL-10 compared to macrophages cultured alone. Morphology changes of macrophages were also measured after co-culture, with, surprisingly, little difference in the groups co-cultured with myoblasts. Pilot experiments suggest there may be an initial lag time greater than 24 hours for myoblasts to affect macrophage phenotype. Future work ideally will include longer time points and optimizing viability and proliferation of myoblasts in co-culture settings.
","abstract_html":"<p>Peripheral artery disease (PAD) is characterized by the development of atherosclerotic plaques on arterial walls, leading to the narrowing of blood vessels, resulting in ischemia in the downstream tissue. In the United States, 12% of the adult population is affected by PAD and its related symptoms. Current surgical revascularization techniques can be effective in part of the patient population, but there is a need for other options. Alternatively, collateral blood vessels, or natural bypass arteries, enlarge to increase blood flow to the ischemic tissue in a process called arteriogenesis, which has been studied as a therapeutic option. Cell-based therapies, such as BM-MNCs, have been investigated as means to enhance arteriogenesis, but have largely failed in clinical trials. An alternative cell-based therapy candidate are myoblasts, or muscle progenitor cells. Myoblasts increase arteriogenesis in murine models and are known to interact with macrophages, which are immune cells that are primary regulators of arteriogenesis. Macrophages can polarize to inflammatory (M1) and regenerative (M2) phenotypes, with the M2 phenotype promoting enhanced arteriogenesis. This interaction suggests that myoblasts may be signaling macrophage polarization to enhance arteriogenesis. The purpose of this study was to determine if myoblasts in vitro can affect macrophage polarization into inflammatory (M1) or regenerative (M2) phenotypes. Protocols for macrophage culture and polarization were implemented, and then macrophages were co-cultured with myoblasts for 24 hours to assess the effects in vitro. Concentrations of known inflammatory (TNF-a) and regenerative (IL-10) cytokines released by macrophages were measured after co-culture with myoblasts. Surprisingly, macrophages co-cultured with myoblasts showed a decrease in both TNF-a and IL-10 compared to macrophages cultured alone. Morphology changes of macrophages were also measured after co-culture, with, surprisingly, little difference in the groups co-cultured with myoblasts. Pilot experiments suggest there may be an initial lag time greater than 24 hours for myoblasts to affect macrophage phenotype. Future work ideally will include longer time points and optimizing viability and proliferation of myoblasts in co-culture settings.</p>","abstract_has_math":false,"creators":["Welch, Olivia"],"institution":null,"degree_name":"MS in Biomedical Engineering","degree_level":null,"degree_discipline":"Biomedical Engineering","degree_department":null,"school":null,"contributors":["Trevor Cardinal","Biomedical Engineering","College of Engineering"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2022,"date_issued":"2022-03-01T08:00:00Z","date_published":"2022-03-01T08:00:00Z","updated_at":"2026-07-24T01:32:37Z","subjects":["Ischemia","Arteriogenesis","Macrophages","Polarization","Myoblasts","Cell Therapy","Biomedical Engineering and Bioengineering"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["10.15368/theses.2022.24"],"render_values":[{"text":"10.15368/theses.2022.24","href":"https://doi.org/10.15368/theses.2022.24","code":true}]}]},"links":{"outbound_url":"https://digitalcommons.calpoly.edu/theses/2631","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Trevor Cardinal","Biomedical Engineering","College of Engineering"]},{"key":"dc:creator","label":"Author","values":["Welch, Olivia"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2022-04-12T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Engineering"]},{"key":"thesis:degree_name","label":"Degree Name","values":["MS in Biomedical Engineering"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Ischemia","Arteriogenesis","Macrophages","Polarization","Myoblasts","Cell Therapy","Biomedical Engineering and Bioengineering"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.calpoly.edu/theses/2631","10.15368/theses.2022.24"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Peripheral artery disease (PAD) is characterized by the development of atherosclerotic plaques on arterial walls, leading to the narrowing of blood vessels, resulting in ischemia in the downstream tissue. In the United States, 12% of the adult population is affected by PAD and its related symptoms. Current surgical revascularization techniques can be effective in part of the patient population, but there is a need for other options. Alternatively, collateral blood vessels, or natural bypass arteries, enlarge to increase blood flow to the ischemic tissue in a process called arteriogenesis, which has been studied as a therapeutic option. Cell-based therapies, such as BM-MNCs, have been investigated as means to enhance arteriogenesis, but have largely failed in clinical trials. An alternative cell-based therapy candidate are myoblasts, or muscle progenitor cells. Myoblasts increase arteriogenesis in murine models and are known to interact with macrophages, which are immune cells that are primary regulators of arteriogenesis. Macrophages can polarize to inflammatory (M1) and regenerative (M2) phenotypes, with the M2 phenotype promoting enhanced arteriogenesis. This interaction suggests that myoblasts may be signaling macrophage polarization to enhance arteriogenesis. The purpose of this study was to determine if myoblasts in vitro can affect macrophage polarization into inflammatory (M1) or regenerative (M2) phenotypes. Protocols for macrophage culture and polarization were implemented, and then macrophages were co-cultured with myoblasts for 24 hours to assess the effects in vitro. Concentrations of known inflammatory (TNF-a) and regenerative (IL-10) cytokines released by macrophages were measured after co-culture with myoblasts. Surprisingly, macrophages co-cultured with myoblasts showed a decrease in both TNF-a and IL-10 compared to macrophages cultured alone. Morphology changes of macrophages were also measured after co-culture, with, surprisingly, little difference in the groups co-cultured with myoblasts. Pilot experiments suggest there may be an initial lag time greater than 24 hours for myoblasts to affect macrophage phenotype. Future work ideally will include longer time points and optimizing viability and proliferation of myoblasts in co-culture settings.
"]},{"key":"dc:title","label":"Title","values":["Impact of Primary Myoblasts on Macrophage Polarization In-Vitro"]}]}],"canonical_facts":{"dc:contributor":["Trevor Cardinal","Biomedical Engineering","College of Engineering"],"dc:creator":["Welch, Olivia"],"dc:date.available":["2022-04-12T07:00:00Z"],"dc:description.abstract":["Peripheral artery disease (PAD) is characterized by the development of atherosclerotic plaques on arterial walls, leading to the narrowing of blood vessels, resulting in ischemia in the downstream tissue. In the United States, 12% of the adult population is affected by PAD and its related symptoms. Current surgical revascularization techniques can be effective in part of the patient population, but there is a need for other options. Alternatively, collateral blood vessels, or natural bypass arteries, enlarge to increase blood flow to the ischemic tissue in a process called arteriogenesis, which has been studied as a therapeutic option. Cell-based therapies, such as BM-MNCs, have been investigated as means to enhance arteriogenesis, but have largely failed in clinical trials. An alternative cell-based therapy candidate are myoblasts, or muscle progenitor cells. Myoblasts increase arteriogenesis in murine models and are known to interact with macrophages, which are immune cells that are primary regulators of arteriogenesis. Macrophages can polarize to inflammatory (M1) and regenerative (M2) phenotypes, with the M2 phenotype promoting enhanced arteriogenesis. This interaction suggests that myoblasts may be signaling macrophage polarization to enhance arteriogenesis. The purpose of this study was to determine if myoblasts in vitro can affect macrophage polarization into inflammatory (M1) or regenerative (M2) phenotypes. Protocols for macrophage culture and polarization were implemented, and then macrophages were co-cultured with myoblasts for 24 hours to assess the effects in vitro. Concentrations of known inflammatory (TNF-a) and regenerative (IL-10) cytokines released by macrophages were measured after co-culture with myoblasts. Surprisingly, macrophages co-cultured with myoblasts showed a decrease in both TNF-a and IL-10 compared to macrophages cultured alone. Morphology changes of macrophages were also measured after co-culture, with, surprisingly, little difference in the groups co-cultured with myoblasts. Pilot experiments suggest there may be an initial lag time greater than 24 hours for myoblasts to affect macrophage phenotype. Future work ideally will include longer time points and optimizing viability and proliferation of myoblasts in co-culture settings.
"],"dc:identifier":["https://digitalcommons.calpoly.edu/theses/2631","10.15368/theses.2022.24"],"dc:subject":["Ischemia","Arteriogenesis","Macrophages","Polarization","Myoblasts","Cell Therapy","Biomedical Engineering and Bioengineering"],"dc:title":["Impact of Primary Myoblasts on Macrophage Polarization In-Vitro"],"thesis:degree_discipline":["Biomedical Engineering"],"thesis:degree_name":["MS in Biomedical Engineering"]},"updated_at":"2026-07-24T01:32:37Z"}