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Söderkvist, Peter
Alternative names
Publications (10 of 147) Show all publications
Malmström, A., Lysiak, M., Winther Kristensen, B., Hovey, E., Henriksson, R. & Söderkvist, P. (2019). Do we really know who has an MGMT methylated glioma?: Results of an international survey regarding use of MGMT analyses for glioma. Neuro-Oncology Practice, 1-9
Open this publication in new window or tab >>Do we really know who has an MGMT methylated glioma?: Results of an international survey regarding use of MGMT analyses for glioma
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2019 (English)In: Neuro-Oncology Practice, ISSN 2054-2577, p. 1-9Article in journal (Refereed) Published
Abstract [en]

Glioma O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation status informs clinical decision making. Worldwide different methods and cutoff levels are used, which can lead to discordant methylation results.We conducted an international survey to clarify which methods are regularly used and why. We also explored opinions regarding international consensus on methods and cutoff.The survey had 152 respondents from 25 countries. MGMT methylation status is determined for all glioblastomas in 37% of laboratories. The most common methods are methylation-specific polymerase chain reaction (msPCR) (37%) and pyrosequencing (34%). A method is selected for simplicity (56%), cost-effectiveness (50%), and reproducibility of results (52%). For sequencing, the number of CpG sites analyzed varies from 1–3 up to more than 16. For 50% of laboratories, the company producing the kit determines which CpG sites are examined, whereas 33% select the sites themselves. Selection of cutoff is equally distributed among a cutoff defined in the literature, by the local laboratory, or by the outside laboratory performing the analysis. This cutoff varies, reported from 1% to 30%, and in 1 laboratory tumor is determined as methylated in case of 1 methylated CpG site of 17 analyzed. Some report tumors as unmethylated or weakly vs highly methylated. An international consensus on MGMT methylation method and cutoff is warranted by 66% and 76% of respondents, respectively. The method preferred would be msPCR (45%) or pyrosequencing (42%), whereas 18% suggest next-generation sequencing.Although analysis of MGMT methylation status is routine, there is controversy regarding laboratory methods and cutoff level. Most respondents favor development of international consensus guidelines.

Place, publisher, year, edition, pages
Oxford: Oxford University Press, 2019
National Category
Medical Bioscience Clinical Laboratory Medicine
Identifiers
urn:nbn:se:liu:diva-160808 (URN)10.1093/nop/npz039 (DOI)
Available from: 2019-10-09 Created: 2019-10-09 Last updated: 2019-10-11Bibliographically approved
Welander, J., Lysiak, M., Brauckhoff, M., Brunaud, L., Söderkvist, P. & Gimm, O. (2018). Activating FGFR1 mutations in sporadic pheochromocytoma. World Journal of Surgery, 42(2), 482-489
Open this publication in new window or tab >>Activating FGFR1 mutations in sporadic pheochromocytoma
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2018 (English)In: World Journal of Surgery, ISSN 0364-2313, E-ISSN 1432-2323, Vol. 42, no 2, p. 482-489Article in journal (Refereed) Published
Abstract [en]

Pheochromocytomas are neuroendocrine tumors of the adrenal glands that cause hypertension. More than a third of the cases are associated with hereditary mutations in a growing list of susceptibility genes, some of which are also somatically altered in sporadic pheochromocytomas. However, for the majority of sporadic pheochromocytomas, a genetic explanation is still lacking. Here we investigated the genomic landscape of sporadic pheochromocytomas with whole-exome sequencing of 16 paired tumor and normal DNA samples, and discovered on average 33 non-silent somatic mutations per tumor. One of the recurrently mutated genes was FGFR1, encoding the fibroblast growth factor receptor 1, which was recently revealed as an oncogene in pilocytic astrocytoma and childhood glioblastoma. Including a subsequent analysis of a larger cohort, activating FGFR1  mutations were detected in three of 80 sporadic pheochromocytomas (3.8%). Gene expression microarray profiling showed that these tumors clustered with NF1- RET- and HRAS-mutated pheochromocytomas, indicating activation of the MAPK and PI3K-AKT signal transduction pathways. The results advance our biological understanding of pheochromocytoma and suggest that somatic FGFR1 activation is an important event in a subset of these tumors.

Place, publisher, year, edition, pages
Springer, 2018
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-114805 (URN)10.1007/s00268-017-4320-0 (DOI)000419886700025 ()29159601 (PubMedID)
Note

Funding agencies: Linkoping University; Swedish Cancer Society; FORSS; LiU Cancer

Available from: 2015-03-04 Created: 2015-03-04 Last updated: 2019-05-03Bibliographically approved
Alkaissi, H., Havarinasab, S., Nielsen, J. B., Söderkvist, P. & Hultman, P. (2018). Bank1 and NF-kappaB as key regulators in anti-nucleolar antibody development. PLoS ONE, 13(7), Article ID e0199979.
Open this publication in new window or tab >>Bank1 and NF-kappaB as key regulators in anti-nucleolar antibody development
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2018 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, no 7, article id e0199979Article in journal (Refereed) Published
Abstract [en]

Systemic autoimmune rheumatic disorders (SARD) represent important causes of morbidity and mortality in humans. The mechanisms triggering autoimmune responses are complex and involve a network of genetic factors. Mercury-induced autoimmunity (HgIA) in mice is an established model to study the mechanisms of the development of antinuclear antibodies (ANA), which is a hallmark in the diagnosis of SARD. A.SW mice with HgIA show a significantly higher titer of antinucleolar antibodies (ANoA) than the B10.S mice, although both share the same MHC class II (H-2). We applied a genome-wide association study (GWAS) to their Hg-exposed F2 offspring to investigate the non-MHC genes involved in the development of ANoA. Quantitative trait locus (QTL) analysis showed a peak logarithm of odds ratio (LOD) score of 3.05 on chromosome 3. Microsatellites were used for haplotyping, and fine mapping was conducted with next generation sequencing. The candidate genes Bank1 (B-cell scaffold protein with ankyrin repeats 1) and Nfkbl (nuclear factor kappa B subunit 1) were identified by additional QTL analysis. Expression of the Bank1 and Nfkb1 genes and their downstream target genes involved in the intracellular pathway (Tlr9,II6, Tnf) was investigated in mercury-exposed A.SW and B10.S mice by real-time PCR. Bank1 showed significantly lower gene expression in the A.SW strain after Hg-exposure, whereas the B10.S strain showed no significant difference. Nfkb1, Tlr9, II6 and Tnf had significantly higher gene expression in the A.SW strain after Hg-exposure, while the B10.S strain showed no difference. This study supports the roles of Bank1 (produced mainly in B-cells) and Nfkbl (produced in most immune cells) as key regulators of ANoA development in HgIA.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2018
National Category
Genetics
Identifiers
urn:nbn:se:liu:diva-150265 (URN)10.1371/journal.pone.0199979 (DOI)000438866600014 ()30016332 (PubMedID)
Note

Funding Agencies|Swedish Research Council Branch of Medicine; County Council of Ostergotland; Linkoping University

Available from: 2018-08-17 Created: 2018-08-17 Last updated: 2019-04-24
Paulsson, J. O., Svahn, F., Welander, J., Brunaud, L., Söderkvist, P., Gimm, O., . . . Juhlin, C. C. (2016). Editorial Material: Absence of the BRAF V600E mutation in pheochromocytoma in JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, vol 39, issue 6, pp 715-716. Journal of Endocrinological Investigation, 39(6), 715-716
Open this publication in new window or tab >>Editorial Material: Absence of the BRAF V600E mutation in pheochromocytoma in JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, vol 39, issue 6, pp 715-716
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2016 (English)In: Journal of Endocrinological Investigation, ISSN 0391-4097, E-ISSN 1720-8386, Vol. 39, no 6, p. 715-716Article in journal, Editorial material (Other academic) Published
Abstract [en]

Purpose Pheochromocytomas (PCCs) are rare endocrine tumors originating from the adrenal medulla. These tumors display a highly heterogeneous mutation profile, and a substantial part of the causative genetic events remains to be explained. Recent studies have reported presence of the activating BRAF V600E mutation in PCC, suggesting a role for BRAF activation in tumor development. This study sought to further investigate the occurrence of the BRAF V600E mutation in these tumors. Methods A cohort of 110 PCCs was screened for the BRAF V600E mutation using direct Sanger sequencing. Results All cases investigated displayed wild-type sequences at nucleotide 1799 in the BRAF gene. Conclusions Taken together with all previously screened tumors up to date, only 1 BRAF V600E mutation has been found among 361 PCCs. These findings imply that the BRAF V600E mutation is a rare event in pheochromocytoma.

Place, publisher, year, edition, pages
SPRINGER, 2016
Keywords
Adrenal; Pheochromocytoma; Sequencing; BRAF; Mutation
National Category
Medical Genetics
Identifiers
urn:nbn:se:liu:diva-129146 (URN)10.1007/s40618-015-0420-6 (DOI)000375920000013 ()26710756 (PubMedID)
Available from: 2016-06-13 Created: 2016-06-13 Last updated: 2018-04-25
Stenman, A., Welander, J., Gustavsson, I., Brunaud, L., Backdahl, M., Söderkvist, P., . . . Larsson, C. (2016). HRAS mutation prevalence and associated expression patterns in pheochromocytoma. Genes, Chromosomes and Cancer, 55(5), 452-459
Open this publication in new window or tab >>HRAS mutation prevalence and associated expression patterns in pheochromocytoma
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2016 (English)In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 55, no 5, p. 452-459Article in journal (Refereed) Published
Abstract [en]

Pheochromocytomas (PCC) and abdominal paragangliomas (PGL) display a highly diverse genetic background and recent gene expression profiling studies have shown that PCC and PGL (together PPGL) alter either kinase signaling pathways or the pseudo-hypoxia response pathway dependent of the genetic composition. Recurrent mutations in the Harvey rat sarcoma viral oncogene homolog (HRAS) have recently been verified in sporadic PPGLs. In order to further establish the HRAS mutation frequency and to characterize the associated expression profiles of HRAS mutated tumors, 156 PPGLs for exon 2 and 3 hotspot mutations in the HRAS gene was screened, and compared with microarray-based gene expression profiles for 93 of the cases. The activating HRAS mutations G13R, Q61R, and Q61K were found in 10/142 PCC (7.0%) and a Q61L mutation was revealed in 1/14 PGL (7.1%). All HRAS mutated cases included in the mRNA expression profiling grouped in Cluster 2, and 21 transcripts were identified as altered when comparing the mutated tumors with 91 HRAS wild-type PPGL. Somatic HRAS mutations were not revealed in cases with known PPGL susceptibility gene mutations and all HRAS mutated cases were benign. The HRAS mutation prevalence of all PPGL published up to date is 5.2% (49/950), and 8.8% (48/548) among cases without a known PPGL susceptibility gene mutation. The findings support a role of HRAS mutations as a somatic driver event in benign PPGL without other known susceptibility gene mutations. HRAS mutated PPGL cluster together with NF1- and RET-mutated tumors associated with activation of kinase-signaling pathways.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-127407 (URN)10.1002/gcc.22347 (DOI)000372913800005 ()26773571 (PubMedID)
Note

Funding Agencies|Swedish Cancer Foundation; StratCan; Swedish Research Council; Cancer Research Foundations of Radiumhemmet; Karolinska Institutet; Stockholm County Council

Available from: 2016-05-02 Created: 2016-04-26 Last updated: 2018-04-25
Noren, E., Verma, D., Söderkvist, P., Weisselberg, T., Söderman, J., Lotfi, K. & Almer, S. (2016). Single Nucleotide Polymorphisms in MORC4, CD14, and TLR4 Are Related to Outcome of Allogeneic Stem Cell Transplantation. Annals of Transplantation, 21, 56-67
Open this publication in new window or tab >>Single Nucleotide Polymorphisms in MORC4, CD14, and TLR4 Are Related to Outcome of Allogeneic Stem Cell Transplantation
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2016 (English)In: Annals of Transplantation, ISSN 1425-9524, E-ISSN 2329-0358, Vol. 21, p. 56-67Article in journal (Refereed) Published
Abstract [en]

Background: Non-HLA genes may contribute to the prognosis after hematopoietic stem cell transplantation. We investigated associations between single nucleotide polymorphisms in regions of MORC4, CD14, TLR4, NOD2, SLC22A4, SLC22A5, CARD8, NLRP3, and CLDN2 and the outcomes of patients undergoing allogeneic stem cell transplantation. Material/Methods: Single nucleotide polymorphisms in selected regions were determined and analyzed for putative associations with overall mortality and acute graft-versus-host disease. Significant associations were further explored by logistic regression, controlling for additional variables. Results: A significant association was identified between overall mortality among recipients and a nonsynonymous coding variant of MORC4 (rs6622126) in the recipient genetic makeup (P=0.029). Since MORC4 is located on the X-chromosome, the results were also analyzed separately for males and females. The association between overall mortality for recipients and the risk allele (rs6622126; A) was confirmed for males with respect to genetic makeup of recipients (P=0.012), donor genetic makeup (P=0.004), and the combined allele composition of the donor and recipient (P=0.001). A significant association was also identified between overall mortality and the recipient risk allele of CD14 (rs2569190; P=0.031), TLR4 (rs4986790; P=0.043), and NOD2 (carriage of at least 1 mutant allele of rs2066844, rs2066845, or rs2066847; P=0.048). Among the investigated genes, only the CD14 (rs2569190) recipient risk allele was significantly associated with acute graft-versus-host disease (P=0.023). Logistic regression models confirmed these findings, except for NOD2, and also identified a significant contribution by age at stem cell transplantation (MORC4, CD14, TLR4), diagnosis (CD14, TLR4), and prophylaxis (MORC4). Conclusions: Genetic variation in MORC4, CD14, and TLR4 may affect the outcome of allogeneic stem cell transplantation.

Place, publisher, year, edition, pages
Warsaw, Poland: International Scientific Literature, 2016
Keywords
Association Studies; Genetic Predisposition to Disease; Graft vs. Host Disease; Polymorphism, Single Nucleotide; Transplantation, Homologous
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-126266 (URN)000371110000001 ()
Available from: 2016-03-21 Created: 2016-03-21 Last updated: 2017-05-03Bibliographically approved
Mosrati, M. A., Willander, K., Jakobsen Falk, I., Hermanson, M., Höglund, M., Stockelberg, D., . . . Söderkvist, P. (2015). Association between TERT promoter polymorphisms and acute myeloid leukemia risk and prognosis. OncoTarget, 6(28), 25109-25120
Open this publication in new window or tab >>Association between TERT promoter polymorphisms and acute myeloid leukemia risk and prognosis
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2015 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 6, no 28, p. 25109-25120Article in journal (Refereed) Published
Abstract [en]

Telomerase reverse transcriptase gene (TERT) promoter mutations are identified in many malignancies but not in hematological malignancies. Here we analyzed TERT and protection of telomeres 1 gene (POT1) mutations, and four different TERT SNVs in 226 acute myeloid leukemia (AML) patients and 806 healthy individuals in a case referent design, where also overall survival was assessed. A significant association for increased risk of AML was found for TERT SNVs, rs2853669 (OR = 2.45, p = 0.00015) and rs2736100 (OR = 1.5, p = 0.03). The overall survival for patients with CC genotype of rs2853669 was significantly shorter compared to those with TT or TC genotypes (p = 0.036 and 0.029 respectively). The influence of TERT rs2853669 CC on survival was confirmed in multivariable Cox regression analysis as an independent risk biomarker in addition to high risk group, higher age and treatment. No hot spot TERT promoter mutations at -228Cgreater thanT or -250Cgreater thanT or POT1 mutations could be identified in this AML cohort. We show that rs2853669 CC may be a risk factor for the development of AML that may also be used as a prognostic marker to identify high risk normal karyotype -AML (NK-AML) patients, for treatment guidance.

Place, publisher, year, edition, pages
Albany, NY, United States: Impact Journals LLC, 2015
Keywords
TERT; SNV; AML; prognostic markers
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-122667 (URN)10.18632/oncotarget.4668 (DOI)000363160100047 ()
Note

Funding Agencies|Swedish Research Council; Swedish Cancer Society; County Council of Ostergotland; AFA Insurance; FORSS

Available from: 2015-11-16 Created: 2015-11-13 Last updated: 2017-12-01Bibliographically approved
van Thuijl, H. F., Mazor, T., Johnson, B. E., Fouse, S. D., Aihara, K., Hong, C., . . . Costello, J. F. (2015). Evolution of DNA repair defects during malignant progression of low-grade gliomas after temozolomide treatment. Acta Neuropathologica, 129(4), 597-607
Open this publication in new window or tab >>Evolution of DNA repair defects during malignant progression of low-grade gliomas after temozolomide treatment
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2015 (English)In: Acta Neuropathologica, ISSN 0001-6322, E-ISSN 1432-0533, Vol. 129, no 4, p. 597-607Article in journal (Refereed) Published
Abstract [en]

Temozolomide (TMZ) increases the overall survival of patients with glioblastoma (GBM), but its role in the clinical management of diffuse low-grade gliomas (LGG) is still being defined. DNA hypermethylation of the O (6) -methylguanine-DNA methyltransferase (MGMT) promoter is associated with an improved response to TMZ treatment, while inactivation of the DNA mismatch repair (MMR) pathway is associated with therapeutic resistance and TMZ-induced mutagenesis. We previously demonstrated that TMZ treatment of LGG induces driver mutations in the RB and AKT-mTOR pathways, which may drive malignant progression to secondary GBM. To better understand the mechanisms underlying TMZ-induced mutagenesis and malignant progression, we explored the evolution of MGMT methylation and genetic alterations affecting MMR genes in a cohort of 34 treatment-na less than ve LGGs and their recurrences. Recurrences with TMZ-associated hypermutation had increased MGMT methylation compared to their untreated initial tumors and higher overall MGMT methylation compared to TMZ-treated non-hypermutated recurrences. A TMZ-associated mutation in one or more MMR genes was observed in five out of six TMZ-treated hypermutated recurrences. In two cases, pre-existing heterozygous deletions encompassing MGMT, or an MMR gene, were followed by TMZ-associated mutations in one of the genes of interest. These results suggest that tumor cells with methylated MGMT may undergo positive selection during TMZ treatment in the context of MMR deficiency.

Place, publisher, year, edition, pages
Springer Verlag (Germany), 2015
Keywords
Low-grade glioma; Temozolomide; Hypermutator; Mismatch repair; MGMT
National Category
Medical Genetics
Identifiers
urn:nbn:se:liu:diva-117202 (URN)10.1007/s00401-015-1403-6 (DOI)000351517200008 ()25724300 (PubMedID)
Note

Funding Agencies|Accelerate Brain Cancer Cure; Grove Foundation; TDC Foundation; Anne and Jason Farber Foundation; UCSF Brain Tumor SPORE grant [NIH P50CA097257]; Dutch Cancer Society (KWF) [2009-4470]; foundation STOPHersentumoren; Edli foundation; LiU Cancer Research Network; Medical Research Council of Southeast Sweden; National Institute Of General Medical Sciences [T32GM008568]; National Institutes of Health [1T32CA15102201]; National Cancer Institute [R01CA169316]; Sontag Foundation; NCI RO1 [R01 CA163687]; Project for Development of Innovative Research on Cancer Therapeutics (P-Direct); Ministry of Education, Culture, Sports, Science and Technology of Japan [23134501, 24221011]

Available from: 2015-04-22 Created: 2015-04-21 Last updated: 2019-10-14
Stenman, A., Svahn, F., Welander, J., Gustavson, B., Söderkvist, P., Gimm, O. & Juhlin, C. C. (2015). Immunohistochemical NF1 Analysis Does not Predict NF1 Gene Mutation Status in Pheochromocytoma.. Endocrine pathology, 26(1), 9-14
Open this publication in new window or tab >>Immunohistochemical NF1 Analysis Does not Predict NF1 Gene Mutation Status in Pheochromocytoma.
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2015 (English)In: Endocrine pathology, ISSN 1046-3976, E-ISSN 1559-0097, Vol. 26, no 1, p. 9-14Article in journal (Refereed) Published
Abstract [en]

Pheochromocytomas (PCCs) are tumors originating from the adrenal medulla displaying a diverse genetic background. While most PCCs are sporadic, about 40 % of the tumors have been associated with constitutional mutations in one of at least 14 known susceptibility genes. As 25 % of sporadic PCCs harbor somatic neurofibromin 1 gene (NF1) mutations, NF1 has been established as the most recurrently mutated gene in PCCs. To be able to pinpoint NF1-related pheochromocytoma (PCC) disease in clinical practice could facilitate the detection of familial cases, but the large size of the NF1 gene makes standard DNA sequencing methods cumbersome. The aim of this study was to examine whether mutations in the NF1 gene could be predicted by immunohistochemistry as a method to identify cases for further genetic characterization. Sixty-seven PCCs obtained from 67 unselected patients for which the somatic and constitutional mutational status of NF1 was known (49 NF1 wild type, 18 NF1 mutated) were investigated for NF1 protein immunoreactivity, and the results were correlated to clinical and genetic data. NF1 immunoreactivity was absent in the majority of the PCCs (44/67; 66 %), including 13 out of 18 cases (72 %) with a somatic or constitutional NF1 mutation. However, only a minority of the NF1 wild-type PCCs (18/49; 37 %) displayed retained NF1 immunoreactivity, thereby diminishing the specificity of the method. We conclude that NF1 immunohistochemistry alone is not a sufficient method to distinguish between NF1-mutated and non-mutated PCCs. In the clinical context, genetic screening therefore remains the most reliable tool to detect NF1-mutated PCCs.

Place, publisher, year, edition, pages
Springer, 2015
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-115262 (URN)10.1007/s12022-014-9348-1 (DOI)000350057500002 ()25403449 (PubMedID)
Available from: 2015-03-11 Created: 2015-03-11 Last updated: 2018-04-25Bibliographically approved
Shahzad, K., Bock, F., Dong, W., Wang, H., Kopf, S., Kohli, S., . . . Isermann, B. (2015). Nlrp3-inflammasome activation in non-myeloid-derived cells aggravates diabetic nephropathy. Kidney International, 87(1), 74-84
Open this publication in new window or tab >>Nlrp3-inflammasome activation in non-myeloid-derived cells aggravates diabetic nephropathy
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2015 (English)In: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, Vol. 87, no 1, p. 74-84Article in journal (Refereed) Published
Abstract [en]

Diabetic nephropathy is a growing health concern with characteristic sterile inflammation. As the underlying mechanisms of this inflammation remain poorly defined, specific therapies targeting sterile inflammation in diabetic nephropathy are lacking. Intriguingly, an association of diabetic nephropathy with inflammasome activation has recently been shown, but the pathophysiological relevance of this finding remains unknown. Within glomeruli, inflammasome activation was detected in endothelial cells and podocytes in diabetic humans and mice and in glucose-stressed glomerular endothelial cells and podocytes in vitro. Abolishing Nlrp3 or caspase-1 expression in bone marrow-derived cells fails to protect mice against diabetic nephropathy. Conversely, Nlrp3-deficient mice are protected against diabetic nephropathy despite transplantation of wild-type bone marrow. Pharmacological IL-1R antagonism prevented or even reversed diabetic nephropathy in mice. Mitochondrial reactive oxygen species (ROS) activate the Nlrp3 inflammasome in glucose or advanced glycation end product stressed podocytes. Inhibition of mitochondrial ROS prevents glomerular inflammasome activation and nephropathy in diabetic mice. Thus, mitochondrial ROS and Nlrp3-inflammasome activation in non-myeloid-derived cells aggravate diabetic nephropathy. Targeting the inflammasome may be a potential therapeutic approach to diabetic nephropathy.

Place, publisher, year, edition, pages
Nature Publishing Group: Open Access Hybrid Model Option A, 2015
Keywords
diabetic nephropathy; endothelial cell; inflammasome; mitochondrial ROS; Nlrp3; podocyte
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-113734 (URN)10.1038/ki.2014.271 (DOI)000346977900011 ()25075770 (PubMedID)
Note

Funding Agencies|Deutsche Forschungsgemeinschaft [IS 67/2-4, TH 1789/1-1, BI 1281/3-1]; EFSD (European Foundation for the Study of Diabetes); DDS (Deutsche Diabetes Stiftung); Hopp Stiftung; Stiftung fur Pathobiochemie und Molekulare Diagnostik; ERC StG; BioSysNet Research group

Available from: 2015-01-30 Created: 2015-01-29 Last updated: 2017-12-05
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