Lp(a): an acute-phase reactant?

Noma, Akio; Abe, Akira; Maeda, Shin; Seishima, Mariko; Makino, Kazuhiko; Yano, Yumihiko; Shimokawa, Kuniyasu

doi:10.1016/0009-3084(94)90164-3

Cited by 70 publications

(51 citation statements)

References 9 publications

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“…Significant amounts of apo(a) mRNA were consistently detected in Several interleukin-6 (IL-6)-responsive elements have been identified in the promoter region of LPA (70), and some studies have suggested that apo(a)/Lp(a) could act as an acute phase protein (71,72)). However, opposite effects have also been reported (73,74).…”

Section: Metabolism Of Lp(a)mentioning

confidence: 99%

Structure, function, and genetics of lipoprotein (a)

Schmidt

Noureen

Kronenberg

et al. 2016

Journal of Lipid Research

414

346

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between apoB-100 of the LDL moiety and one of the kringle domains in apo(a) (4,5,(14)(15)(16). The assembly of Lp(a) is believed to occur at the hepatocyte cell membrane surface (17), but other scenarios have also been proposed [reviewed in (18, 19)].Lp(a) was originally described as a dichotomous (Lp+, Lp) genetic trait (20), but it soon became evident that it is quantitative rather than qualitative in nature (21-23). Lp(a) plasma concentrations are highly heritable (24-28). The major locus controlling the Lp(a) concentrations is the LPA gene (MIM 152200; ENSG00000198670) on the reverse strand of chromosome 6q27 (29-31), which encodes the apo(a) component of Lp(a) (25,26,(32)(33)(34). Close LPA orthologs are found in all apes and in Old World monkeys. INTRA-AND INTER-POPULATION DIFFERENCES INLp ( INTRODUCTION TO THE LIPOPROTEIN (a) TRAITHuman lipoprotein (a) [Lp(a)] is a macromolecular complex in plasma that was first described in 1963 by the Norwegian physician Kåre Berg (1). Ever since its discovery, this enigmatic particle has intrigued basic researchers and clinicians due to its unknown physiological function and its association with atherosclerotic diseases, in particular coronary heart disease (CHD) [reviewed in (2)]. Lp(a) is composed of one molecule of a LDL-particle containing apoB-100 and one molecule of a large highly polymorphic glycoprotein named apo(a) (3-6). A characteristic feature of apo(a) is the presence of loop-like structures called kringles (7,8). Kringle domains are triple loop structures stabilized by three internal disulfide bonds and are also present in other coagulation factors, such as plasminogen (PLG), prothrombin, urokinase, and tissue-type PLG activators (9-12). In contrast to PLG, the linker domain between kringles is glycosylated in apo(a). The apo(a) is synthesized by the liver (13). The two components of Lp(a) are covalently linked together by a disulfide bond

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Section: Metabolism Of Lp(a)mentioning

confidence: 99%

Structure, function, and genetics of lipoprotein (a)

Schmidt

Noureen

Kronenberg

et al. 2016

Journal of Lipid Research

414

346

View full text Add to dashboard Cite

show abstract

“…5,6 Also, Lp(a) levels have repeatedly been linked to acute-phase responses. [7][8][9][10] On the other hand, negative acute-phase characteristics and decreases in catabolic states have also been shown to occur. 11,12 In vitro experiments show that Lp(a) messenger RNA (mRNA) expression can be positively regulated by interleukin-6 (IL-6), whereas it can be suppressed by transforming growth factor ␤1 (TGF-␤1) and tumor necrosis factor-␣ (TNF-␣), suggesting that in vivo Lp(a) levels may be dependent on the balance between stimulatory and inhibitory cytokines, 13 which could help to explain the variation of Lp(a) levels with regard to different clinical settings.…”

Section: To the Editormentioning

confidence: 99%

Increased Lipoprotein(a) levels are not a steady prothrombotic defect

Korte

Greiner

Feldges

et al. 2001

Blood

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In conclusion, the 1040T/C SNP located in the coding region of the TAFI gene and resulting in the Thr325Ile substitution is associated with TAFI plasma levels, just like other SNPs in and around this gene. Presently, it is not known which SNP is/are responsible for this effect on TAFI levels. On the other hand, studies using recombinant proteins have demonstrated a functional effect of the Thr325Ile substitution on the stability of activated TAFI resulting in altered antifibrinolytic activity. The possibility that the same TAFI haplotype will affect levels and antifibrinolytic activity in opposite directions will hamper the interpretation of genetic association studies using this SNP.

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“…A previous study which analysed Lp(a) at two time points (3rd and 28th days post MI) showed a 12% difference between the first and second samples and concluded that Lp(a) increases immediately post MI and return to baseline after four weeks. 8 But Andreassen et al 9 and Noma et al 10 showed that increment in Lp(a) was delayed and rose only after seven days after MI. The findings in this study, where Lp(a) concentrations were measured serially by apo(a) size insensitive method, show that unlike CRP and TC, Lp(a) does not behave like an APR.…”

Section: Discussionmentioning

confidence: 99%

Serum lipoprotein(a) concentrations do not change significantly in the immediate seven-day period post myocardial infarction

et al. 2014

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Background: Lipoprotein(a) is an independent predictor of cardiovascular disease and its variability after myocardial infarction was assessed in this study. Methods: Lipoprotein(a) was analysed by a size insensitive latex immunoturbidimetric end point assay in samples from days 0 to 7 in 31 patients admitted with myocardial infarction. Results: Median lipoprotein(a) changed by À0.9%, À0.1% and 9.6% on days 1, 2-3 and 4-7, respectively, and was not statistically significant. Median total cholesterol reduced by 8.7%, 9.1%, 14.5% and C-reactive protein increased by 68.4%, 510%, 502% over days 1, 2-3, 4-7, respectively. Conclusions: Unlike total cholesterol and C-reactive protein, lipoprotein(a) does not demonstrate significant variability for up to seven days after myocardial infarction and measurements made during this period after myocardial infarction are physiologically meaningful.

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Lp(a): an acute-phase reactant?

Cited by 70 publications

References 9 publications

Structure, function, and genetics of lipoprotein (a)

Structure, function, and genetics of lipoprotein (a)

Increased Lipoprotein(a) levels are not a steady prothrombotic defect

Serum lipoprotein(a) concentrations do not change significantly in the immediate seven-day period post myocardial infarction

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