Endogenous Galectin-8 protects against Th17 infiltration and fibrosis following acute kidney injury

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dc.article.number192
dc.catalogadorpva
dc.contributor.authorPerez-Moreno, Elisa
dc.contributor.authorPeña, Adely de la
dc.contributor.authorToledo, Tomás
dc.contributor.authorSaez, Javiera
dc.contributor.authorPérez-Molina, Francisca
dc.contributor.authorEspinoza, Sofía
dc.contributor.authorMetz, Claudia
dc.contributor.authorDíaz-Valdivia, Nicole
dc.contributor.authorAzócar, Lorena
dc.contributor.authorPrado, Carolina
dc.contributor.authorPacheco, Rodrigo
dc.contributor.authorSegovia-Miranda, Fabian
dc.contributor.authorGodoy, Alejandro S.
dc.contributor.authorAmador, Cristian A.
dc.contributor.authorFeuerhake González, Teo
dc.contributor.authorGonzález, Alfonso
dc.contributor.authorSoza, Andrea
dc.date.accessioned2025-05-28T16:54:58Z
dc.date.available2025-05-28T16:54:58Z
dc.date.issued2025
dc.date.updated2025-05-18T00:03:09Z
dc.description.abstractBackground Acute kidney injury (AKI) is a serious clinical condition characterized by a rapid decline in renal function, often progressing to chronic kidney disease (CKD) and fibrosis. The endogenous mechanisms influencing kidney injury resolution or maladaptive repair remain poorly understood. Galectin‑8 (Gal‑8), a tandem‑repeat β‑galactosidebinding lectin, plays a role in epithelial cell proliferation, epithelial‑mesenchymal transition, and immune regulation, all of which are critical in AKI outcomes. While exogenous Gal‑8 administration has shown renoprotective effects, its endogenous role in kidney injury progression and resolution remains unclear. Methods To investigate the endogenous role of Gal‑8 in AKI, we compared the responses of Gal‑8 knockout (Gal8‑KO; Lgals8−/− bearing a β‑gal cassette under the Lgals8 gene promoter) and wild‑type (Lgals8+/+) mice in a nephrotoxic folic acid (FA)‑induced AKI model. Renal Gal‑8 expression was assessed by β‑galactosidase staining, lectin‑marker colocalization, and RT‑qPCR. Renal function, structure, and immune responses were evaluated at the acute (day 2) and fibrotic (day 14) phases of injury. Plasma creatinine levels were measured to assess renal function, while histological analyses evaluated tubular damage, renal inflammation, and extracellular matrix deposition. Flow cytometry was performed to characterize the immune response, focusing on pro‑inflammatory T cells. Results Galectin‑8 was predominantly expressed in the renal cortex, localizing to tubules, glomeruli, and blood vessels, with its levels decreasing by half following AKI. Both Lgals8+/+ and Lgals8−/− mice exhibited similar renal function and structure impairments during the acute phase, though Lgals8+/+ mice showed slightly worse damage. By the fibrotic phase, Lgals8−/− mice exhibited more pronounced cortical damage and fibrosis, characterized by increased type I and III collagen deposition and enhanced Th17 cell infiltration, while myofibroblast activation remained comparable to that of Lgals8+/+ mice. Conclusions Endogenous Gal‑8 does not significantly protect the kidney during the acute phase and is dispensable for cell proliferation and death in response to AKI. However, it is crucial in preventing maladaptive repair by regulating.
dc.fechaingreso.objetodigital2025-05-18
dc.format.extent19 páginas
dc.fuente.origenBiomed Central
dc.identifier.citationMolecular Medicine. 2025 May 16;31(1):192
dc.identifier.doi10.1186/s10020-025-01245-y
dc.identifier.issn1528-3658
dc.identifier.urihttps://doi.org/10.1186/s10020-025-01245-y
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/104508
dc.information.autorucEscuela de Medicina; Feuerhake González, Teo; 0000-0002-7065-2309; 186147
dc.issue.numero1
dc.language.isoen
dc.nota.accesocontenido completo
dc.publisherSpringer Nature
dc.revistaMolecular Medicine
dc.rightsacceso abierto
dc.rights.holderThe Author(s)
dc.rights.licenseAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectGalectin‑8
dc.subjectAcute kidney injury
dc.subjectAKI
dc.subjectFibrosis
dc.subjectChronic kidney disease
dc.subjectCDK
dc.subjectInflammation and Th17
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEndogenous Galectin-8 protects against Th17 infiltration and fibrosis following acute kidney injury
dc.typeartículo
dc.volumen31
sipa.codpersvinculados186147
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