Amyloidosis

Gorevic, P D; Franklin, E C

doi:10.1146/annurev.me.32.020181.001401

Cited by 27 publications

(10 citation statements)

References 10 publications

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“…Its serum concentration increases 1,000-fold after acute inflammation, being regulated primarily by the 200 -300-fold increase in SAA gene transcription (32,34,35). In mice, the SAA gene family consists of four genes, SAA1, SAA2, SAA3, and SAA5, and a pseudogene (36,37).…”

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confidence: 99%

“…Whereas expression of SAA1, SAA2, and SAA3 is dramatically induced after inflammation and each contributes equally to the increased SAA mRNA levels in the liver, SAA5 expression is induced to a much lower level and with different induction kinetics (38,39). In addition to being highly regulated by the inflammatory cytokines, expression of SAA1 and SAA2 are also highly cell type-specific, restricted to the liver hepatocytes (32,34,35). Studies of the rat SAA1 promoter demonstrate that 304 bp of its 5Ј-flanking sequence are sufficient not only for its liver cell-specific expression but also for its cytokine-induced expression in response to inflammatory mediators (40).…”

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confidence: 99%

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Transcription Factor AP-2 Functions as a Repressor That Contributes to the Liver-specific Expression of Serum Amyloid A1 Gene

Ren

Liao

2001

Journal of Biological Chemistry

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We previously identified transcription factor AP-2 as the nuclear factor that interacts with the tissue-specific repressor element in the rat serum amyloid A1 (SAA1) promoter. In this report, we provide evidence for a second AP-2-binding site and show that both AP-2 sites participate in mediating the transcription repression of SAA1 promoter. This proximal AP-2 site overlaps with the NFB-binding site known to be essential for SAA1 promoter activity. Protein binding competition experiments demonstrated that AP-2 and NFB binding to these overlapping sites were mutually exclusive. Furthermore, the addition of AP-2 easily displaced prebound NFB, whereas NFB could not displace AP-2. These results thus suggest that one mechanism by which AP-2 negatively regulates SAA1 promoter activity may be by antagonizing the function of NFB. Consistent with a repression function, transient expression of AP-2 in HepG2 cells inhibited conditioned medium-induced SAA1 promoter activation. This inhibition was dependent on functional AP-2-binding sites, since mutation of AP-2-binding sites abolished inhibitory effects of AP-2 in HepG2 cells as well as resulted in derepression of the SAA1 promoter in HeLa cells. In addition to SAA1, we found that several other liver gene promoters also contain putative AP-2-binding sites. Some of these sequences could specifically inhibit AP-2⅐DNA complex formation, and for the human complement C3 promoter, overexpression of AP-2 also could repress its cytokinemediated activation. Finally, stable expression of AP-2 in hepatoma cells significantly reduced the expression of endogenous SAA, albumin, and ␣-fetoprotein genes. Taken together, our results suggest that AP-2 may function as a transcription repressor to inhibit the expression of not only SAA1 gene but also other liver genes in nonhepatic cells.

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confidence: 99%

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confidence: 99%

Transcription Factor AP-2 Functions as a Repressor That Contributes to the Liver-specific Expression of Serum Amyloid A1 Gene

Ren

Liao

2001

Journal of Biological Chemistry

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“…Due to hyperchemo-taxis of these cells in BD, colchicine has been used with some success [23,24], Moreover, colchicine may inhibit precursor protein synthesis or may inhibit cells responsi ble for proteolysis of serum amyloid A protein (SA A) [25]. This drug is effective prophylactically in FMF [22,26], but has only been employed sporadically for other types of secondary amyloidosis [14,27].…”

Section: Discussionmentioning

confidence: 99%

The Expanding Spectrum of a Disease

Tasdemir

Sıvrı²,

Turgan³

et al. 1989

Nephron

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In this report, we present a series of 6 patients with Behçet’s disease (BD) associated with amyloidosis whose illnesses date back at least 4 years. In all the cases, nephrotic syndrome heralded the onset of amyloidosis, which was diagnosed by percutaneous kidney biopsies. After the diagnosis of amyloidosis, all subjects received colchicine, and steroids were discontinued. Three patients have benefited from treatment. It was suggested that amyloidosis may be an intrinsic feature of BD or that the suppurative lesions may play a role in the accumulation of amyloid in the tissues. The literature was reviewed and discussed.

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“…Immunoperoxidase studies with antisera to AA protein, prealbumin, P-component and X and k light chains were performed in selected Congo-red-positive samples as described by Gorovic [ 19].…”

Section: Methodsmentioning

confidence: 99%

Deposition of Nonamyloid Material in Connective Tissue in Uraemia

Kachel¹,

Altmeyer

Kühn

et al. 1984

Blood Purif

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Carpal tunnel syndrome was recently described as a late complication in patients on long-term regular dialysis treatment (RDT). Perineural tissue excized from carpal tunnel stained Congo-red-positive, indicating that it might be amyloid. The aim of this study was to further characterize the deposited material and to investigate predilection sites for amyloid deposition like skin and rectal mucosa in RDT patients and in chronic renal failure patients being still on conservative treatment. Congo-red-positive material could be detected in the corium of the skin in RDT patients, and to a minor degree in conservatively treated uraemic patients. By immunological techniques and electron microscopy, these deposits could not be identified as amyloid. In electron microscopy, fine, granular basement-membrane-like material was found in the perineural tissue as well as in the skin of uraemic patients. This material is most likely altered collagen.

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Amyloidosis

Cited by 27 publications

References 10 publications

Transcription Factor AP-2 Functions as a Repressor That Contributes to the Liver-specific Expression of Serum Amyloid A1 Gene

Transcription Factor AP-2 Functions as a Repressor That Contributes to the Liver-specific Expression of Serum Amyloid A1 Gene

The Expanding Spectrum of a Disease

Deposition of Nonamyloid Material in Connective Tissue in Uraemia

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