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  1. Article ; Online: Acute kidney injury during the first week of life: time for an update?

    Vidal, Enrico / Ray, Patricio E

    Pediatric nephrology (Berlin, Germany)

    2024  

    Language English
    Publishing date 2024-02-09
    Publishing country Germany
    Document type Editorial
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-024-06310-y
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  2. Article: HIV-1 Nef acts in synergy with APOL1-G1 to induce nephrocyte cell death in a new

    Zhu, Jun-Yi / Fu, Yulong / van de Leemput, Joyce / Yu, Ying / Li, Jinliang / Ray, Patricio E / Han, Zhe

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Background: People carrying two : Method: We generated transgenic (Tg) flies that express : Results: We found that HIV-1 Nef acts in synergy with APOL1-G1 resulting in nephrocyte structural and functional defects. Specifically, HIV-1 Nef itself ... ...

    Abstract Background: People carrying two
    Method: We generated transgenic (Tg) flies that express
    Results: We found that HIV-1 Nef acts in synergy with APOL1-G1 resulting in nephrocyte structural and functional defects. Specifically, HIV-1 Nef itself can induce endoplasmic reticulum (ER) stress (without affecting autophagy). Through a different pathway, Nef exacerbates the organelle acidification defects and reduced autophagy induced by APOL1-G1. The synergy between HIV-1 Nef and APOL1-G1 is built on their joint effects on elevating ER stress, triggering nephrocyte dysfunction and ultimately cell death.
    Conclusions: A new
    Language English
    Publishing date 2024-03-10
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.08.584069
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  3. Article ; Online: APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway

    Jun-yi Zhu / Jin-Gu Lee / Yulong Fu / Joyce van de Leemput / Patricio E. Ray / Zhe Han

    Disease Models & Mechanisms, Vol 16, Iss

    2023  Volume 12

    Keywords apol1 ; podocyte ; nephrocyte ; drosophila ; endocytosis ; autophagy ; Medicine ; R ; Pathology ; RB1-214
    Language English
    Publishing date 2023-12-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: A SNARE protective pool antagonizes APOL1 renal toxicity in Drosophila nephrocytes.

    Lee, Jin-Gu / Fu, Yulong / Zhu, Jun-Yi / Wen, Pei / van de Leemput, Joyce / Ray, Patricio E / Han, Zhe

    Cell & bioscience

    2023  Volume 13, Issue 1, Page(s) 199

    Abstract: Background: People of Sub-Saharan African ancestry are at higher risk of developing chronic kidney disease (CKD), attributed to the Apolipoprotein L1 (APOL1) gene risk alleles (RA) G1 and G2. The underlying mechanisms by which the APOL1-RA precipitate ... ...

    Abstract Background: People of Sub-Saharan African ancestry are at higher risk of developing chronic kidney disease (CKD), attributed to the Apolipoprotein L1 (APOL1) gene risk alleles (RA) G1 and G2. The underlying mechanisms by which the APOL1-RA precipitate CKD remain elusive, hindering the development of potential treatments.
    Results: Using a Drosophila genetic modifier screen, we found that SNARE proteins (Syx7, Ykt6, and Syb) play an important role in preventing APOL1 cytotoxicity. Reducing the expression of these SNARE proteins significantly increased APOL1 cytotoxicity in fly nephrocytes, the equivalent of mammalian podocytes, whereas overexpression of Syx7, Ykt6, or Syb attenuated their toxicity in nephrocytes. These SNARE proteins bound to APOL1-G0 with higher affinity than APOL1-G1/G2, and attenuated APOL1-G0 cytotoxicity to a greater extent than either APOL1-RA.
    Conclusions: Using a Drosophila screen, we identified SNARE proteins (Syx7, Ykt6, and Syb) as antagonists of APOL1-induced cytotoxicity by directly binding APOL1. These data uncovered a new potential protective role for certain SNARE proteins in the pathogenesis of APOL1-CKD and provide novel therapeutic targets for APOL1-associated nephropathies.
    Language English
    Publishing date 2023-11-04
    Publishing country England
    Document type Journal Article
    ZDB-ID 2593367-X
    ISSN 2045-3701
    ISSN 2045-3701
    DOI 10.1186/s13578-023-01147-8
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  5. Article ; Online: APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway.

    Zhu, Jun-Yi / Lee, Jin-Gu / Fu, Yulong / van de Leemput, Joyce / Ray, Patricio E / Han, Zhe

    Disease models & mechanisms

    2023  Volume 16, Issue 12

    Abstract: People of African ancestry who carry the APOL1 risk alleles G1 or G2 are at high risk of developing kidney diseases through not fully understood mechanisms that impair the function of podocytes. It is also not clear whether the APOL1-G1 and APOL1-G2 risk ...

    Abstract People of African ancestry who carry the APOL1 risk alleles G1 or G2 are at high risk of developing kidney diseases through not fully understood mechanisms that impair the function of podocytes. It is also not clear whether the APOL1-G1 and APOL1-G2 risk alleles affect these cells through similar mechanisms. Previously, we have developed transgenic Drosophila melanogaster lines expressing either the human APOL1 reference allele (G0) or APOL1-G1 specifically in nephrocytes, the cells homologous to mammalian podocytes. We have found that nephrocytes that expressed the APOL1-G1 risk allele display accelerated cell death, in a manner similar to that of cultured human podocytes and APOL1 transgenic mouse models. Here, to compare how the APOL1-G1 and APOL1-G2 risk alleles affect the structure and function of nephrocytes in vivo, we generated nephrocyte-specific transgenic flies that either expressed the APOL1-G2 or both G1 and G2 (G1G2) risk alleles on the same allele. We found that APOL1-G2- and APOL1-G1G2-expressing nephrocytes developed more severe changes in autophagic pathways, acidification of organelles and the structure of the slit diaphragm, compared to G1-expressing nephrocytes, leading to their premature death. We conclude that both risk alleles affect similar key cell trafficking pathways, leading to reduced autophagy and suggesting new therapeutic targets to prevent APOL1 kidney diseases.
    MeSH term(s) Animals ; Mice ; Humans ; Drosophila melanogaster/metabolism ; Apolipoprotein L1/genetics ; Apolipoprotein L1/metabolism ; Kidney Diseases ; Cell Death ; Mice, Transgenic ; Autophagy/genetics ; Mammals/metabolism
    Chemical Substances Apolipoprotein L1 ; APOL1 protein, human
    Language English
    Publishing date 2023-12-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.050223
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  6. Article ; Online: Association of circulating fibroblast growth factor-2 with progression of HIV-chronic kidney diseases in children.

    Ray, Patricio E / Li, Jinliang / Das, Jharna R / Yu, Jing

    Pediatric nephrology (Berlin, Germany)

    2021  Volume 36, Issue 12, Page(s) 3933–3944

    Abstract: Background: Children living with HIV frequently show high plasma levels of fibroblast growth factor-2 (FGF-2/bFGF). FGF-2 accelerates the progression of several experimental kidney diseases; however, the role of circulating FGF-2 in childhood HIV- ... ...

    Abstract Background: Children living with HIV frequently show high plasma levels of fibroblast growth factor-2 (FGF-2/bFGF). FGF-2 accelerates the progression of several experimental kidney diseases; however, the role of circulating FGF-2 in childhood HIV-chronic kidney diseases (HIV-CKDs) is unknown. We carried out this study to determine whether high plasma FGF-2 levels were associated with the development of HIV-CKDs in children.
    Methods: The plasma and urine FGF-2 levels were measured in 84 children (< 12 years of age) living with HIV during the pre-modern antiretroviral era, and followed for at least 3 years to determine the prevalence of proteinuria and HIV-CKDs. We also assessed the distribution of the kidney FGF-2 binding sites by autoradiography and Alcian blue staining, and explored potential mechanisms by which circulating FGF-2 may precipitate HIV-CKDs in cultured kidney epithelial and mononuclear cells derived from children with HIV-CKDs.
    Results: High plasma FGF-2 levels were associated with a high viral load. Thirteen children (~ 15%) developed HIV-CKDs and showed a large reservoir of FGF-2 low-affinity binding sites in the kidney, which can facilitate the recruitment of circulating FGF-2. Children with high plasma and urine FGF-2 levels had 73-fold increased odds (95% CI 9-791) of having HIV-CKDs relative to those with normal FGF-2 values. FGF-2 induced the proliferation and decreased the expression of APOL-1 mRNA in podocytes, and increased the attachment and survival of infected mononuclear cells cultured from children with HIV-CKDs.
    Conclusions: High plasma FGF-2 levels appear to be an additional risk factor for developing progressive childhood HIV-CKDs.
    MeSH term(s) Child ; Disease Progression ; Fibroblast Growth Factor 2/blood ; HIV Infections/diagnosis ; Humans ; Kidney ; Renal Insufficiency, Chronic/diagnosis
    Chemical Substances Fibroblast Growth Factor 2 (103107-01-3)
    Language English
    Publishing date 2021-06-14
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-021-05075-y
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  7. Article ; Online: A SNARE protective pool antagonizes APOL1 renal toxicity in Drosophila nephrocytes

    Jin-Gu Lee / Yulong Fu / Jun-yi Zhu / Pei Wen / Joyce van de Leemput / Patricio E. Ray / Zhe Han

    Cell & Bioscience, Vol 13, Iss 1, Pp 1-

    2023  Volume 14

    Abstract: Abstract Background People of Sub-Saharan African ancestry are at higher risk of developing chronic kidney disease (CKD), attributed to the Apolipoprotein L1 (APOL1) gene risk alleles (RA) G1 and G2. The underlying mechanisms by which the APOL1-RA ... ...

    Abstract Abstract Background People of Sub-Saharan African ancestry are at higher risk of developing chronic kidney disease (CKD), attributed to the Apolipoprotein L1 (APOL1) gene risk alleles (RA) G1 and G2. The underlying mechanisms by which the APOL1-RA precipitate CKD remain elusive, hindering the development of potential treatments. Results Using a Drosophila genetic modifier screen, we found that SNARE proteins (Syx7, Ykt6, and Syb) play an important role in preventing APOL1 cytotoxicity. Reducing the expression of these SNARE proteins significantly increased APOL1 cytotoxicity in fly nephrocytes, the equivalent of mammalian podocytes, whereas overexpression of Syx7, Ykt6, or Syb attenuated their toxicity in nephrocytes. These SNARE proteins bound to APOL1-G0 with higher affinity than APOL1-G1/G2, and attenuated APOL1-G0 cytotoxicity to a greater extent than either APOL1-RA. Conclusions Using a Drosophila screen, we identified SNARE proteins (Syx7, Ykt6, and Syb) as antagonists of APOL1-induced cytotoxicity by directly binding APOL1. These data uncovered a new potential protective role for certain SNARE proteins in the pathogenesis of APOL1-CKD and provide novel therapeutic targets for APOL1-associated nephropathies.
    Keywords SNARE proteins ; SNARE protective pool ; APOL1 ; Renal toxicity ; Nephrocytes ; Serum resistance-associated (SRA) protein ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2023-11-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
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  8. Article ; Online: HIV-associated nephropathy: a diagnosis in evolution.

    Ray, Patricio E

    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

    2012  Volume 27, Issue 11, Page(s) 3969–3972

    Abstract: HIV-1 associated nephropathy (HIVAN) is a clinical and renal histological disease characterized by the presence of heavy proteinuria associated with focal segmental glomerulosclerosis and microcystic tubular dilatation. These renal lesions lead to renal ... ...

    Abstract HIV-1 associated nephropathy (HIVAN) is a clinical and renal histological disease characterized by the presence of heavy proteinuria associated with focal segmental glomerulosclerosis and microcystic tubular dilatation. These renal lesions lead to renal enlargement and rapid progression to kidney failure. People from African ancestry show a unique susceptibility to develop HIVAN. The study by Wearne and colleagues, which includes the largest group of patients of African ancestry with HIVAN studied so far, describes a novel renal histological variant of HIVAN, and suggests that antiretroviral therapies improve the clinical outcome of all HIV-associated renal diseases. These findings, when interpreted in the context of recent advances in our understanding of the molecular pathogenesis and genetics of HIVAN, will facilitate the recognition of all clinical variants of HIVAN as well the planning of better screening, prevention, and treatment programs for all HIV nephropathies.
    MeSH term(s) AIDS-Associated Nephropathy/drug therapy ; AIDS-Associated Nephropathy/pathology ; Female ; Humans ; Kidney/pathology ; Male
    Language English
    Publishing date 2012-05-13
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 90594-x
    ISSN 1460-2385 ; 0931-0509
    ISSN (online) 1460-2385
    ISSN 0931-0509
    DOI 10.1093/ndt/gfs114
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  9. Article ; Online: Can we cure HIV-1-associated nephropathy in transgenic mice?

    Ray, Patricio E

    Kidney international

    2012  Volume 81, Issue 9, Page(s) 811–813

    Abstract: HIV-1-associated nephropathy (HIVAN) is a rapidly progressive form of focal segmental glomerulosclerosis. HIV transgenic mice can develop a HIVAN-like renal disease. Zhong et al. show that the oral administration of a cyclic nucleotide phosphodiesterase ... ...

    Abstract HIV-1-associated nephropathy (HIVAN) is a rapidly progressive form of focal segmental glomerulosclerosis. HIV transgenic mice can develop a HIVAN-like renal disease. Zhong et al. show that the oral administration of a cyclic nucleotide phosphodiesterase 4 inhibitor and a retinoic acid receptor-α agonist can prevent the development of HIVAN in transgenic mice, acting through a cAMP-dependent mechanism that is independent of HIV-1 genes. These findings suggest that endogenous host factors play a critical role in HIVAN.
    MeSH term(s) AIDS-Associated Nephropathy/prevention & control ; Aminopyridines/pharmacology ; Animals ; Benzamides/pharmacology ; Benzoates/pharmacology ; Cyclopropanes/pharmacology ; Female ; HIV Infections/drug therapy ; HIV-1/genetics ; Kidney Tubules/drug effects ; Male ; Phosphodiesterase 4 Inhibitors/pharmacology ; Renal Insufficiency/prevention & control ; Tetrahydronaphthalenes/pharmacology
    Chemical Substances Aminopyridines ; Benzamides ; Benzoates ; Cyclopropanes ; Phosphodiesterase 4 Inhibitors ; Tetrahydronaphthalenes ; Roflumilast (0P6C6ZOP5U) ; Am 580 (102121-60-8)
    Language English
    Publishing date 2012-04-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1038/ki.2012.13
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    Zs.A 797: Show issues Location:
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  10. Article ; Online: Childhood HIV-associated nephropathy: 36 years later.

    Ray, Patricio E / Li, Jinliang / Das, Jharna R / Tang, Pingtao

    Pediatric nephrology (Berlin, Germany)

    2020  Volume 36, Issue 8, Page(s) 2189–2201

    Abstract: HIV-associated nephropathy (HIVAN) predominantly affects people of African ancestry living with HIV who do not receive appropriate antiretroviral therapy (ART). Childhood HIVAN is characterized by heavy proteinuria and decreased kidney function. Kidney ... ...

    Abstract HIV-associated nephropathy (HIVAN) predominantly affects people of African ancestry living with HIV who do not receive appropriate antiretroviral therapy (ART). Childhood HIVAN is characterized by heavy proteinuria and decreased kidney function. Kidney histology shows mesangial expansion, classic or collapsing glomerulosclerosis, and microcystic renal tubular dilatation leading to kidney enlargement. The pathogenesis of HIVAN involves the kidney recruitment of inflammatory cells and the infection of kidney epithelial cells. In addition, both viral and genetic factors play key roles in this disease. Modern ART has improved the outcome and decreased the prevalence of childhood HIVAN. However, physicians have had modest success providing chronic ART to children and adolescents, and we continue to see children with HIVAN all over the world. This article discusses the progress made during the last decade in our understanding of the pathogenesis and treatment of childhood HIVAN, placing particular emphasis on the mechanisms that mediate the infection of kidney epithelial cells, and the roles of cytokines, the HIV-Tat gene, and the Apolipoprotein-1 (APOL1) gene risk variants in this disease. In view of the large number of children living with HIV at risk of developing HIVAN, better prevention and treatment programs are needed to eradicate this disease.
    MeSH term(s) AIDS-Associated Nephropathy/diagnosis ; AIDS-Associated Nephropathy/epidemiology ; AIDS-Associated Nephropathy/genetics ; Adolescent ; Apolipoprotein L1 ; HIV Infections/complications ; HIV Infections/drug therapy ; HIV Infections/epidemiology ; HIV-1 ; Humans ; Kidney
    Chemical Substances APOL1 protein, human ; Apolipoprotein L1
    Language English
    Publishing date 2020-10-12
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-020-04756-4
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