دورية أكاديمية
Gal3 Plays a Deleterious Role in a Mouse Model of Endotoxemia
العنوان: | Gal3 Plays a Deleterious Role in a Mouse Model of Endotoxemia |
---|---|
المؤلفون: | Fernández-Martín, Juan Carlos, Espinosa-Oliva, Ana M., García-Domínguez, Irene, Rosado-Sánchez, Isaac, Pacheco, Yolanda M., Moyano, Rosario, García Monterde, José, Venero, José L., Pablos, Rocío M. de |
المساهمون: | Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Junta de Andalucía, Instituto de Salud Carlos III |
بيانات النشر: | Multidisciplinary Digital Publishing Institute |
سنة النشر: | 2022 |
المجموعة: | Digital.CSIC (Consejo Superior de Investigaciones Científicas / Spanish National Research Council) |
مصطلحات موضوعية: | Electron microscopy, Endotoxemia, Galectin-3, Lipopolysaccharide, Sepsis |
الوصف: | Lipopolysaccharide (LPS)-induced endotoxemia induces an acute systemic inflammatory response that mimics some important features of sepsis, the disease with the highest mortality rate worldwide. In this work, we have analyzed a murine model of endotoxemia based on a single intraperitoneal injection of 5 mg/kg of LPS. We took advantage of galectin-3 (Gal3) knockout mice and found that the absence of Gal3 decreased the mortality rate oflethal endotoxemia in the first 80 h after the administration of LPS, along with a reduction in the tissular damage in several organs measured by electron microscopy. Using flow cytometry, we demonstrated that, in control conditions, peripheral immune cells, especially monocytes, exhibited high levels of Gal3, which were early depleted in response to LPS injection, thus suggesting Gal3 release under endotoxemia conditions. However, serum levels of Gal3 early decreased in response to LPS challenge (1 h), an indication that Gal3 may be extravasated to peripheral organs. Indeed, analysis of Gal3 in peripheral organs revealed a robust up-regulation of Gal3 36 h after LPS injection. Taken together, these results demonstrate the important role that Gal3 could play in the development of systemic inflammation, a well-established feature of sepsis, thus opening new and promising therapeutic options for these harmful conditions. ; This research was funded by grants by the Spanish Ministerio de Ciencia, Innovación y Universidades/FEDER/UE RTI2018-098645-B-100), Junta de Andalucía (Consejería de Economía y Conocimiento, US-1264806) and FIS (PI18/01216). YMP was supported by the Consejería de Salud y Bienestar Social of Junta de Andalucía through the ‘‘NicolásMonardes’’ programme [C-0013-2017]. ; Peer reviewed |
نوع الوثيقة: | article in journal/newspaper |
وصف الملف: | application/pdf |
اللغة: | English |
تدمد: | 1661-6596 1422-0067 35163089 |
العلاقة: | #PLACEHOLDER_PARENT_METADATA_VALUE#; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/RTI2018-098645-B-I00/ES/PAPEL DE LA GALECTINA-3 EN LA RESPUESTA INMUNE ASOCIADA A ENFERMEDADES DEL SISTEMA NERVIOSO CENTRAL. IMPLICACION EN ENFERMEDADES NEURODEGENERATIVAS Y GLIOBLASTOMA MULTIFORME/; Publisher's version; https://doi.org/10.3390/ijms23031170Test; Sí; International Journal of Molecular Sciences 23(3): 1170 (2022); http://hdl.handle.net/10261/305873Test; http://dx.doi.org/10.13039/501100011011Test; http://dx.doi.org/10.13039/501100011033Test; http://dx.doi.org/10.13039/501100000780Test; http://dx.doi.org/10.13039/501100004587Test; 2-s2.0-85122989086; https://api.elsevier.com/content/abstract/scopus_id/85122989086Test |
DOI: | 10.3390/ijms23031170 |
DOI: | 10.13039/501100011011 |
DOI: | 10.13039/501100011033 |
DOI: | 10.13039/501100000780 |
DOI: | 10.13039/501100004587 |
الإتاحة: | https://doi.org/10.3390/ijms2303117010.13039/50110001101110.13039/50110001103310.13039/50110000078010.13039/501100004587Test http://hdl.handle.net/10261/305873Test https://api.elsevier.com/content/abstract/scopus_id/85122989086Test |
حقوق: | open |
رقم الانضمام: | edsbas.BA69A887 |
قاعدة البيانات: | BASE |
تدمد: | 16616596 14220067 35163089 |
---|---|
DOI: | 10.3390/ijms23031170 |