{"id":{"repo_id":"calpoly","oai_identifier":"oai:digitalcommons.calpoly.edu:theses-2556"},"canonical_url":"https://search.dev.ndltd.org/etd/calpoly/oai:digitalcommons.calpoly.edu:theses-2556","repository":{"repo_id":"calpoly","name":"Cal Poly","base_url":"https://digitalcommons.calpoly.edu/do/oai/"},"display":{"title":"The Use of Sphingomyelin to Protect Against UV Induced DNA Damage in Human Keratinocytes","abstract":"<p>Non melanoma skin cancer (NMSC) is a serious condition caused by chronic ultraviolet (UV) exposure that leads to DNA damage in skin. UV radiation has the potential to lead to DNA damage, which triggers biochemical pathways within a cell. The result is that the cell either undergoes cell cycle arrest, giving the cell time to repair DNA damage, or apoptosis. Sunscreen is the most commonly used treatment for preventing UV induced skin damage, but it involves a number of undesirable and toxic side effects including damaging the dermis, premature aging of skin and underweight child births. This has led to interest in finding safer alternatives to prevent UV damage without the negative side effects of sunscreen. In particular, bovine milk sphingomyelin (SM) is a compound that has the potential to protect against UV damage without any of the dangerous side effects of sunscreen. Here we present the use of SM for UV protection of human keratinocytes (KRTs) to prevent DNA mutations that result from UV exposure. In particular, analysis of the expression of DNA damage biomarkers p21 and p53 was done to determine the potential of SM to prevent DNA damage associated with UV exposure. Both non-SM treated KRTs and KRTs treated with 0.1% SM media 24 hours prior to UV radiation were fixed and IF-stained at 24 hours following 40 mJ/cm<sup>2</sup> of UV exposure. Significant differences in both p21 and p53 were observed between the SM treated and non-SM treated cells at the UV dosage level (via t-test; p</p>","abstract_html":"&lt;p&gt;Non melanoma skin cancer (NMSC) is a serious condition caused by chronic ultraviolet (UV) exposure that leads to DNA damage in skin. UV radiation has the potential to lead to DNA damage, which triggers biochemical pathways within a cell. The result is that the cell either undergoes cell cycle arrest, giving the cell time to repair DNA damage, or apoptosis. Sunscreen is the most commonly used treatment for preventing UV induced skin damage, but it involves a number of undesirable and toxic side effects including damaging the dermis, premature aging of skin and underweight child births. This has led to interest in finding safer alternatives to prevent UV damage without the negative side effects of sunscreen. In particular, bovine milk sphingomyelin (SM) is a compound that has the potential to protect against UV damage without any of the dangerous side effects of sunscreen. Here we present the use of SM for UV protection of human keratinocytes (KRTs) to prevent DNA mutations that result from UV exposure. In particular, analysis of the expression of DNA damage biomarkers p21 and p53 was done to determine the potential of SM to prevent DNA damage associated with UV exposure. Both non-SM treated KRTs and KRTs treated with 0.1% SM media 24 hours prior to UV radiation were fixed and IF-stained at 24 hours following 40 mJ/cm&lt;sup&gt;2&lt;/sup&gt; of UV exposure. Significant differences in both p21 and p53 were observed between the SM treated and non-SM treated cells at the UV dosage level (via t-test; p&lt;/p&gt;","abstract_has_math":false,"creators":["Campbell, Kevin"],"institution":null,"degree_name":"MS in Biomedical Engineering","degree_level":null,"degree_discipline":"Biomedical and General Engineering","degree_department":null,"school":null,"contributors":["Lily Laiho"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-06-01T07:00:00Z","date_published":"2015-06-01T07:00:00Z","updated_at":"2026-07-24T01:32:42Z","subjects":["Keratinocytes","p21","p53","UV radiation","sphingomyelin","skin cancer"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["10.15368/theses.2015.72"],"render_values":[{"text":"10.15368/theses.2015.72","href":"https://doi.org/10.15368/theses.2015.72","code":true}]}]},"links":{"outbound_url":"https://digitalcommons.calpoly.edu/theses/1413","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Lily Laiho"]},{"key":"dc:creator","label":"Author","values":["Campbell, Kevin"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2015-06-12T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical and General 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":["Keratinocytes","p21","p53","UV radiation","sphingomyelin","skin cancer"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.calpoly.edu/theses/1413","10.15368/theses.2015.72"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p>Non melanoma skin cancer (NMSC) is a serious condition caused by chronic ultraviolet (UV) exposure that leads to DNA damage in skin. UV radiation has the potential to lead to DNA damage, which triggers biochemical pathways within a cell. The result is that the cell either undergoes cell cycle arrest, giving the cell time to repair DNA damage, or apoptosis. Sunscreen is the most commonly used treatment for preventing UV induced skin damage, but it involves a number of undesirable and toxic side effects including damaging the dermis, premature aging of skin and underweight child births. This has led to interest in finding safer alternatives to prevent UV damage without the negative side effects of sunscreen. In particular, bovine milk sphingomyelin (SM) is a compound that has the potential to protect against UV damage without any of the dangerous side effects of sunscreen. Here we present the use of SM for UV protection of human keratinocytes (KRTs) to prevent DNA mutations that result from UV exposure. In particular, analysis of the expression of DNA damage biomarkers p21 and p53 was done to determine the potential of SM to prevent DNA damage associated with UV exposure. Both non-SM treated KRTs and KRTs treated with 0.1% SM media 24 hours prior to UV radiation were fixed and IF-stained at 24 hours following 40 mJ/cm<sup>2</sup> of UV exposure. Significant differences in both p21 and p53 were observed between the SM treated and non-SM treated cells at the UV dosage level (via t-test; p</p>"]},{"key":"dc:title","label":"Title","values":["The Use of Sphingomyelin to Protect Against UV Induced DNA Damage in Human Keratinocytes"]}]}],"canonical_facts":{"dc:contributor":["Lily Laiho"],"dc:creator":["Campbell, Kevin"],"dc:date.available":["2015-06-12T07:00:00Z"],"dc:description.abstract":["<p>Non melanoma skin cancer (NMSC) is a serious condition caused by chronic ultraviolet (UV) exposure that leads to DNA damage in skin. UV radiation has the potential to lead to DNA damage, which triggers biochemical pathways within a cell. The result is that the cell either undergoes cell cycle arrest, giving the cell time to repair DNA damage, or apoptosis. Sunscreen is the most commonly used treatment for preventing UV induced skin damage, but it involves a number of undesirable and toxic side effects including damaging the dermis, premature aging of skin and underweight child births. This has led to interest in finding safer alternatives to prevent UV damage without the negative side effects of sunscreen. In particular, bovine milk sphingomyelin (SM) is a compound that has the potential to protect against UV damage without any of the dangerous side effects of sunscreen. Here we present the use of SM for UV protection of human keratinocytes (KRTs) to prevent DNA mutations that result from UV exposure. In particular, analysis of the expression of DNA damage biomarkers p21 and p53 was done to determine the potential of SM to prevent DNA damage associated with UV exposure. Both non-SM treated KRTs and KRTs treated with 0.1% SM media 24 hours prior to UV radiation were fixed and IF-stained at 24 hours following 40 mJ/cm<sup>2</sup> of UV exposure. Significant differences in both p21 and p53 were observed between the SM treated and non-SM treated cells at the UV dosage level (via t-test; p</p>"],"dc:identifier":["https://digitalcommons.calpoly.edu/theses/1413","10.15368/theses.2015.72"],"dc:subject":["Keratinocytes","p21","p53","UV radiation","sphingomyelin","skin cancer"],"dc:title":["The Use of Sphingomyelin to Protect Against UV Induced DNA Damage in Human Keratinocytes"],"thesis:degree_discipline":["Biomedical and General Engineering"],"thesis:degree_name":["MS in Biomedical Engineering"]},"updated_at":"2026-07-24T01:32:42Z"}