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We report herein that\n                    <jats:italic>Drosophila<\/jats:italic>\n                    adults exhibit a defective blood\u2013brain barrier, elevated innate immune responses, and astrocyte swelling upon consecutive strikes with a high-impact trauma device. RNA sequencing (RNA-seq) analysis of these astrocytes revealed upregulated expression of genes encoding PDGF and VEGF receptor-related (Pvr, a receptor tyrosine kinase), adaptor protein complex 1 (AP-1\n                    <jats:italic>,<\/jats:italic>\n                    a transcription factor complex of the c-Jun N-terminal kinase pathway) composed of Jun-related antigen (Jra) and kayak (kay), and matrix metalloproteinase 1 (Mmp1) following TBI. Interestingly, Pvr is both required and sufficient for AP-1 and Mmp1 upregulation, while knockdown of AP-1 expression in the background of Pvr overexpression in astrocytes rescued Mmp1 upregulation upon TBI, indicating that Pvr acts as the upstream receptor for the downstream AP-1\u2013Mmp1 transduction. Moreover, dynamin-associated endocytosis was found to be an important regulatory step in downregulating Pvr signaling. Our results identify a new Pvr\u2013AP-1\u2013Mmp1 signaling pathway in astrocytes in response to TBI, providing potential targets for developing new therapeutic strategies for TBI.\n                  <\/jats:p>","DOI":"10.7554\/elife.87258","type":"journal-article","created":{"date-parts":[[2023,6,13]],"date-time":"2023-06-13T08:23:56Z","timestamp":1686644636000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.87258","source":"Crossref","is-referenced-by-count":7,"title":["A Pvr\u2013AP-1\u2013Mmp1 signaling pathway is activated in astrocytes upon traumatic brain injury"],"prefix":"10.7554","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1309-036X","authenticated-orcid":true,"given":"Tingting","family":"Li","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02aee5m12","id-type":"ROR","asserted-by":"publisher"}],"name":"Key Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, University of Chinese 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