{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T02:05:12Z","timestamp":1784081112283,"version":"3.55.0"},"reference-count":14,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T00:00:00Z","timestamp":1784073600000},"content-version":"vor","delay-in-days":54,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"name":"Y\u0131ld\u0131z Technical University"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Inflammation"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Infectious diseases exacerbate atherosclerosis-associated morbidity and mortality by inducing sustained inflammatory responses characterized by elevated IL-6, TNF-\u03b1, IFN-\u03b3, and CXCL10. Persistent CXCL10-driven recruitment of CXCR3\u207a immune cells promotes endothelial dysfunction and atherosclerotic progression. Although mesenchymal stem cells (MSCs) respond to inflammatory cues and secrete CXCL10, the contribution of CXCL10\/CXCR3 signaling to intrinsic MSC immunomodulatory programming remains poorly understood. The objective of this study is to investigate whether CXCL10 signaling can modulate MSC-mediated immunoregulation. To address this, Wharton\u2019s jelly\u2013derived MSCs (WJ-MSCs) were genetically engineered to express a membrane-anchored CXCL10\u2013Lactadherin C1\/C2 fusion protein (CXCL10-LACTC1\/C2). This strategy was designed to recapitulate physiological, localized, and sustained CXCL10 signaling, enabling spatially restricted chemokine presentation that more closely mimics cell-associated CXCL10 in inflammatory microenvironments compared with soluble CXCL10. The Lactadherin C1\/C2 domain was selected to achieve stable, physiological membrane anchoring without introducing artificial transmembrane domains or compromising CXCL10 bioactivity. CXCL10-LACTC1\/C2\u2013expressing MSCs exhibited increased expression of key immunoregulatory mediators, including IDO1, TGF-\u03b21, and IL4I1. Furthermore, conditioned medium derived from these MSCs attenuated TNF-\u03b1\u2013induced inflammatory responses in human umbilical vein endothelial cells (HUVECs), as indicated by the modulation of endothelial activation and homeostasis markers (ICAM-1, PECAM-1, KDR, vWF, and NRF2) and improvement of cell viability. Collectively, these findings provide mechanistic insight into CXCL10-mediated MSC immunoregulation and support further investigation of MSC-based and cell-free therapeutic strategies aimed at mitigating CXCL10-driven endothelial inflammation in infection-associated vascular injury and atherosclerotic disease progression.<\/jats:p>","DOI":"10.1007\/s10753-026-02518-2","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T05:44:26Z","timestamp":1779428666000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CXCL10-LACTC1\/C2 Expressing Mesenchymal Stem Cell Conditioned Medium Attenuates TNF-\u03b1-Induced Gene Expressions and Cell Viability in HUVECs"],"prefix":"10.1007","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6168-2058","authenticated-orcid":false,"given":"Kaya","family":"Molo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-2504-6542","authenticated-orcid":false,"given":"Ruken","family":"Ege","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3977-839X","authenticated-orcid":false,"given":"K\u00fcbra","family":"Ati\u0307k","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1278-053X","authenticated-orcid":false,"given":"Elif","family":"\u00c7\u0131tak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-6243-428X","authenticated-orcid":false,"given":"Or\u00e7un","family":"\u00c7ulcuo\u011flu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9393-554X","authenticated-orcid":false,"given":"Hakan","family":"Dar\u0131c\u0131","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3060-2806","authenticated-orcid":false,"given":"Emel","family":"Ordu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,22]]},"reference":[{"issue":"11","key":"2518_CR1","doi-asserted-by":"publisher","first-page":"1087","DOI":"10.1016\/j.clinthera.2023.09.020","volume":"45","author":"L Nedkoff","year":"2023","unstructured":"Nedkoff, L., T. 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The tool was not used for study design, data generation, data analysis, interpretation of results, or formulation of scientific conclusions. All experimental procedures, data analyses, and interpretations were performed and validated by the authors, who take full responsibility for the content of the manuscript.","order":1,"name":"Ethics","label":"Use of Artificial Intelligence Tools","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"The authors declare no competing interests.","order":2,"name":"Ethics","label":"Competing interests","group":{"name":"EthicsHeading","label":"Declarations"}}],"article-number":"164"}}