{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/90721"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/90721","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"THE EFFECT OF SDF1α ON SKELETAL MUSCLE REGENERATION AFTER COMPARTMENT SYNDROME INJURY","abstract":"Introduction: Skeletal muscle dysfunction, whether due to injury, disease or age, can be debilitating to normal life. There are few effective treatments for severe skeletal muscle injuries. SDF1α is a chemokine which promotes migration of stem cells through binding to the CXCR4 receptor and has been suggested to enhance tissue vascularization. In this preliminary study, we tested the effects of SDF1α treatment on the recovery of skeletal muscle function and tissue morphology in a rat compartment syndrome (CS) injury model. We have previously demonstrated that this model causes damage to muscular, vascular, and neural compartments as seen in patients[1]. Materials and Methods: Male Lewis rats (~12 months of age) were injured as previously described [1] and divided into either SDF1α , saline , SC treatment with SDF1α, or SC treatment groups. Three days after injury, SDF1α (50 μL - 100ng/animal) , saline , SC treatment with SDF1α , or SC treatment was injected into the injured tibialis anterior (TA) muscle. In vivo muscle function (isometric torque) was determined prior to injury and 7 and 14 days after injury via stimulation of the peroneal nerve. Histological assessments and qPCR were used to determine the tissue and molecular effects of SDF1α treatment. Results: Our data showed that SDF1α treatment resulted in no statistical significance for muscle function, fibrosis, regenerating myofibers, vascularization, or qPCR, but found significance in degenerating myofibers and GFP positive myofibers in SDF1α group . Conclusion: In conclusion, we found no statistical significance in muscle function, fibrosis, vascularization, or qPCR, but f ound significance in degenerating myofibers and GFP positive myofibers in SDF1α group. More experiments will need to be done to confirm these findings.","abstract_html":"Introduction: Skeletal muscle dysfunction, whether due to injury, disease or age, can be debilitating to normal life. There are few effective treatments for severe skeletal muscle injuries. SDF1α is a chemokine which promotes migration of stem cells through binding to the CXCR4 receptor and has been suggested to enhance tissue vascularization. In this preliminary study, we tested the effects of SDF1α treatment on the recovery of skeletal muscle function and tissue morphology in a rat compartment syndrome (CS) injury model. We have previously demonstrated that this model causes damage to muscular, vascular, and neural compartments as seen in patients[1]. Materials and Methods: Male Lewis rats (~12 months of age) were injured as previously described [1] and divided into either SDF1α , saline , SC treatment with SDF1α, or SC treatment groups. Three days after injury, SDF1α (50 μL - 100ng/animal) , saline , SC treatment with SDF1α , or SC treatment was injected into the injured tibialis anterior (TA) muscle. In vivo muscle function (isometric torque) was determined prior to injury and 7 and 14 days after injury via stimulation of the peroneal nerve. Histological assessments and qPCR were used to determine the tissue and molecular effects of SDF1α treatment. Results: Our data showed that SDF1α treatment resulted in no statistical significance for muscle function, fibrosis, regenerating myofibers, vascularization, or qPCR, but found significance in degenerating myofibers and GFP positive myofibers in SDF1α group . Conclusion: In conclusion, we found no statistical significance in muscle function, fibrosis, vascularization, or qPCR, but f ound significance in degenerating myofibers and GFP positive myofibers in SDF1α group. More experiments will need to be done to confirm these findings.","abstract_has_math":false,"creators":["Moschouris, Kathryn Elizabeth"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018","date_published":"2018","updated_at":"2026-07-27T22:02:17Z","subjects":["Compartment Syndrome"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/90721","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Moschouris, Kathryn Elizabeth"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2018-05-24T08:36:07Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2019-05-23T08:30:12Z"]},{"key":"dc:date.issued","label":"Date","values":["2018"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Compartment Syndrome"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/90721"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Introduction: Skeletal muscle dysfunction, whether due to injury, disease or age, can be debilitating to normal life. There are few effective treatments for severe skeletal muscle injuries. SDF1α is a chemokine which promotes migration of stem cells through binding to the CXCR4 receptor and has been suggested to enhance tissue vascularization. In this preliminary study, we tested the effects of SDF1α treatment on the recovery of skeletal muscle function and tissue morphology in a rat compartment syndrome (CS) injury model. We have previously demonstrated that this model causes damage to muscular, vascular, and neural compartments as seen in patients[1]. Materials and Methods: Male Lewis rats (~12 months of age) were injured as previously described [1] and divided into either SDF1α , saline , SC treatment with SDF1α, or SC treatment groups. Three days after injury, SDF1α (50 μL - 100ng/animal) , saline , SC treatment with SDF1α , or SC treatment was injected into the injured tibialis anterior (TA) muscle. In vivo muscle function (isometric torque) was determined prior to injury and 7 and 14 days after injury via stimulation of the peroneal nerve. Histological assessments and qPCR were used to determine the tissue and molecular effects of SDF1α treatment. Results: Our data showed that SDF1α treatment resulted in no statistical significance for muscle function, fibrosis, regenerating myofibers, vascularization, or qPCR, but found significance in degenerating myofibers and GFP positive myofibers in SDF1α group . Conclusion: In conclusion, we found no statistical significance in muscle function, fibrosis, vascularization, or qPCR, but f ound significance in degenerating myofibers and GFP positive myofibers in SDF1α group. More experiments will need to be done to confirm these findings."]},{"key":"dc:title","label":"Title","values":["THE EFFECT OF SDF1α ON SKELETAL MUSCLE REGENERATION AFTER COMPARTMENT SYNDROME INJURY"]}]}],"canonical_facts":{"dc:creator":["Moschouris, Kathryn Elizabeth"],"dc:date.accessioned":["2018-05-24T08:36:07Z"],"dc:date.available":["2019-05-23T08:30:12Z"],"dc:date.issued":["2018"],"dc:description.abstract":["Introduction: Skeletal muscle dysfunction, whether due to injury, disease or age, can be debilitating to normal life. There are few effective treatments for severe skeletal muscle injuries. SDF1α is a chemokine which promotes migration of stem cells through binding to the CXCR4 receptor and has been suggested to enhance tissue vascularization. In this preliminary study, we tested the effects of SDF1α treatment on the recovery of skeletal muscle function and tissue morphology in a rat compartment syndrome (CS) injury model. We have previously demonstrated that this model causes damage to muscular, vascular, and neural compartments as seen in patients[1]. Materials and Methods: Male Lewis rats (~12 months of age) were injured as previously described [1] and divided into either SDF1α , saline , SC treatment with SDF1α, or SC treatment groups. Three days after injury, SDF1α (50 μL - 100ng/animal) , saline , SC treatment with SDF1α , or SC treatment was injected into the injured tibialis anterior (TA) muscle. In vivo muscle function (isometric torque) was determined prior to injury and 7 and 14 days after injury via stimulation of the peroneal nerve. Histological assessments and qPCR were used to determine the tissue and molecular effects of SDF1α treatment. Results: Our data showed that SDF1α treatment resulted in no statistical significance for muscle function, fibrosis, regenerating myofibers, vascularization, or qPCR, but found significance in degenerating myofibers and GFP positive myofibers in SDF1α group . Conclusion: In conclusion, we found no statistical significance in muscle function, fibrosis, vascularization, or qPCR, but f ound significance in degenerating myofibers and GFP positive myofibers in SDF1α group. More experiments will need to be done to confirm these findings."],"dc:identifier.uri":["http://hdl.handle.net/10339/90721"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:subject":["Compartment Syndrome"],"dc:title":["THE EFFECT OF SDF1α ON SKELETAL MUSCLE REGENERATION AFTER COMPARTMENT SYNDROME INJURY"],"dc:type":["Thesis"]},"updated_at":"2026-07-27T22:02:17Z"}