NLRX1 does not play a role in diabetes nor the development of diabetic nephropathy induced by multiple low doses of streptozotocin

Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus that results in both tubular and glomerular injury. Low-grade inflammation and oxidative stress are two mechanisms known to drive the progression of DN. Nucleotide-binding leucine-rich repeat containing family member X1 (...

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Vydáno v:	PloS one Ročník 14; číslo 3; s. e0214437
Hlavní autoři:	Scantlebery, Angelique M. L., Uil, Melissa, Butter, Loes M., Poelman, Renée, Claessen, Nike, Girardin, Stephen E., Florquin, Sandrine, Roelofs, Joris J. T. H., Leemans, Jaklien C.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Public Library of Science 25.03.2019 Public Library of Science (PLoS)
Témata:	Animals Antioxidants Authorship Biology and Life Sciences Body weight Body weight loss Butter Cellular stress response Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic nephropathies Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy Dose-Response Relationship, Drug Fibrosis Glucose Hemoglobin Hyperglycemia Inflammation Kidney - drug effects Kidney - metabolism Kidney - pathology Kidney diseases Kidneys Leucine Male Medicine and Health Sciences Metabolism Mice Mice, Inbred C57BL Microvasculature Mitochondria Mitochondrial Proteins - deficiency Mitochondrial Proteins - metabolism Nephropathy Oxidative phosphorylation Oxidative stress Oxidative Stress - drug effects Pathogenesis Pathology Phenotype Phenotypes Phosphorylation Physiological effects Polydipsia Polyuria Proteins Streptozocin Streptozocin - pharmacology Tumor necrosis factor-TNF Type 1 diabetes Urination disorders Weight loss Netherlands
ISSN:	1932-6203, 1932-6203
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Abstract	Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus that results in both tubular and glomerular injury. Low-grade inflammation and oxidative stress are two mechanisms known to drive the progression of DN. Nucleotide-binding leucine-rich repeat containing family member X1 (NLRX1) is an innate immune receptor, uniquely located in mitochondria, that has been found to regulate inflammatory responses and to dampen renal oxidative stress by regulating oxidative phosphorylation. For this reason, we investigated the role of NLRX1 in the development of DN in a Type 1 Diabetes mouse model. We analyzed the effect of NLRX1 deficiency on diabetes development and the accompanied renal damage, inflammation, and fibrosis. We found that multiple low doses of streptozotocin induced body weight loss, polydipsia, hyperglycemia, glycosuria, and a mild DN phenotype in wildtype and NLRX1-deficient mice, without significant differences between these mouse strains. Despite increased NLRX1 expression in diabetic wildtype mice, NLRX1 deficiency did not affect the diabetic phenotype induced by streptozotocin treatment, as reflected by similar levels of polyuria, microalbuminuria, and increased renal markers of oxidative stress and inflammation in wildtype and NLRX1-deficient mice. The present findings show that NLRX1 does not mediate the development of streptozotocin-induced diabetes and diabetic-induced nephropathy in mice after multiple low doses of streptozotocin. This data implies that, while NLRX1 can be triggered by cellular stress, its regulatory and functional effects may be dependent on the specific physiological conditions. In the case of DN, NLRX1 may be neither helpful nor harmful, but rather a marker of metabolic stress.
AbstractList	Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus that results in both tubular and glomerular injury. Low-grade inflammation and oxidative stress are two mechanisms known to drive the progression of DN. Nucleotide-binding leucine-rich repeat containing family member X1 (NLRX1) is an innate immune receptor, uniquely located in mitochondria, that has been found to regulate inflammatory responses and to dampen renal oxidative stress by regulating oxidative phosphorylation. For this reason, we investigated the role of NLRX1 in the development of DN in a Type 1 Diabetes mouse model. We analyzed the effect of NLRX1 deficiency on diabetes development and the accompanied renal damage, inflammation, and fibrosis. We found that multiple low doses of streptozotocin induced body weight loss, polydipsia, hyperglycemia, glycosuria, and a mild DN phenotype in wildtype and NLRX1-deficient mice, without significant differences between these mouse strains. Despite increased NLRX1 expression in diabetic wildtype mice, NLRX1 deficiency did not affect the diabetic phenotype induced by streptozotocin treatment, as reflected by similar levels of polyuria, microalbuminuria, and increased renal markers of oxidative stress and inflammation in wildtype and NLRX1-deficient mice. The present findings show that NLRX1 does not mediate the development of streptozotocin-induced diabetes and diabetic-induced nephropathy in mice after multiple low doses of streptozotocin. This data implies that, while NLRX1 can be triggered by cellular stress, its regulatory and functional effects may be dependent on the specific physiological conditions. In the case of DN, NLRX1 may be neither helpful nor harmful, but rather a marker of metabolic stress. Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus that results in both tubular and glomerular injury. Low-grade inflammation and oxidative stress are two mechanisms known to drive the progression of DN. Nucleotide-binding leucine-rich repeat containing family member X1 (NLRX1) is an innate immune receptor, uniquely located in mitochondria, that has been found to regulate inflammatory responses and to dampen renal oxidative stress by regulating oxidative phosphorylation. For this reason, we investigated the role of NLRX1 in the development of DN in a Type 1 Diabetes mouse model. We analyzed the effect of NLRX1 deficiency on diabetes development and the accompanied renal damage, inflammation, and fibrosis. We found that multiple low doses of streptozotocin induced body weight loss, polydipsia, hyperglycemia, glycosuria, and a mild DN phenotype in wildtype and NLRX1-deficient mice, without significant differences between these mouse strains. Despite increased NLRX1 expression in diabetic wildtype mice, NLRX1 deficiency did not affect the diabetic phenotype induced by streptozotocin treatment, as reflected by similar levels of polyuria, microalbuminuria, and increased renal markers of oxidative stress and inflammation in wildtype and NLRX1-deficient mice. The present findings show that NLRX1 does not mediate the development of streptozotocin-induced diabetes and diabetic-induced nephropathy in mice after multiple low doses of streptozotocin. This data implies that, while NLRX1 can be triggered by cellular stress, its regulatory and functional effects may be dependent on the specific physiological conditions. In the case of DN, NLRX1 may be neither helpful nor harmful, but rather a marker of metabolic stress.Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus that results in both tubular and glomerular injury. Low-grade inflammation and oxidative stress are two mechanisms known to drive the progression of DN. Nucleotide-binding leucine-rich repeat containing family member X1 (NLRX1) is an innate immune receptor, uniquely located in mitochondria, that has been found to regulate inflammatory responses and to dampen renal oxidative stress by regulating oxidative phosphorylation. For this reason, we investigated the role of NLRX1 in the development of DN in a Type 1 Diabetes mouse model. We analyzed the effect of NLRX1 deficiency on diabetes development and the accompanied renal damage, inflammation, and fibrosis. We found that multiple low doses of streptozotocin induced body weight loss, polydipsia, hyperglycemia, glycosuria, and a mild DN phenotype in wildtype and NLRX1-deficient mice, without significant differences between these mouse strains. Despite increased NLRX1 expression in diabetic wildtype mice, NLRX1 deficiency did not affect the diabetic phenotype induced by streptozotocin treatment, as reflected by similar levels of polyuria, microalbuminuria, and increased renal markers of oxidative stress and inflammation in wildtype and NLRX1-deficient mice. The present findings show that NLRX1 does not mediate the development of streptozotocin-induced diabetes and diabetic-induced nephropathy in mice after multiple low doses of streptozotocin. This data implies that, while NLRX1 can be triggered by cellular stress, its regulatory and functional effects may be dependent on the specific physiological conditions. In the case of DN, NLRX1 may be neither helpful nor harmful, but rather a marker of metabolic stress.
Audience	Academic
Author	Girardin, Stephen E. Claessen, Nike Roelofs, Joris J. T. H. Butter, Loes M. Uil, Melissa Poelman, Renée Florquin, Sandrine Scantlebery, Angelique M. L. Leemans, Jaklien C.
AuthorAffiliation	2 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada 1 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, North Holland, The Netherlands National Institutes of Health, UNITED STATES
AuthorAffiliation_xml	– name: National Institutes of Health, UNITED STATES – name: 1 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, North Holland, The Netherlands – name: 2 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
Author_xml	– sequence: 1 givenname: Angelique M. L. orcidid: 0000-0001-9303-6042 surname: Scantlebery fullname: Scantlebery, Angelique M. L. – sequence: 2 givenname: Melissa surname: Uil fullname: Uil, Melissa – sequence: 3 givenname: Loes M. surname: Butter fullname: Butter, Loes M. – sequence: 4 givenname: Renée surname: Poelman fullname: Poelman, Renée – sequence: 5 givenname: Nike surname: Claessen fullname: Claessen, Nike – sequence: 6 givenname: Stephen E. surname: Girardin fullname: Girardin, Stephen E. – sequence: 7 givenname: Sandrine surname: Florquin fullname: Florquin, Sandrine – sequence: 8 givenname: Joris J. T. H. surname: Roelofs fullname: Roelofs, Joris J. T. H. – sequence: 9 givenname: Jaklien C. surname: Leemans fullname: Leemans, Jaklien C.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/30908533$$D View this record in MEDLINE/PubMed
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CitedBy_id	crossref_primary_10_1016_j_cyto_2022_156055 crossref_primary_10_3892_etm_2021_9640 crossref_primary_10_1016_j_ejphar_2020_173276 crossref_primary_10_3389_fimmu_2019_02419 crossref_primary_10_1111_imm_13291 crossref_primary_10_1007_s00424_019_02316_w
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 LMB, RP, NC also contributed equally to this work and JR and JL share last authorship. Competing Interests: The authors have declared that no competing interests exist.
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Snippet	Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus that results in both tubular and glomerular injury. Low-grade inflammation and...
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SubjectTerms	Animals Antioxidants Authorship Biology and Life Sciences Body weight Body weight loss Butter Cellular stress response Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic nephropathies Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy Dose-Response Relationship, Drug Fibrosis Glucose Hemoglobin Hyperglycemia Inflammation Kidney - drug effects Kidney - metabolism Kidney - pathology Kidney diseases Kidneys Leucine Male Medicine and Health Sciences Metabolism Mice Mice, Inbred C57BL Microvasculature Mitochondria Mitochondrial Proteins - deficiency Mitochondrial Proteins - metabolism Nephropathy Oxidative phosphorylation Oxidative stress Oxidative Stress - drug effects Pathogenesis Pathology Phenotype Phenotypes Phosphorylation Physiological effects Polydipsia Polyuria Proteins Streptozocin Streptozocin - pharmacology Tumor necrosis factor-TNF Type 1 diabetes Urination disorders Weight loss
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Title	NLRX1 does not play a role in diabetes nor the development of diabetic nephropathy induced by multiple low doses of streptozotocin
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