Serum amyloid A gene expression and AA amyloid formation in A/J and SJL/J mice.
Serum amyloid A (SAA) gene expression and AA amyloid fibril formation were studied in A/J and SJL/J mice, two strains which have been reported to possess defects in AA fibril formation. Four types of inflammatory stimulation were employed: acute inflammation stimulated with lipopolysaccharide (LPS), chronic inflammation with casein in complete Freund's adjuvant, amyloidosis with injection of amyloid enhancing factor (AEF) together with casein in complete Freund's adjuvant, and non-amyloidogenic inflammation in the presence of AEF with injection of AEF together with LPS. Both A/J and SJL/J mice developed splenic amyloidosis 1 day after initiation of chronic inflammation in the presence of AEF. No amyloid deposits were detected during any of the other types of inflammation. Amyloidotic mice exhibited decreased amounts of SAA mRNA in liver and spleen concomitant with decreased amounts of SAA in serum. Alpha-I-acid glycoprotein mRNA was present in liver throughout the course of AEF accelerated amyloidosis, indicating that decreased SAA gene expression and AA fibril formation is not part of a general inhibitory effect of AEF on protein synthesis.
Thorndike Memorial Laboratory, Department of Medicine, Boston City Hospital, MA 02118, USA.
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Rokita
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Shirahama
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Cohen
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JD
Sipe
D000818:Animals; D005260:Female; D005786:Gene Expression Regulation; D008099:Liver / Q000032:analysis; D051379:Mice; D008815:Mice, Inbred Strains; D009961:Orosomucoid / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D000685:Serum Amyloid A Protein / Q000096:biosynthesis* / Q000235:genetics*; D013154:Spleen / Q000032:analysis
D009961:Orosomucoid; D012333:RNA, Messenger; D000685:Serum Amyloid A Protein