Immunohistochemical study of Krüppel-like factor 4 in the spinal cords of rats with experimental autoimmune encephalomyelitis

• Published in: Acta histochemica Vol. 117; no. 6; pp. 521 - 527
• Main Authors: Ahn, Meejung, Kim, Jeongtae, Park, Changnam, Jung, Kyungsook, Moon, Changjong, Shin, Taekyun
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.07.2015
• Subjects: Animals; Astrocytes; Encephalomyelitis, Autoimmune, Experimental - genetics; Encephalomyelitis, Autoimmune, Experimental - metabolism; Experimental autoimmune encephalomyelitis; Female; Immunohistochemistry - methods; KLF4; Kruppel-Like Transcription Factors - genetics; Kruppel-Like Transcription Factors - metabolism; Macrophages; Male; Rats; Spinal Cord - metabolism; PBS; ABC; KLF; Astrocytes; MS; EAE; Experimental autoimmune encephalomyelitis; CNS; Macrophages; KLF4; LPS; GFAP; NF-κB; FITC; PPAR; iNOS; MBP; TRITC; CFA; GKLF
• ISSN: 0065-1281; 1618-0372
• DOI: 10.1016/j.acthis.2015.03.012

•Krüppel-like factor (KLF) 4 is significantly increased in EAE affected spinal cords.•KLF4, constitutively expressed in neurons and glial cells, is up-regulated in EAE.•KLF4 was detected in some macrophages as well as in reactive astrocytes in EAE.•Increased KLF4 in rat EAE may modulate CNS inflammation. The expression and localization of Krüppel-like factor (KLF) 4, a class of zinc-finger transcription factors, was investigated in the spinal cords of rats with experimental autoimmune encephalomyelitis (EAE) using western blotting and immunohistochemistry. KLF4 expression was increased significantly in EAE-affected spinal cords compared with normal rat spinal cords. The elevated levels of KLF4 in the spinal cords of rats with EAE remained significant, even during the recovery stage of EAE. The cellular phenotype of KLF4 in EAE lesions consisted of some T cells, macrophages, and reactive astrocytes, whereas it was expressed constitutively in resting astrocytes and neurons, but not in ramified microglial cells in normal spinal cords. Collectively, we postulate that autoimmune T cells and macrophages activate KLF4 and subsequently do not proliferate or exhibit phenotypic switching from M1 to M2 macrophages, respectively. In addition, we hypothesize that the increased and sustained expression of KLF4 in reactive astrocytes during EAE was associated with suppressed CNS inflammation, as well as reduced numbers of pro-inflammatory T cells and M1 macrophages.