{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T02:15:10Z","timestamp":1793153710819,"version":"4.5.0"},"reference-count":76,"publisher":"American Spinal Injury Association","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objectives:<\/jats:title>\n                    <jats:p>The aim of this study was to determine whether circulating concentrations of activation- and apoptosis-derived endothelial cell-derived microvesicles (EMVs) differ between adults after subacute (time since injury \u22646 months) and chronic (time since injury &gt;12 months) spinal cord injury (SCI).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      Peripheral blood was collected from 43 adults (age range 18-71 years): 12 non-injured adults (9 male\/3 female), 16 adults with subacute cervical and high thoracic (C2-T3) motor complete injuries (13 male\/3 female; time since injury 1-3 months), and 15 adults with chronic cervical and high thoracic (C1-T2) motor complete injuries (14 male\/1 female; time since injury 12-52 months). EMVs were defined by markers of endothelial origin either by activation (CD62e\n                      <jats:sup>+<\/jats:sup>\n                      ) or apoptosis (CD31\n                      <jats:sup>+<\/jats:sup>\n                      \/CD42b\n                      <jats:sup>\u2212<\/jats:sup>\n                      ) by flow cytometry. Activation-derived but not apoptosis-derived EMVs were significantly higher (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; .05) in adults with chronic SCI (median [IQR], 139 [83-181] EMVs\/\u03bcL) compared with adults with subacute SCI (median [IQR], 99 [83-104] EMVs\/\u03bcL) and non-injured adults (median [IQR], 74 [51-104] EMVs\/\u03bcL). In contrast, apoptosis-derived but not activation-derived EMVs were significantly higher (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; .05) in adults with subacute SCI (mean \u00b1\n                      <jats:italic>SD<\/jats:italic>\n                      , 77 \u00b1 17 EMVs\/\u03bcL) compared with adults with chronic SCI (mean \u00b1\n                      <jats:italic>SD<\/jats:italic>\n                      , 55 \u00b1 19 EMVs\/\u03bcL) and non-injured adults (mean \u00b1\n                      <jats:italic>SD<\/jats:italic>\n                      , 52 \u00b1 25 EMVs\/\u03bcL). Differential expression of circulating EMVs in adults with SCI during the subacute and chronic phase of injury may represent a biomarker of the vascular environment associated with each condition. Our findings suggest that the vascular phenotype is markedly different in subacute compared with the chronic SCI and provide insight into endothelial function after SCI.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.46292\/sci24-00068","type":"journal-article","created":{"date-parts":[[2025,6,24]],"date-time":"2025-06-24T11:41:19Z","timestamp":1750765279000},"page":"29-38","source":"Crossref","is-referenced-by-count":2,"title":["Different Circulating Endothelial Microvesicle Subtype Signature in Subacute and Chronic Spinal Cord Injury"],"prefix":"10.46292","volume":"31","author":[{"given":"Andrew J.","family":"Park","sequence":"first","affiliation":[{"name":"Rocky Mountain Regional Spinal Injury System, Craig Hospital, Englewood, Colorado"},{"name":"University of Colorado, Department of Physical Medicine and Rehabilitation, Aurora, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah K.","family":"Fandl","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vinicius P.","family":"Garcia","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Auburn R.","family":"Berry","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kendra N.","family":"Wegerson","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily I.","family":"Ostrander","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah L.","family":"Cardenas","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noah M.","family":"DeSouza","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jared J.","family":"Greiner","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Stauffer","sequence":"additional","affiliation":[{"name":"Division of Cardiology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado"},{"name":"Division of Cardiology, Denver Health Medical Center, Denver, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher A.","family":"DeSouza","sequence":"additional","affiliation":[{"name":"Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"25425","reference":[{"issue":"7","key":"b1","series-title":"J Am Coll Cardiol","first-page":"741","article-title":"Increased risk of myocardial infarction, heart failure, and atrial fibrillation after spinal cord injury","volume":"83","author":"Yoo\n              JE","year":"2024","unstructured":"Yoo\n              JE\n            , KimM, KimB, et al. 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Increased risk of myocardial infarction, heart failure, and atrial fibrillation after spinal cord injury. J Am Coll Cardiol. 2024;83(7):741-751. doi:10.1016\/j.jacc.2023.12.010."},{"issue":"6","key":"b2","series-title":"Spinal Cord","first-page":"310","article-title":"The relationship between neurological level of injury and symptomatic cardiovascular disease risk in the aging spinal injured","volume":"39","author":"Groah\n              SL","year":"2001","unstructured":"Groah\n              SL\n            , WeitzenkampD, SettP, SoniB, SavicG. The relationship between neurological level of injury and symptomatic cardiovascular disease risk in the aging spinal injured. Spinal Cord. 2001;39(6):310-7. doi:10.1038\/sj.sc.3101162."},{"issue":"3","key":"b3","series-title":"Int Heart J","first-page":"325","article-title":"Evaluating the prevalence of silent coronary artery disease in asymptomatic patients with spinal cord injury","volume":"47","author":"Lee\n              CS","year":"2006","unstructured":"Lee\n              CS\n            , LuYH, LeeST, LinCC, DingHJ. Evaluating the prevalence of silent coronary artery disease in asymptomatic patients with spinal cord injury. Int Heart J. 2006;47(3):325-330. doi:10.1536\/ihj.47.325."},{"issue":"1","key":"b4","series-title":"Atherosclerosis","first-page":"29","article-title":"Carotid intima-media thickness is increased in patients with spinal cord injury independent of traditional cardiovascular risk factors","volume":"202","author":"Matos-Souza\n              JR","year":"2009","unstructured":"Matos-Souza\n              JR\n            , PithonKR, OzahataTM, et al. Carotid intima-media thickness is increased in patients with spinal cord injury independent of traditional cardiovascular risk factors. Atherosclerosis. 2009;202(1):29-31. doi:10.1016\/j.atherosclerosis.2008.04.013."},{"issue":"12","key":"b5","series-title":"Spinal Cord","first-page":"775","article-title":"Measurement of coronary artery calcification by electron beam computerized tomography in persons with chronic spinal cord injury: Evidence for increased atherosclerotic burden","volume":"45","author":"Orakzai\n              SH","year":"2007","unstructured":"Orakzai\n              SH\n            , OrakzaiRH, AhmadiN, et al. Measurement of coronary artery calcification by electron beam computerized tomography in persons with chronic spinal cord injury: Evidence for increased atherosclerotic burden. 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Association of circulating endothelial microparticles with cardiometabolic risk factors in the Framingham Heart Study. Eur Heart J. 2014;35(42):2972-2979. doi:10.1093\/eurheartj\/ehu153."},{"issue":"11","key":"b31","series-title":"Exp Physiol","first-page":"1560","article-title":"Type 2 diabetes and older age contribute to elevated plasma microparticle concentrations independent of chronic stroke","volume":"103","author":"Landers-Ramos\n              RQ","year":"2018","unstructured":"Landers-Ramos\n              RQ\n            , SerraMC, BlumenthalJB, RyanAS, Hafer-MackoCE, PriorSJ. Type 2 diabetes and older age contribute to elevated plasma microparticle concentrations independent of chronic stroke. 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