While diseases such as cancer and diabetes, or surgery and traumatic injury can cause hypoxia through a decrease in blood circulation to bodily regions or decrease cardiac output they can also associate with hypoxia-induced pain. Clinically, opioids, such as morphine, are used to modulate pain. The mu-opioid receptors (MORs) are one of three main types of opioid receptors and are key mediators in morphine-induced analgesia. Therefore, in this study, the effect of hypoxia on MOR gene expression was examined using human neuronal cells treated with DFO to create a hypoxic-mimic condition. We found that MOR expression was shown to decrease over increased exposure times to DFO. Recently, our laboratory reported that receptor associated C kinase (RACK-1), interacting with the transcription regulator Poly C Binding Protein (PCBP-1), can negatively regulate MOR gene expression using a yeast two-hybrid screening system. RT-PCR analysis revealed an increased in RACK-1 expression while a decrease in MOR expression under DFO treatment was observed. These results supported our recent finding that RACK-1 participates in the regulation of MOR expression. Neuronal cells surviving the DFO insult also displayed activation of the JAK/STAT pathway through Western blot analysis. Due to activation, the suppressors of cytokine signaling (SOCS) proteins, negative regulators of the JAK/STAT pathway, were investigated and detected via RT-PCR. These results suggest that there is an up-regulation of the SOCS proteins under hypoxia, and it may play a role in a form of neuroprotection by aiding in the decrease of inflammation associated with the JAK/STAT pathway.
","abstract_html":"<p>While diseases such as cancer and diabetes, or surgery and traumatic injury can cause hypoxia through a decrease in blood circulation to bodily regions or decrease cardiac output they can also associate with hypoxia-induced pain. Clinically, opioids, such as morphine, are used to modulate pain. The mu-opioid receptors (MORs) are one of three main types of opioid receptors and are key mediators in morphine-induced analgesia. Therefore, in this study, the effect of hypoxia on MOR gene expression was examined using human neuronal cells treated with DFO to create a hypoxic-mimic condition. We found that MOR expression was shown to decrease over increased exposure times to DFO. Recently, our laboratory reported that receptor associated C kinase (RACK-1), interacting with the transcription regulator Poly C Binding Protein (PCBP-1), can negatively regulate MOR gene expression using a yeast two-hybrid screening system. RT-PCR analysis revealed an increased in RACK-1 expression while a decrease in MOR expression under DFO treatment was observed. These results supported our recent finding that RACK-1 participates in the regulation of MOR expression. Neuronal cells surviving the DFO insult also displayed activation of the JAK/STAT pathway through Western blot analysis. Due to activation, the suppressors of cytokine signaling (SOCS) proteins, negative regulators of the JAK/STAT pathway, were investigated and detected via RT-PCR. These results suggest that there is an up-regulation of the SOCS proteins under hypoxia, and it may play a role in a form of neuroprotection by aiding in the decrease of inflammation associated with the JAK/STAT pathway.</p>","abstract_has_math":false,"creators":["Candelora, Jennifer"],"institution":null,"degree_name":"MS Biology","degree_level":"Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Jane L. Ko, PhD","Constantine Bitsaktsis, PhD","Jessica Cottrell, PhD"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-07-01T07:00:00Z","date_published":"2014-07-01T07:00:00Z","updated_at":"2026-07-24T04:32:52Z","subjects":["DFO","hyoxia","MOR","SOCS","Medicine and Health Sciences","Neuroscience and Neurobiology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarship.shu.edu/dissertations/1982","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Jane L. Ko, PhD","Constantine Bitsaktsis, PhD","Jessica Cottrell, PhD"]},{"key":"dc:creator","label":"Author","values":["Candelora, Jennifer"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2014-06-30T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["MS Biology"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["DFO","hyoxia","MOR","SOCS","Medicine and Health Sciences","Neuroscience and Neurobiology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarship.shu.edu/dissertations/1982"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["While diseases such as cancer and diabetes, or surgery and traumatic injury can cause hypoxia through a decrease in blood circulation to bodily regions or decrease cardiac output they can also associate with hypoxia-induced pain. Clinically, opioids, such as morphine, are used to modulate pain. The mu-opioid receptors (MORs) are one of three main types of opioid receptors and are key mediators in morphine-induced analgesia. Therefore, in this study, the effect of hypoxia on MOR gene expression was examined using human neuronal cells treated with DFO to create a hypoxic-mimic condition. We found that MOR expression was shown to decrease over increased exposure times to DFO. Recently, our laboratory reported that receptor associated C kinase (RACK-1), interacting with the transcription regulator Poly C Binding Protein (PCBP-1), can negatively regulate MOR gene expression using a yeast two-hybrid screening system. RT-PCR analysis revealed an increased in RACK-1 expression while a decrease in MOR expression under DFO treatment was observed. These results supported our recent finding that RACK-1 participates in the regulation of MOR expression. Neuronal cells surviving the DFO insult also displayed activation of the JAK/STAT pathway through Western blot analysis. Due to activation, the suppressors of cytokine signaling (SOCS) proteins, negative regulators of the JAK/STAT pathway, were investigated and detected via RT-PCR. These results suggest that there is an up-regulation of the SOCS proteins under hypoxia, and it may play a role in a form of neuroprotection by aiding in the decrease of inflammation associated with the JAK/STAT pathway.
"]},{"key":"dc:title","label":"Title","values":["Effects of DFO-Induced Hypoxia on Key Signaling Mediators"]}]}],"canonical_facts":{"dc:contributor":["Jane L. Ko, PhD","Constantine Bitsaktsis, PhD","Jessica Cottrell, PhD"],"dc:creator":["Candelora, Jennifer"],"dc:date.available":["2014-06-30T07:00:00Z"],"dc:description.abstract":["While diseases such as cancer and diabetes, or surgery and traumatic injury can cause hypoxia through a decrease in blood circulation to bodily regions or decrease cardiac output they can also associate with hypoxia-induced pain. Clinically, opioids, such as morphine, are used to modulate pain. The mu-opioid receptors (MORs) are one of three main types of opioid receptors and are key mediators in morphine-induced analgesia. Therefore, in this study, the effect of hypoxia on MOR gene expression was examined using human neuronal cells treated with DFO to create a hypoxic-mimic condition. We found that MOR expression was shown to decrease over increased exposure times to DFO. Recently, our laboratory reported that receptor associated C kinase (RACK-1), interacting with the transcription regulator Poly C Binding Protein (PCBP-1), can negatively regulate MOR gene expression using a yeast two-hybrid screening system. RT-PCR analysis revealed an increased in RACK-1 expression while a decrease in MOR expression under DFO treatment was observed. These results supported our recent finding that RACK-1 participates in the regulation of MOR expression. Neuronal cells surviving the DFO insult also displayed activation of the JAK/STAT pathway through Western blot analysis. Due to activation, the suppressors of cytokine signaling (SOCS) proteins, negative regulators of the JAK/STAT pathway, were investigated and detected via RT-PCR. These results suggest that there is an up-regulation of the SOCS proteins under hypoxia, and it may play a role in a form of neuroprotection by aiding in the decrease of inflammation associated with the JAK/STAT pathway.
"],"dc:identifier":["https://scholarship.shu.edu/dissertations/1982"],"dc:subject":["DFO","hyoxia","MOR","SOCS","Medicine and Health Sciences","Neuroscience and Neurobiology"],"dc:title":["Effects of DFO-Induced Hypoxia on Key Signaling Mediators"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["MS Biology"]},"updated_at":"2026-07-24T04:32:52Z"}