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4. #2641 MiR-200b induces ZEB1 mediated upregulation of Matriptase and affects expression of podocin

Author

Tati, Ramesh, primary, Müller-Deile, Janina, additional, Walentinsson, Anna, additional, Sopel, Nina, additional, Lassen, Emelie, additional, Ebefors, Kerstin, additional, Söderberg, Magnus, additional, Daniel, Christoph, additional, Hansen, Pernille B L, additional, Schiffer, Mario, additional, Nystrom, Jenny, additional, and Buvall, Lisa, additional

Published
2024
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13. The role of dendrin in IgA nephropathy

Author

Levin, Anna, Schwarz, Angelina, Hulkko, Jenny, He, Liqun, Sun, Ying, Barany, Peter, Bruchfeld, Annette, Herthelius, Maria, Wennberg, Lars, Ebefors, Kerstin, Patrakka, Jaakko, Betsholtz, Christer, Nyström, Jenny, Mölne, Johan, Hultenby, Kjell, Witasp, Anna, Wernerson, Annika, Levin, Anna, Schwarz, Angelina, Hulkko, Jenny, He, Liqun, Sun, Ying, Barany, Peter, Bruchfeld, Annette, Herthelius, Maria, Wennberg, Lars, Ebefors, Kerstin, Patrakka, Jaakko, Betsholtz, Christer, Nyström, Jenny, Mölne, Johan, Hultenby, Kjell, Witasp, Anna, and Wernerson, Annika

Abstract

Background Immunoglobulin A nephropathy (IgAN) and its systemic variant IgA vasculitis (IgAV) damage the glomeruli, resulting in proteinuria, hematuria and kidney impairment. Dendrin is a podocyte-specific protein suggested to be involved in the pathogenesis of IgAN. Upon cell injury, dendrin translocates from the slit diaphragm to the nucleus, where it is suggested to induce apoptosis and cytoskeletal changes, resulting in proteinuria and accelerated disease progression in mice. Here we investigated gene and protein expression of dendrin in relation to clinical and histopathological findings to further elucidate its role in IgAN/IgAV. Methods Glomerular gene expression was measured using microarray on 30 IgAN/IgAV patients, 5 patients with membranous nephropathy (MN) and 20 deceased kidney donors. Dendrin was spatially evaluated on kidney tissue sections by immunofluorescence (IF) staining (IgAN patients, n = 4; nephrectomized kidneys, n = 3) and semi-quantified by immunogold electron microscopy (IgAN/IgAV patients, n = 21; MN, n = 5; living kidney donors, n = 6). Histopathological grading was performed according to the Oxford and Banff classifications. Clinical data were collected at the time of biopsy and follow-up. Results Dendrin mRNA levels were higher (P = .01) in IgAN patients compared with MN patients and controls and most prominently in patients with preserved kidney function and fewer chronic histopathological changes. Whereas IF staining did not differ between groups, immunoelectron microscopy revealed that a higher relative nuclear dendrin concentration in IgAN patients was associated with a slower annual progression rate and milder histopathological changes. Conclusion Dendrin messenger RNA levels and relative nuclear protein concentrations are increased and associated with a more benign phenotype and progression in IgAN/IgAV patients.

Published
2023
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14. The pattern of CNI nephrotoxicity differs between treatments.

Author

Nyström, Jenny and Ebefors, Kerstin

Subjects
*LABORATORY rats, *UNFOLDED protein response, *CARDIOTOXICITY, *PATHOLOGICAL physiology, *CARRIER proteins, *HYPERKALEMIA
Abstract

The article discusses the differences in nephrotoxicity (kidney damage) caused by two commonly used immunosuppressant drugs, cyclosporine A (CsA) and tacrolimus (Tac), which are used to prevent organ rejection after transplantation. The study conducted on rats found that while both drugs caused significant damage to the kidneys, they affected different renal compartments. CsA mainly affected the proximal tubules, while Tac affected the microvasculature (glomerular filtration barrier). The study highlights the need for personalized treatment regimens to reduce the nephrotoxic effects of these drugs in organ transplant patients. [Extracted from the article]

Published
2024
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15. The role of dendrin in IgA nephropathy

Author

Levin, Anna, primary, Schwarz, Angelina, additional, Hulkko, Jenny, additional, He, Liqun, additional, Sun, Ying, additional, Barany, Peter, additional, Bruchfeld, Annette, additional, Herthelius, Maria, additional, Wennberg, Lars, additional, Ebefors, Kerstin, additional, Patrakka, Jaakko, additional, Betsholtz, Christer, additional, Nyström, Jenny, additional, Mölne, Johan, additional, Hultenby, Kjell, additional, Witasp, Anna, additional, and Wernerson, Annika, additional

Published
2022
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22. Impaired glomerular and tubular antioxidative defense mechanisms in nephrotic syndrome

Author

Granqvist, Anna, Nilsson, Ulf A., Ebefors, Kerstin, Haraldsson, Borje, and Nystrom, Jenny

Subjects
Thioredoxin -- Physiological aspects, Thioredoxin -- Genetic aspects, Thioredoxin -- Research, Gene expression -- Research, Antioxidants -- Physiological aspects, Antioxidants -- Research, Nephrotic syndrome -- Risk factors, Nephrotic syndrome -- Genetic aspects, Nephrotic syndrome -- Care and treatment, Nephrotic syndrome -- Research, Biological sciences
Abstract

The molecular mechanisms behind acquired nephrotic syndrome (NS) are still largely unknown. One possible explanation for the development of proteinuria is oxidative damage to the glomerular cells. Our hypothesis was that the oxidative defense is weakened in NS, and we focused on measurements of the oxidative-antioxidative status in the glomerular and tubular parts of the nephron. Gene expression was analyzed in renal biopsies from patients with NS. In addition, to compare the acute and chronic phases of the disease, we studied puromycin-treated rats. In the biopsy material, the expression of enzymes involved in the antioxidative defense was higher in the tubulointerstitial compartment than in the glomerular cells. Real-time PCR analysis revealed a decreased glomerular expression in nephrotic kidneys for the antioxidant enzymes catalase and glutathione peroxidase-3, and -4. The tubular gene expression was downregulated for catalase, glutathione peroxidase-3, and thioredoxin reductase-1 and -2. The altered gene expression was accompanied by increased lipid peroxidation in urine. In rats, serum concentrations of ascorbyl-free radicals, measured with electron spin resonance, were elevated in the acute phase of the disease, suggesting increased oxidative stress in the circulation. In addition, we saw an increase in the plasma antioxidant capacity combined with a decreased oxidation of proteins in sera from nephrotic rats, but not from humans. In conclusion, there is a marked downregulation of several antioxidative enzymes in nephrotic kidneys, especially in glomerular structures. Our data suggest that oxidative damage to glomerular cells may contribute significantly to the course and prognosis of nephrotic syndrome. puromycin aminonucleoside; oxidative stress doi: 10.1152/ajprenal.00124.2010.

Published
2010

23. Novel insights into the disease transcriptome of human diabetic glomeruli and tubulointerstitium

Author

Levin, Anna, primary, Reznichenko, Anna, additional, Witasp, Anna, additional, Liu, Peidi, additional, Greasley, Peter J, additional, Sorrentino, Antonio, additional, Blondal, Thorarinn, additional, Zambrano, Sonia, additional, Nordström, Johan, additional, Bruchfeld, Annette, additional, Barany, Peter, additional, Ebefors, Kerstin, additional, Erlandsson, Fredrik, additional, Patrakka, Jaakko, additional, Stenvinkel, Peter, additional, Nyström, Jenny, additional, and Wernerson, Annika, additional

Published
2020
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26. Endothelin receptor-A mediates degradation of the glomerular endothelial surface layer via pathologic crosstalk between activated podocytes and glomerular endothelial cells

Author

Ebefors, Kerstin, primary, Wiener, Robert J., additional, Yu, Liping, additional, Azeloglu, Evren U., additional, Yi, Zhengzi, additional, Jia, Fu, additional, Zhang, Weijia, additional, Baron, Margaret H., additional, He, John C., additional, Haraldsson, Börje, additional, and Daehn, Ilse, additional

Published
2019
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28. The effect of androgen excess on maternal metabolism, placental function and fetal growth in obese dams

Author

Fornes, Romina, Maliqueo, Manuel, Hu, Min, Hadi, Laila, Jimenez-Andrade, Juan M., Ebefors, Kerstin, Nyström, Jenny, Labrie, Fernand, Jansson, Thomas, Benrick, Anna, Stener-Victorin, Elisabet, Fornes, Romina, Maliqueo, Manuel, Hu, Min, Hadi, Laila, Jimenez-Andrade, Juan M., Ebefors, Kerstin, Nyström, Jenny, Labrie, Fernand, Jansson, Thomas, Benrick, Anna, and Stener-Victorin, Elisabet

Abstract

Pregnant women with polycystic ovary syndrome (PCOS) are often overweight or obese. To study the effects of maternal androgen excess in obese dams on metabolism, placental function and fetal growth, female C57Bl6J mice were fed a control (CD) or a high fat/high sucrose (HF/HS) diet for 4-10 weeks, and then mated. On gestational day (GD) 15.5-17.5, dams were injected with dihydrotestosterone (CD-DHT, HF/HS-DHT) or a vehicle (CD-Veh, HF/HS-Veh). HF/HS dams had higher fat content, both before mating and on GD18.5, with no difference in glucose homeostasis, whereas the insulin sensitivity was higher in DHT-exposed dams. Compared to the CD groups, the livers from HF/HS dams weighed more on GD18.5, the triglyceride content was higher, and there was a dysregulation of liver enzymes related to lipogenesis and higher mRNA expression of Fitm1. Fetuses from HF/HS-Veh dams had lower liver triglyceride content and mRNA expression of Srebf1c. Maternal DHT exposure, regardless of diet, decreased fetal liver Pparg mRNA expression and increased placental androgen receptor protein expression. Maternal diet-induced obesity, together with androgen excess, affects maternal and fetal liver function as demonstrated by increased triglyceride content and dysfunctional expression of enzymes and transcription factors involved in de novo lipogenesis and fat storage., CC BY 4.0

Published
2017
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30. Orellanine specifically targets renal clear cell carcinoma

Author

Buvall, Lisa, primary, Hedman, Heidi, additional, Khramova, Alina, additional, Najar, Deman, additional, Bergwall, Lovisa, additional, Ebefors, Kerstin, additional, Sihlbom, Carina, additional, Lundstam, Sven, additional, Herrmann, Anders, additional, Wallentin, Hanna, additional, Roos, Emelie, additional, Nilsson, Ulf A., additional, Johansson, Martin, additional, Törnell, Jan, additional, Haraldsson, Börje, additional, and Nyström, Jenny, additional

Published
2017
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33. Glomerular Endothelial Mitochondrial Dysfunction Is Essential and Characteristic of Diabetic Kidney Disease Susceptibility

Author

Qi, Haiying, primary, Casalena, Gabriella, additional, Shi, Shaolin, additional, Yu, Liping, additional, Ebefors, Kerstin, additional, Sun, Yezhou, additional, Zhang, Weijia, additional, D’Agati, Vivette, additional, Schlondorff, Detlef, additional, Haraldsson, Börje, additional, Böttinger, Erwin, additional, and Daehn, Ilse, additional

Published
2016
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36. Molecular mechanisms of the kidney in health and disease

Author

Ebefors, Kerstin

Subjects
kidney, gene expression, glomerulus, proteoglycans, urologic and male genital diseases
Abstract

In 2010, 307 Swedish patients received a new kidney through transplantation, and the first of April 2011, 603 patients were on the kidney transplant waiting list. In Sweden over 8000 patients are presently in active uremic care with about half in dialysis and the other half with a functional kidney graft. The numbers of patients in need of active uremic care are escalating and so are the costs for renal health care, in Sweden as in most of the western world. For patients with end stage renal disease active uremic care is the last option for survival since there is no cure or specific treatment for most renal diseases. The lack of treatment options often leaves steroids and chemotherapy as the only available choices. In order to find more specific treatment and to cure or delay the progress of renal disease we need to learn more about the molecular background of these diseases. To increase our understanding of the molecular mechanisms behind renal disease we have studied the gene expression in both an animal model of the nephrotic syndrome in rat as well as in human material in form of renal biopsies and cell cultures. The most common renal diseases all start in the glomerulus, the capillary tuft in the nephron where the ultrafiltration of blood takes place, and therefore we have focused on gene expression in the glomerulus. When investigating the gene expression in glomeruli from healthy kidney donors and from mice we found a core cluster of conserved, highly glomerulus-specific genes. Normal function of some of these genes in the glomerulus is already known to be of importance to the filtration barrier and mutations in certain of them are tightly connected to proteinuria. The discovered core cluster also contained genes that so far has not been coupled to renal function and disease, and can therefore be used as a new source of kidney glomerular-specific genes and biomarkers. By studying gene expression in rats with nephrotic syndrome and in patients with renal disease we found that expression of a special family of extracellular matrix proteins, called proteoglycans, was changed in renal disease compared to healthy controls. Proteoglycans are multifunctional proteins with functions ranging from holding and releasing signal molecules to making up part of the extracellular matrix structure. In patients with IgA nephropathy we found that the proteoglycan perlecan had an increased gene expression compared to control, and that the gene expression correlated to the excretion of protein in the urine and even to the progress rate of the disease. This suggests that perlecan could likely be used as a molecular marker for IgA nephropathy and as such help us to further understand the progression of the disease. In addition we have developed a unique method of culturing cells from patients with renal disease and we believe that this will give us new information about the molecular mechanism of this disorder and help us develop more specific and individualized treatment for patients with kidney failure.

Published
2011

38. Glomerular Endothelial Mitochondrial Dysfunction Is Essential and Characteristic of Diabetic Kidney Disease Susceptibility.

Author

Qi, Haiying, Casalena, Gabriella, Shi, Shaolin, Liping Yu, Ebefors,2, Kerstin, Sun,1, Yezhou, Weijia Zhang,1, D'Agati, Vivette, Schlondorff, Detlef, Haraldsson, Börje, Böttinger, Erwin, Daehn, Ilse, Yu, Liping, Ebefors, Kerstin, Sun, Yezhou, and Zhang, Weijia

Subjects
KIDNEY disease diagnosis, GLOMERULAR filtration rate, ENDOTHELIAL cells, MITOCHONDRIAL membranes, DISEASE susceptibility, DNA metabolism, ALBUMINURIA, ANIMAL experimentation, ANIMALS, ANTIOXIDANTS, CELL receptors, CELLULAR signal transduction, DIABETES, DIABETIC nephropathies, ENDOTHELINS, ENDOTHELIUM, ENZYME-linked immunosorbent assay, EPITHELIAL cells, FLOW cytometry, HIGH performance liquid chromatography, TYPE 1 diabetes, KIDNEY glomerulus, MICE, MITOCHONDRIA, ORGANOPHOSPHORUS compounds, PIPERIDINE, POLYMERASE chain reaction, RESEARCH funding, SCANNING electron microscopy, OXYGEN consumption, DEOXYRIBONUCLEOSIDES, PHARMACODYNAMICS
Abstract

The molecular signaling mechanisms between glomerular cell types during initiation/progression of diabetic kidney disease (DKD) remain poorly understood. We compared the early transcriptome profile between DKD-resistant C57BL/6J and DKD-susceptible DBA/2J (D2) glomeruli and demonstrated a significant downregulation of essential mitochondrial genes in glomeruli from diabetic D2 mice, but not in C57BL/6J, with comparable hyperglycemia. Diabetic D2 mice manifested increased mitochondrial DNA lesions (8-oxoguanine) exclusively localized to glomerular endothelial cells after 3 weeks of diabetes, and these accumulated over time in addition to increased urine secretion of 8-oxo-deoxyguanosine. Detailed assessment of glomerular capillaries from diabetic D2 mice demonstrated early signs of endothelial injury and loss of fenestrae. Glomerular endothelial mitochondrial dysfunction was associated with increased glomerular endothelin-1 receptor type A (Ednra) expression and increased circulating endothelin-1 (Edn1). Selective Ednra blockade or mitochondrial-targeted reactive oxygen species scavenging prevented mitochondrial oxidative stress of endothelial cells and ameliorated diabetes-induced endothelial injury, podocyte loss, albuminuria, and glomerulosclerosis. In human DKD, increased urine 8-oxo-deoxyguanosine was associated with rapid DKD progression, and biopsies from patients with DKD showed increased mitochondrial DNA damage associated with glomerular endothelial EDNRA expression. Our studies show that DKD susceptibility was linked to mitochondrial dysfunction, mediated largely by Edn1-Ednra in glomerular endothelial cells representing an early event in DKD progression, and suggest that cross talk between glomerular endothelial injury and podocytes leads to defects and depletion, albuminuria, and glomerulosclerosis. [ABSTRACT FROM AUTHOR]

Published
2017
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42. Melanocortin 1 Receptor Agonists Reduce Proteinuria

Author

Lindskog, Annika, primary, Ebefors, Kerstin, additional, Johansson, Martin E., additional, Stefánsson, Bergur, additional, Granqvist, Anna, additional, Arnadottir, Margret, additional, Berg, Anna-Lena, additional, Nyström, Jenny, additional, and Haraldsson, Börje, additional

Published
2010
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44. The role of dendrin in IgA nephropathy.

Author

Levin A, Schwarz A, Hulkko J, He L, Sun Y, Barany P, Bruchfeld A, Herthelius M, Wennberg L, Ebefors K, Patrakka J, Betsholtz C, Nyström J, Mölne J, Hultenby K, Witasp A, and Wernerson A

Subjects
Mice, Animals, Kidney Glomerulus pathology, Nerve Tissue Proteins metabolism, Proteinuria etiology, Glomerulonephritis, IGA complications, Glomerulonephritis, Membranous metabolism, IgA Vasculitis complications
Abstract

Background: Immunoglobulin A nephropathy (IgAN) and its systemic variant IgA vasculitis (IgAV) damage the glomeruli, resulting in proteinuria, hematuria and kidney impairment. Dendrin is a podocyte-specific protein suggested to be involved in the pathogenesis of IgAN. Upon cell injury, dendrin translocates from the slit diaphragm to the nucleus, where it is suggested to induce apoptosis and cytoskeletal changes, resulting in proteinuria and accelerated disease progression in mice. Here we investigated gene and protein expression of dendrin in relation to clinical and histopathological findings to further elucidate its role in IgAN/IgAV., Methods: Glomerular gene expression was measured using microarray on 30 IgAN/IgAV patients, 5 patients with membranous nephropathy (MN) and 20 deceased kidney donors. Dendrin was spatially evaluated on kidney tissue sections by immunofluorescence (IF) staining (IgAN patients, n = 4; nephrectomized kidneys, n = 3) and semi-quantified by immunogold electron microscopy (IgAN/IgAV patients, n = 21; MN, n = 5; living kidney donors, n = 6). Histopathological grading was performed according to the Oxford and Banff classifications. Clinical data were collected at the time of biopsy and follow-up., Results: Dendrin mRNA levels were higher (P = .01) in IgAN patients compared with MN patients and controls and most prominently in patients with preserved kidney function and fewer chronic histopathological changes. Whereas IF staining did not differ between groups, immunoelectron microscopy revealed that a higher relative nuclear dendrin concentration in IgAN patients was associated with a slower annual progression rate and milder histopathological changes., Conclusion: Dendrin messenger RNA levels and relative nuclear protein concentrations are increased and associated with a more benign phenotype and progression in IgAN/IgAV patients., (© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)

Published
2023
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