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Biomedical subjects

Anna Nogalska

Publications and source records attributed to Anna Nogalska.

9 recordsLinked to original sources

An immune-associated mitochondrial DNA variant with sex differences reveals a putative novel microprotein called MASL.

The use of mitochondrial wide association studies (MiWAS) to link mitochondrial DNA variants (mtSNPs) to phenotypes of interest has uncovered important connections between mitochondrial genes and human health. The recent introduction of a re-annotated mitochondrial genome that accounts for small open reading frames (sORFs) with protein coding potential suggests the existence of mitochondrial-derived microproteins, many of which remain uncharacterized. Thus, considering the re-annotated mitochondrial genome when conducting genomic analyses such as MiWAS facilitates the mapping of mtSNPs back to microprotein-encoding sORFs and uncovers interactions between mitochondrial microproteins and biological systems. Here, we employ MiWAS of venous blood samples from the Health and Retirement Study (HRS) and identify a mtSNP associated with sex-specific changes to immune composition. After accounting for re-annotation, we map the identified mtSNP back to a sORF that encodes a novel microprotein, termed MASL (Mitochondrial Associated Small d-Loop peptide). Complementary phenome-wide association studies (PheWAS) in HRS and and UK Biobank confirm interactions between this mtSNP and immune phenotypes of interest, and our targeted RNA-Seq method (mitoSNP-seq) elucidates sex-differences in gene expression and functional pathways potentially altered by this mtSNP that may be relevant to the associated microprotein. Early characterization of the MASL microprotein shows sex-differences in circulating MASL levels in human plasma, and sex-specific interactions when comparing male and female mice treated with synthesized MASL. Together, the results of this study not only contribute to our understanding of mitochondrial dynamics in immunity, but also provide early characterization of a novel mitochondrial-derived microprotein with sex-specific modulatory effects.

Genomics↗

The potential role of sterol regulatory element binding protein transcription factors in renal injury.

The disturbed lipid metabolism is a permanent finding in renal failure. It is supposed to be a main reason for the accelerated atherosclerosis and high cardiovascular and cerebrovascular mortality of patients with renal failure. Sterol regulatory element binding proteins (SREBPs) are the transcription factors involved in the regulation of lipid homeostasis. They are responsible for the transcription activation of genes associated with the synthesis of fatty acids, triglycerides, and cholesterol. SREBP-1 gene expression in adipose tissue and SREBP-2 in liver are significantly elevated in renal failure. This is accompanied with the up-regulation of genes encoding enzymes of both fatty acids and cholesterol synthesis and significant serum lipid enhancement. Moreover, it has been shown that a destructive accumulation of lipids in the kidney structures is associated with enhanced kidney SREBP gene expression and increased lipid production. This was found even in the absence of any abnormalities in serum lipids. One may suppose that SREBP transcription factors play an important role in disturbed lipid metabolism in renal failure.

Disease Progression↗

Gender- and age-related changes in 6-phosphogluconate dehydrogenase gene expression in white adipose tissue of rats (Rattus norvegicus) are not related to serum testosterone concentration.

Previously, we have shown that the age-related changes in 6-phosphogluconate dehydrogenase (6PGDH) activity depend on sex, and that oestradiol is playing a crucial role in the regulation of 6PGDH gene expression in rat liver, but not in other tissues [Pankiewicz, A., Sledzinski, T., Nogalska, A., Swierczynski, J., 2003. Tissue specific, sex and age-related differences in the 6-phosphogluconate dehydrogenase gene expression. Int. J. Biochem. Cell Biol. 35, 235-245.]. To complete the knowledge on the influence of sex hormones on 6PGDH activity, experiments have been performed on the effect of testosterone on 6PGDH gene expression in rat white adipose tissue and liver. The results presented here disclosed that in young male rats high serum testosterone concentration was associated with high white adipose tissue 6PGDH activity. After orchidectomy, a decrease in serum testosterone concentration (both in young and old rats) was observed. In contrast, no changes in white adipose tissue and liver 6PGDH activity were found. In female rats, both young and old, serum testosterone concentration was below the limit of detection, whereas 6PGDH activity was much higher in young than in old animals. Moreover, the testosterone administration to 9-month old male rats (which displayed much lower serum testosterone concentration that young animals) resulted in no effect on 6PGDH activity either in WAT or in the liver. In conclusion, the results presented in this paper indicate that testosterone does not play any role in the age- and gender-related differences in 6PGDH gene expression in white adipose tissue.

Adipose Tissue↗

Homocysteine-induced endoplasmic reticulum protein (Herp) is up-regulated in sporadic inclusion-body myositis and in endoplasmic reticulum stress-induced cultured human muscle fibers.

Herp is a stress-response protein localized in the endoplasmic reticulum (ER) membrane. Herp was proposed to improve ER-folding, decrease ER protein load, and participate in ER-associated degradation (ERAD). Intra-muscle-fiber ubiquitinated multiprotein-aggregates containing, among other proteins, either amyloid-beta (Abeta) or phosphorylated tau are characteristic of sporadic inclusion-body myositis (s-IBM). ER stress and proteasome inhibition appear to play a role in s-IBM pathogenesis. We have now studied Herp in s-IBM muscle fibers and in ER-stress-induced or proteasome-inhibited cultured human muscle fibers. In s-IBM muscle fibers: (i) Herp was strongly immunoreactive in the form of aggregates, which co-localized with Abeta, GRP78, and beta2 proteasome subunit; (ii) Herp mRNA and protein were increased. In ER-stress-induced cultured human muscle fibers: (i) Herp immunoreactivity was diffusely increased; (ii) Herp mRNA and protein were increased. In proteasome-inhibited cultured human muscle fibers: (i) Herp immunoreactivity was in the form of aggregates; (ii) Herp protein was increased, but its mRNA was not. Accordingly, in s-IBM muscle fibers: (i) increase of Herp might be due to both ER-stress and proteasome inhibition; (ii) co-localization of Herp with Abeta, proteasome, and ER-chaperone GRP78 could reflect its possible role in processing and degradation of cytotoxic proteins in ER.

Amyloid beta-Peptides↗

Leptin decreases lipogenic enzyme gene expression through modification of SREBP-1c gene expression in white adipose tissue of aging rats.

Aging is associated with a significant reduction of lipogenic enzyme gene expression and lipogenesis in white adipose tissue (WAT). The age-related increase of lep gene expression could be, in part, responsible for these changes. Considering that sterol regulatory element binding protein 1c (SREBP-1c) plays an important role in regulation of lipogenic enzyme gene expression, it is likely that the age-related decrease of WAT lipogenic potential could be a consequence of the inhibition of SREBP-1c gene expression by leptin. We determined whether the increase of lep gene expression would account for the age-related decrease in SREBP-1c and its direct target, main lipogenic enzymes acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), by assaying the messenger RNA (mRNA) levels of SREBP-1c, FAS, ACC, and leptin in WAT of 2-month-old (young) and 20-month-old (old) rats. Leptin mRNA level was much higher in the old animals, whereas in contrast, old rats displayed much lower mRNA levels of SREBP-1c and lipogenic enzymes. Moreover, experimentally increased plasma leptin concentration in young rats to the value observed in old rats resulted in the decrease of SREBP-1c, FAS, and ACC mRNA levels in WAT. Thus, the increase of lep gene expression could, in part, account for the reduced SREBP-1c gene expression and, consequently, the diminished lipogenic activity in WAT of old animals.

Acetyl-CoA Carboxylase↗

Potential role of high serum leptin concentration in age-related decrease of fatty acid synthase gene expression in rat white adipose tissue.

Ageing in rats is associated with significant reduction of lipogenic enzymes genes expression and the rate of fatty acids synthesis in white adipose tissue. Since resistance to insulin and/or triiodothyronine is not directly related to reduction in lipogenic enzymes activity in white adipose tissue of old rats, we have proposed recently that the age-related increase in leptin gene expression and high serum leptin concentration could, at least partly, account for the down regulation of lipogenic enzymes gene expression. To test this hypothesis, in this paper we experimentally (by single intraperitoneal injection of recombinant leptin) increased plasma leptin concentration in young rats to the level observed in old animals, and we examined its effect on fatty acids synthase (FAS) gene expression in white adipose tissue. The results presented in this paper indicate that leptin administration to young rats, in amount that cause the increase in serum leptin concentration to that found in old rats, significantly decreased the white adipose tissue FAS gene expression. We propose, therefore, that leptin could play a causative role in the down-regulation of lipogenic enzyme gene expression observed with ageing.

Adipose Tissue↗

Upregulation of lipogenic enzymes genes expression in white adipose tissue of rats with chronic renal failure is associated with higher level of sterol regulatory element binding protein-1.

Chronic renal failure (CRF) frequently results in hypertriglyceridemia and elevated plasma concentration of very-low-density lipoprotein (VLDL). These abnormalities are thought to be primarily due to depressed lipoprotein lipase and hepatic lipase activities, as well as impaired clearance of plasma lipoproteins. Some results suggest that not only lipoproteins catabolism but also their overproduction might contribute to hypertriglyceridemia in CRF. Because sterol regulatory element binding protein (SREBP) plays an important role in the regulation of lipid homeostasis, increased level of this transcription factor might be involved in modulating lipid metabolism in CRF. The purpose of the present study is to determine whether there is an altered regulation of the SREBP-1 in CRF rats and whether the altered regulation of SREBP-1 is associated with the upregulation of lipogenic enzymes genes expression in CRF rats. In the white adipose tissue (WAT) of CRF rats, marked increases in the microsomal (precursor) and nuclear (mature) forms of SREBP-1 have been found. The increase in SREBP-1 was associated with an increased level of lipogenic enzymes (acetyl-coenzyme A [CoA] carboxylase [ACC], adenosine triphosphate-citrate lyase [ACL], fatty acid synthase [FAS], glucose 6-phosphate dehydrogenase [G6PDH], 6-phosphogluconate dehydrogenase [6PGDH], and malic enzyme [ME]) genes expression. In turn, this was associated with an increased rate of fatty acids synthesis in WAT and a significant increase in plasma triacylglycerol (TAG) and VLDL concentration. Our study indicates that WAT SREBP-1 expression is increased in CRF rats and that SREBP-1 may play an important role in the increased fatty acid synthesis. These results reveal another facet of disturbed lipid metabolism in CRF.

Adipose Tissue↗

The age-related inverse relationship between ob and lipogenic enzymes genes expression in rat white adipose tissue.

To determine whether increase of serum leptin (the known natural inhibitor of lipogenic enzymes gene expression) concentration would account for the age-related decrease in lipogenesis (a) serum leptin concentration; (b) leptin mRNA abundance; (c) the rate of fatty acid synthesis in vivo; (d) lipogenic enzymes activity and (e) mRNA levels were assayed in white adipose tissue (WAT) of male young and old rats. We found that leptin mRNA abundance in WAT and serum leptin concentration was much lower in young than in old animals. In contrast, the rate of fatty acid synthesis in WAT was much higher in young animals. The old rats displayed much lower lipogenic enzymes activities (acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), ATP-citrate lyase (ACL), malic enzyme (ME), glucose 6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase 6PGDH) and mRNA abundance as compared to young rats. Considering the inverse relationship between serum leptin concentration and lipogenic enzymes genes expression and known inhibitory effect of leptin on lipogenic enzymes gene expression, one can conclude that the increase of ob gene expression could at least partly account for the reduced WAT lipogenic enzymes genes expression in old animals.

ATP Citrate (pro-S)-Lyase↗

Tissue specific, sex and age--related differences in the 6-phosphogluconate dehydrogenase gene expression.

Data presented in thid paper indicate that: (1) the age-related changes in 6-phosphogluconate dehydrogenase (6PGDH) activity depend on sex and tissue. No differences in the liver 6PGDH activity between young (1-month-old) males and females were found. In adult males, the activity was the same as in young animals but, in adult females, it reached the value twice as high as in the young. In adipose tissue (both white and brown) and kidney cortex, the enzyme activity decreased with age both in males and females. There were no differences between males and females 6PGDH activity in brain, heart and skeletal muscle. (2) The sex and age-related changes in the liver 6PGDH activity occur predominantly at the level of mRNA cellular concentration. (3) In the liver of ovariectomized rats decrease of 6PGDH activity and mRNA level was observed. Oestradiol administration to ovariectomized rats restored liver 6PGDH activity and liver 6PGDH mRNA levels to that observed in controls. No changes in 6PGDH activity and mRNA levels were found in white adipose tissue (WAT) of ovariectomized adult rats and in ovariectomized rats treated with oestradiol. (4) Oestradiol administration to males caused an increase of liver 6PGDH activity and mRNA levels to values observed in females, but was without an effect on WAT 6PGDH activity and mRNA level. (5) These results suggest that 6PGDH activity in different tissues is not regulated in coordinate fashion and that oestradiol plays an important role in the liver enzyme activity regulation.

Adipose Tissue↗