{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T18:59:29Z","timestamp":1785437969587,"version":"3.56.0"},"posted":{"date-parts":[[2025,10,6]]},"group-title":"Cell Biology","reference-count":110,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,10,6]],"date-time":"2025-10-06T00:00:00Z","timestamp":1759708800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["R35NS111582"],"award-info":[{"award-number":["R35NS111582"]}],"id":[{"id":"https:\/\/ror.org\/01s5ya894","id-type":"ROR","asserted-by":"publisher"}]},{"name":"The Ray W Poppleton Endowment"},{"award":["NS105864"],"award-info":[{"award-number":["NS105864"]}],"id":[{"id":"https:\/\/ror.org\/01s5ya894","id-type":"ROR","asserted-by":"publisher"}]},{"award":["Presidential Fellowship"],"award-info":[{"award-number":["Presidential Fellowship"]}],"id":[{"id":"https:\/\/ror.org\/00rs6vg23","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Spinal cord injury (SCI) triggers systemic pathology beyond the nervous system, including bone marrow failure that can worsen infection risk, anemia, and motor recovery. Here we identify a neuroendocrine mechanism that rapidly imprints long-lasting dysfunction in hematopoietic stem cells (HSCs), which sustain lifelong production of immune cells, red blood cells, and platelets. Rather than mounting a canonical stress-hematopoietic response, SCI HSCs enter a broadly repressed state marked by chromatin closure and suppression of programs required for cell-cycle entry, genome maintenance, and redox defense. This maladaptive state leads to persistent DNA damage, impaired oxidative stress resolution, pancytopenia, and loss of long-term HSC regenerative capacity. Mechanistically, SCI-induced glucocorticoid surges drive glucocorticoid receptor-dependent repression of DNA repair genes, including\n                  <jats:italic>Lig1<\/jats:italic>\n                  and\n                  <jats:italic>Fen1<\/jats:italic>\n                  . Acute glucocorticoid receptor blockade after SCI restores durable hematopoiesis, revealing an early therapeutic window to preserve hematopoietic integrity after neurotrauma.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Graphical abstract<\/jats:title>\n                  <jats:fig id=\"ufig1\" position=\"float\" orientation=\"portrait\" fig-type=\"figure\">\n                    <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"680535v2_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                  <\/jats:fig>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Key Findings<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>Acute SCI prevents induction of normal stress-induced repair programs in HSCs.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>SCI HSPCs exhibit increased chromatin compaction.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>SCI compromises HSC genome-maintenance and redox capabilities.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>SCI HSCs have defects in normal cell cycle regulation, are hypersensitive to genotoxic stress, and are deficient in long-term reconstitution.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>Early glucocorticoid receptor (GR) blockade restores long-term hematopoiesis, supporting a GR-dependent but reversible repression mechanism.<\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                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