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Galectin-1 enhances TNFalpha-induced inflammatory responses in Sertoli cells through activation of MAPK signalling

Lei, Tao ; Moos, Sven ; Klug, Jörg ; Aslani, Ferial ; Bhushan, Sudhanshu ; Wahle, Eva ; Fröhlich, Suada ; Meinhardt, Andreas ; Fijak, Monika

Originalveröffentlichung: (2018) Scientific Reports 8(1):3741 doi: 10.1038/s41598-018-22135-w
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URN: urn:nbn:de:hebis:26-opus-145629

Sammlung: Open Access - Publikationsfonds
Universität Justus-Liebig-Universität Gießen
Institut: Department of Anatomy and Cell Biology
Fachgebiet: Medizin
DDC-Sachgruppe: Medizin
Dokumentart: Aufsatz
Sprache: Englisch
Erstellungsjahr: 2018
Publikationsdatum: 15.05.2019
Kurzfassung auf Englisch: Galectin-1 (Gal-1) is a pleiotropic lectin involved in the modulation of immune responses. Using a model of rat experimental autoimmune orchitis (EAO), we investigated the role of Gal-1 in testicular inflammation. EAO is characterized by leukocytic infiltrates in the interstitium, damage of spermatogenesis and production of inflammatory mediators like TNFalpha and MCP1 causing infertility. In normal rat testis Gal-1 was mainly expressed in Sertoli cells and germ cells. In the inflamed testis, Gal-1 expression was significantly downregulated most likely due to germ cell loss. Analyses of lectin binding and expression of glucosaminyl- and sialyltransferases indicated that the glycan composition on the cell surface of Sertoli and peritubular cells becomes less favourable for Gal-1 binding under inflammatory conditions. In primary Sertoli cells Gal-1 expression was found to be upregulated after TNFalpha challenge. Pretreatment with Gal-1 synergistically and specifically enhanced TNFalpha-induced expression of MCP1, IL-1alpha, IL-6 and TNFalpha in Sertoli cells. Combined stimulation of Sertoli cells with Gal-1 and TNFα enhanced the phosphorylation of MAP kinases as compared to TNFalpha or Gal-1 alone. Taken together, our data show that Gal-1 modulates inflammatory responses in Sertoli cells by enhancing the pro-inflammatory activity of TNFalpha via stimulation of MAPK signalling.
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