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  1. Article ; Online: Hedgehog signaling indirectly affects tubular cell survival after obstructive kidney injury.

    Rauhauser, Alysha A / Ren, Chongyu / Lu, Dongmei / Li, Binghua / Zhu, Jili / McEnery, Kayla / Vadnagara, Komal / Zepeda-Orozco, Diana / Zhou, Xin J / Lin, Fangming / Jetten, Anton M / Attanasio, Massimo

    American journal of physiology. Renal physiology

    2015  Volume 309, Issue 9, Page(s) F770–8

    Abstract: Hedgehog (Hh) is an evolutionary conserved signaling pathway that has important functions in kidney morphogenesis and adult organ maintenance. Recent work has shown that Hh signaling is reactivated in the kidney after injury and is an important mediator ... ...

    Abstract Hedgehog (Hh) is an evolutionary conserved signaling pathway that has important functions in kidney morphogenesis and adult organ maintenance. Recent work has shown that Hh signaling is reactivated in the kidney after injury and is an important mediator of progressive fibrosis. Pericytes and fibroblasts have been proposed to be the principal cells that respond to Hh ligands, and pharmacological attenuation of Hh signaling has been considered as a possible treatment for fibrosis, but the effect of Hh inhibition on tubular epithelial cells after kidney injury has not been reported. Using genetically modified mice in which tubule-derived hedgehog signaling is increased and mice in which this pathway is conditionally suppressed in pericytes that express the proteoglycan neuron glial protein 2 (NG2), we found that suppression of Hh signaling is associated with decreased macrophage infiltration and tubular proliferation but also increased tubular apoptosis, an effect that correlated with the reduction of tubular β-catenin activity. Collectively, our data suggest a complex function of hedgehog signaling after kidney injury in initiating both reparative and proproliferative, prosurvival processes.
    MeSH term(s) Acute Kidney Injury/etiology ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/pathology ; Acute Kidney Injury/prevention & control ; Animals ; Antigens/metabolism ; Apoptosis ; Cell Proliferation ; Cell Survival ; Disease Models, Animal ; Hedgehog Proteins/antagonists & inhibitors ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Kidney Tubules/drug effects ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Pericytes/metabolism ; Pericytes/pathology ; Proteoglycans/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/drug effects ; Smoothened Receptor ; Ureteral Obstruction/complications ; Veratrum Alkaloids/pharmacology ; Zinc Finger Protein GLI1 ; beta Catenin/metabolism
    Chemical Substances Antigens ; CTNNB1 protein, mouse ; Gli protein, mouse ; Gli5 protein, mouse ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Nerve Tissue Proteins ; Proteoglycans ; Receptors, G-Protein-Coupled ; Shh protein, mouse ; Smo protein, mouse ; Smoothened Receptor ; Veratrum Alkaloids ; Zinc Finger Protein GLI1 ; beta Catenin ; chondroitin sulfate proteoglycan 4 ; ihh protein, mouse ; cyclopamine (ZH658AJ192)
    Language English
    Publishing date 2015-11-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00232.2015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Increased hedgehog signaling in postnatal kidney results in aberrant activation of nephron developmental programs.

    Li, Binghua / Rauhauser, Alysha A / Dai, Julie / Sakthivel, Ramanavelan / Igarashi, Peter / Jetten, Anton M / Attanasio, Massimo

    Human molecular genetics

    2011  Volume 20, Issue 21, Page(s) 4155–4166

    Abstract: Hedgehog (Hh) is a core signaling pathway implicated in fundamental processes during embryonic kidney development. We previously found that loss-of-function mutations in the transcription factor GLIS2, a putative vertebrate ortholog of Drosophila Ci, ... ...

    Abstract Hedgehog (Hh) is a core signaling pathway implicated in fundamental processes during embryonic kidney development. We previously found that loss-of-function mutations in the transcription factor GLIS2, a putative vertebrate ortholog of Drosophila Ci, cause nephronophthisis type 7 in humans and mice. Kidney tubular cells in Glis2-knockout mice acquire mesenchymal phenotype, but the cellular mechanisms of this transition are unknown. Here, we demonstrate that Glis2 is a functional component of Hh signaling and is necessary to suppress this pathway in the postnatal kidney. In the epithelial compartment, Glis2 opposes Gli1 activity by binding cis-acting regulatory sequences in the 5' flanking regions of Snai1 and Wnt4, thereby inhibiting de-differentiation of tubular cells. We conclude that Glis2 is necessary to inhibit Hh signaling and to maintain the mature tubular epithelial phenotype in the adult kidney. This is the first description of a molecular mechanism that links the Hh signaling pathway to cystic kidney diseases and can open new avenues for the treatment of diverse ciliopathies.
    MeSH term(s) Animals ; Animals, Newborn ; Cell Differentiation/genetics ; Cells, Cultured ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Developmental ; HEK293 Cells ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Nephrons/growth & development ; Nephrons/metabolism ; Nephrons/pathology ; Nerve Tissue Proteins/metabolism ; PAX2 Transcription Factor/metabolism ; Phenotype ; Protein Binding ; Regulatory Sequences, Nucleic Acid/genetics ; Signal Transduction ; Snail Family Transcription Factors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Wnt4 Protein/genetics ; Wnt4 Protein/metabolism ; Zinc Finger Protein GLI1
    Chemical Substances Gli1 protein, mouse ; Gli5 protein, mouse ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Nerve Tissue Proteins ; PAX2 Transcription Factor ; Pax2 protein, mouse ; SNAI1 protein, human ; Snai1 protein, mouse ; Snail Family Transcription Factors ; Transcription Factors ; Wnt4 Protein ; Wnt4 protein, mouse ; Zinc Finger Protein GLI1 ; sna protein, Drosophila
    Language English
    Publishing date 2011-08-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddr339
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3469: Show issues Location:
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  3. Article ; Online: Loss of Glis2/NPHP7 causes kidney epithelial cell senescence and suppresses cyst growth in the Kif3a mouse model of cystic kidney disease.

    Lu, Dongmei / Rauhauser, Alysha / Li, Binghua / Ren, Chongyu / McEnery, Kayla / Zhu, Jili / Chaki, Moumita / Vadnagara, Komal / Elhadi, Sarah / Jetten, Anton M / Igarashi, Peter / Attanasio, Massimo

    Kidney international

    2016  Volume 89, Issue 6, Page(s) 1307–1323

    Abstract: Enlargement of kidney tubules is a common feature of multiple cystic kidney diseases in humans and mice. However, while some of these pathologies are characterized by cyst expansion and organ enlargement, in others, progressive interstitial fibrosis and ... ...

    Abstract Enlargement of kidney tubules is a common feature of multiple cystic kidney diseases in humans and mice. However, while some of these pathologies are characterized by cyst expansion and organ enlargement, in others, progressive interstitial fibrosis and kidney atrophy prevail. The Kif3a knockout mouse is an established non-orthologous mouse model of cystic kidney disease. Conditional inactivation of Kif3a in kidney tubular cells results in loss of primary cilia and rapid cyst growth. Conversely, loss of function of the gene GLIS2/NPHP7 causes progressive kidney atrophy, interstitial inflammatory infiltration, and fibrosis. Kif3a null tubular cells have unrestrained proliferation and reduced stabilization of p53 resulting in a loss of cell cycle arrest in the presence of DNA damage. In contrast, loss of Glis2 is associated with activation of checkpoint kinase 1, stabilization of p53, and induction of cell senescence. Interestingly, the cystic phenotype of Kif3a knockout mice is partially rescued by genetic ablation of Glis2 and pharmacological stabilization of p53. Thus, Kif3a is required for cell cycle regulation and the DNA damage response, whereas cell senescence is significantly enhanced in Glis2 null cells. Hence, cell senescence is a central feature in nephronophthisis type 7 and Kif3a is unexpectedly required for efficient DNA damage response and cell cycle arrest.
    MeSH term(s) Animals ; Cell Cycle Checkpoints/genetics ; Cellular Senescence/genetics ; Checkpoint Kinase 1/metabolism ; Cilia/pathology ; Cysts/genetics ; DNA Damage/genetics ; Disease Models, Animal ; Epithelial Cells/cytology ; Epithelial Cells/physiology ; Fibrosis ; Flow Cytometry ; Fluorescent Antibody Technique ; Humans ; Imidazoles/pharmacology ; Kidney Diseases, Cystic/genetics ; Kidney Tubules/cytology ; Kidney Tubules/physiology ; Kinesin/genetics ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/physiology ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Phenotype ; Piperazines/pharmacology ; Proto-Oncogene Proteins c-mdm2/antagonists & inhibitors ; RNA Interference ; RNA, Small Interfering/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Gli5 protein, mouse ; Imidazoles ; Kif3a protein, mouse ; Kruppel-Like Transcription Factors ; Nerve Tissue Proteins ; Piperazines ; RNA, Small Interfering ; Tumor Suppressor Protein p53 ; nutlin 3 (53IA0V845C) ; Mdm2 protein, mouse (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Checkpoint Kinase 1 (EC 2.7.11.1) ; Chek1 protein, mouse (EC 2.7.11.1) ; Kinesin (EC 3.6.4.4)
    Language English
    Publishing date 2016-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.03.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 797: Show issues Location:
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  4. Article ; Online: Protein tyrosine-O-sulfation in the retina.

    Kanan, Yogita / Hoffhines, Adam / Rauhauser, Alysha / Murray, Anne / Al-Ubaidi, Muayyad R

    Experimental eye research

    2009  Volume 89, Issue 4, Page(s) 559–567

    Abstract: Tyrosine-O-sulfation, a post-translational modification, is catalyzed by two independent tyrosylprotein sulfotransferases (TPSTs). As an initial step towards understanding the role of TPSTs in retinal function, this study was undertaken to determine the ... ...

    Abstract Tyrosine-O-sulfation, a post-translational modification, is catalyzed by two independent tyrosylprotein sulfotransferases (TPSTs). As an initial step towards understanding the role of TPSTs in retinal function, this study was undertaken to determine the extent to which tyrosine-O-sulfation of proteins is utilized in the retina. A previously characterized anti-sulfotyrosine antibody was used to determine the presence and localization of tyrosine-O-sulfated proteins (TOSPs) in the retina. Using Western blot, RT-PCR and immunohistochemical analyses, we detected TOSPs in the retinas from diverse species, including frog, fish, mouse and human. Some of the variability in the observed sizes of retinal TOSPs in the mouse, at least, may result from differential patterns of glycosylation; however, there seem to be species-specific sulfated retinal proteins as well. TOSPs were detected in most of the retinal layers as well as in the retinal pigment epithelium from human and mouse. Several retinal TOSPs were detected in the inter-photoreceptor matrix, which is consistent with the secreted nature of some sulfated proteins. Transcripts for both TPST-1 and TPST-2 were expressed in both the human and mouse retinas. These data show that retinal protein tyrosine-O-sulfation is highly conserved which suggest a functional significance of these proteins to retinal function and structure.
    MeSH term(s) Animals ; Anura ; Blotting, Western ; Cattle ; Cell Line ; Chickens ; Dogs ; Fishes ; Humans ; Immunohistochemistry ; Male ; Mice ; Mice, Inbred C3H ; Middle Aged ; Protein Processing, Post-Translational ; Rats ; Retina/metabolism ; Retinal Pigment Epithelium/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sciuridae ; Species Specificity ; Sulfotransferases ; Swine ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism
    Chemical Substances tyrosine O-sulfate (29166358BF) ; Tyrosine (42HK56048U) ; Sulfotransferases (EC 2.8.2.-) ; protein-tyrosine sulfotransferase (EC 2.8.2.20)
    Language English
    Publishing date 2009-06-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80122-7
    ISSN 1096-0007 ; 0014-4835
    ISSN (online) 1096-0007
    ISSN 0014-4835
    DOI 10.1016/j.exer.2009.05.010
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    Zs.A 163: Show issues Location:
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  5. Article ; Online: Loss of diacylglycerol kinase epsilon in mice causes endothelial distress and impairs glomerular Cox-2 and PGE2 production.

    Zhu, Jili / Chaki, Moumita / Lu, Dongmei / Ren, Chongyu / Wang, Shan-Shan / Rauhauser, Alysha / Li, Binghua / Zimmerman, Susan / Jun, Bokkyoo / Du, Yong / Vadnagara, Komal / Wang, Hanquin / Elhadi, Sarah / Quigg, Richard J / Topham, Matthew K / Mohan, Chandra / Ozaltin, Fatih / Zhou, Xin J / Marciano, Denise K /
    Bazan, Nicolas G / Attanasio, Massimo

    American journal of physiology. Renal physiology

    2016  Volume 310, Issue 9, Page(s) F895–908

    Abstract: ... Loirat C, Lifton RP. Nat Genet 45: 531-536, 2013; Ozaltin F, Li BH, Rauhauser A, An SW, Soylemezoglu O ...

    Abstract Thrombotic microangiopathy (TMA) is a disorder characterized by microvascular occlusion that can lead to thrombocytopenia, hemolytic anemia, and glomerular damage. Complement activation is the central event in most cases of TMA. Primary forms of TMA are caused by mutations in genes encoding components of the complement or regulators of the complement cascade. Recently, we and others have described a genetic form of TMA caused by mutations in the gene diacylglycerol kinase-ε (DGKE) that encodes the lipid kinase DGKε (Lemaire M, Fremeaux-Bacchi V, Schaefer F, Choi MR, Tang WH, Le Quintrec M, Fakhouri F, Taque S, Nobili F, Martinez F, Ji WZ, Overton JD, Mane SM, Nurnberg G, Altmuller J, Thiele H, Morin D, Deschenes G, Baudouin V, Llanas B, Collard L, Majid MA, Simkova E, Nurnberg P, Rioux-Leclerc N, Moeckel GW, Gubler MC, Hwa J, Loirat C, Lifton RP. Nat Genet 45: 531-536, 2013; Ozaltin F, Li BH, Rauhauser A, An SW, Soylemezoglu O, Gonul II, Taskiran EZ, Ibsirlioglu T, Korkmaz E, Bilginer Y, Duzova A, Ozen S, Topaloglu R, Besbas N, Ashraf S, Du Y, Liang CY, Chen P, Lu DM, Vadnagara K, Arbuckle S, Lewis D, Wakeland B, Quigg RJ, Ransom RF, Wakeland EK, Topham MK, Bazan NG, Mohan C, Hildebrandt F, Bakkaloglu A, Huang CL, Attanasio M. J Am Soc Nephrol 24: 377-384, 2013). DGKε is unrelated to the complement pathway, which suggests that unidentified pathogenic mechanisms independent of complement dysregulation may result in TMA. Studying Dgke knockout mice may help to understand the pathogenesis of this disease, but no glomerular phenotype has been described in these animals so far. Here we report that Dgke null mice present subclinical microscopic anomalies of the glomerular endothelium and basal membrane that worsen with age and develop glomerular capillary occlusion when exposed to nephrotoxic serum. We found that induction of cyclooxygenase-2 and of the proangiogenic prostaglandin E2 are impaired in Dgke null kidneys and are associated with reduced expression of the antithrombotic cell adhesion molecule platelet endothelial cell adhesion molecule-1/CD31 in the glomerular endothelium. Notably, prostaglandin E2 supplementation was able to rescue motility defects of Dgke knockdown cells in vitro and to restore angiogenesis in a test in vivo. Our results unveil an unexpected role of Dgke in the induction of cyclooxygenase-2 and in the regulation of glomerular prostanoids synthesis under stress.
    MeSH term(s) Aging/pathology ; Animals ; Cell Movement ; Cyclooxygenase 2/biosynthesis ; Diacylglycerol Kinase/genetics ; Dinoprostone/biosynthesis ; Endothelium/pathology ; Glomerulonephritis/enzymology ; Glomerulonephritis/metabolism ; Glomerulonephritis/pathology ; Kidney Function Tests ; Kidney Glomerulus/enzymology ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neovascularization, Physiologic ; Wound Healing
    Chemical Substances Cyclooxygenase 2 (EC 1.14.99.1) ; Diacylglycerol Kinase (EC 2.7.1.107) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2016-05-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00431.2015
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  6. Article ; Online: DGKE variants cause a glomerular microangiopathy that mimics membranoproliferative GN.

    Ozaltin, Fatih / Li, Binghua / Rauhauser, Alysha / An, Sung-Wan / Soylemezoglu, Oguz / Gonul, Ipek Isik / Taskiran, Ekim Z / Ibsirlioglu, Tulin / Korkmaz, Emine / Bilginer, Yelda / Duzova, Ali / Ozen, Seza / Topaloglu, Rezan / Besbas, Nesrin / Ashraf, Shazia / Du, Yong / Liang, Chaoying / Chen, Phylip / Lu, Dongmei /
    Vadnagara, Komal / Arbuckle, Susan / Lewis, Deborah / Wakeland, Benjamin / Quigg, Richard J / Ransom, Richard F / Wakeland, Edward K / Topham, Matthew K / Bazan, Nicolas G / Mohan, Chandra / Hildebrandt, Friedhelm / Bakkaloglu, Aysin / Huang, Chou-Long / Attanasio, Massimo

    Journal of the American Society of Nephrology : JASN

    2012  Volume 24, Issue 3, Page(s) 377–384

    Abstract: Renal microangiopathies and membranoproliferative GN (MPGN) can manifest similar clinical presentations and histology, suggesting the possibility of a common underlying mechanism in some cases. Here, we performed homozygosity mapping and whole exome ... ...

    Abstract Renal microangiopathies and membranoproliferative GN (MPGN) can manifest similar clinical presentations and histology, suggesting the possibility of a common underlying mechanism in some cases. Here, we performed homozygosity mapping and whole exome sequencing in a Turkish consanguineous family and identified DGKE gene variants as the cause of a membranoproliferative-like glomerular microangiopathy. Furthermore, we identified two additional DGKE variants in a cohort of 142 unrelated patients diagnosed with membranoproliferative GN. This gene encodes the diacylglycerol kinase DGKε, which is an intracellular lipid kinase that phosphorylates diacylglycerol to phosphatidic acid. Immunofluorescence confocal microscopy demonstrated that mouse and rat Dgkε colocalizes with the podocyte marker WT1 but not with the endothelial marker CD31. Patch-clamp experiments in human embryonic kidney (HEK293) cells showed that DGKε variants affect the intracellular concentration of diacylglycerol. Taken together, these results not only identify a genetic cause of a glomerular microangiopathy but also suggest that the phosphatidylinositol cycle, which requires DGKE, is critical to the normal function of podocytes.
    MeSH term(s) Amino Acid Sequence ; Animals ; Base Sequence ; Cohort Studies ; Consanguinity ; DNA/genetics ; Diacylglycerol Kinase/genetics ; Diacylglycerol Kinase/metabolism ; Diagnosis, Differential ; Diglycerides/metabolism ; Female ; Genetic Variation ; Glomerulonephritis, Membranoproliferative/enzymology ; Glomerulonephritis, Membranoproliferative/genetics ; Glomerulonephritis, Membranoproliferative/pathology ; HEK293 Cells ; Humans ; Kidney Diseases/enzymology ; Kidney Diseases/genetics ; Kidney Diseases/pathology ; Kidney Glomerulus/enzymology ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Pedigree ; Podocytes/metabolism ; Polymorphism, Single Nucleotide ; Rats ; Sequence Homology, Amino Acid ; Turkey
    Chemical Substances Diglycerides ; DNA (9007-49-2) ; DGKE protein, human (EC 2.7.1.107) ; Diacylglycerol Kinase (EC 2.7.1.107)
    Language English
    Publishing date 2012-12-28
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2012090903
    Database MEDical Literature Analysis and Retrieval System OnLINE

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