Evidence map›Paper›PMID 30201495›Full record

ArticleThe American journal of pathology2018

Role of Apolipoprotein L1 in Human Parietal Epithelial Cell Transition.

Vinod Kumar, Himanshu Vashistha, Xiqian Lan, Nirupama Chandel, Kamesh Ayasolla, Seyedeh Shadafarin Marashi Shoshtari, Rukhsana Aslam, Nitpriya Paliwal, Frank Abbruscato, Joanna Mikulak and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. The metabolic effects of APOL1 in humans.Pflugers Archiv : European journal of physiology · 2023
    Review
  6. Review
  7. The Pathology Lesion Patterns of Podocytopathies: How and why?Frontiers in cell and developmental biology · 2022
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Lessons From APOL1 Animal Models.Frontiers in medicine · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. APOL1 and kidney cell function.American journal of physiology. Renal physiology · 2019
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 8 institutions in 4 countries.

Vinod KumarImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Himanshu VashisthaInstitute of Translational Research, the Ochsner Clinic, New Orleans, Louisiana.
Xiqian LanImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Nirupama ChandelImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Kamesh AyasollaImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Seyedeh Shadafarin Marashi ShoshtariImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Rukhsana AslamImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Nitpriya PaliwalImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Frank AbbruscatoInstitute of Translational Research, the Ochsner Clinic, New Orleans, Louisiana.
Joanna MikulakHumanitas Clinical and Research Center, Rozzano, Milan, Italy.
Waldemar PopikHealth Disparities and HIV, Meharry Medical College, Nashville, Tennessee.
Mohamed G AttaNephrogy Division, Johns Hopkins Hospital, Baltimore, Maryland.
Praveen N ChanderDepartment of Pathology, New York Medical College, Valhalla, New York.
Ashwani MalhotraImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York.
Catherine Meyer-SchwesingerNephrology Division, University of Hamburg, Hamburg, Germany.
Karl SkoreckiTechnion-Israel Institute of Technology, Rambam Health Care Campus, Haifa, Israel.
Pravin C SinghalImmunology and Inflammation Center, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, New York. Electronic address: psinghal@northwell.edu.
Feinstein Institute for Medical Research · USOchsner Medical Center · USHumanitas University · ITJohns Hopkins Hospital · USMeharry Medical College · USNew York Medical College · USTechnion – Israel Institute of Technology · ILUniversität Hamburg · DE

Funding

HIV ASSOCIATED NEPHROPATHY IN DRUG ADDICTSR01DA012111 · NIDA · LONG ISLAND JEWISH MEDICAL CENTER · PI SINGHAL, PRAVIN C · 1998 to 2007
$3.6M
Epigenetic factors and HIV-associated NephropathyR01DK098074 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2013 to 2016
$2.5M
APOL1 in Diabetic PodocytopathyR01DK118017 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2018 to 2021
$2.0M
NIDA NIH HHS R01 DA012111NIDDK NIH HHS R01 DK098074NIDDK NIH HHS R01 DK118017
6 · The paper itself

Abstract

Human parietal epithelial cells (PECs) are progenitor cells that sustain podocyte homeostasis. We hypothesized that the lack of apolipoprotein (APO) L1 ensures the PEC phenotype, but its induction initiates PEC transition (expression of podocyte markers). APOL1 expression and down-regulation of miR193a coincided with the expression of podocyte markers during the transition. The induction of APOL1 also stimulated transition markers in human embryonic kidney cells (cells with undetectable APOL1 protein expression). APOL1 silencing in PECs up-regulated miR193a expression, suggesting the possibility of a reciprocal feedback relationship between APOL1 and miR193a. HIV, interferon-γ, and vitamin D receptor agonist down-regulated miR193a expression and induced APOL1 expression along with transition markers in PECs. Luciferase assay suggested a putative interaction between miR193a and APOL1. Since silencing of APOL1 attenuated HIV-, vitamin D receptor agonist-, miR193a inhibitor-, and interferon-γ-induced expression of transition markers, APOL1 appears to be a critical functional constituent of the miR193a- APOL1 axis in PECs. This notion was confirmed by further enhanced expression of PEC markers in APOL1 mRNA-silenced PECs. In vivo studies, glomeruli in patients with HIV, and HIV/APOL1 transgenic mice had foci of PECs expressing synaptopodin, a transition marker. APOL1 likely regulates PEC molecular phenotype through modulation of miR193a expression, and APOL1 and miR193a share a reciprocal feedback relationship.

Indexed as

Gene Expression RegulationAIDS-Associated NephropathyAnimalsApolipoprotein L1Case-Control StudiesEpithelial CellsHEK293 CellsHep G2 CellsHumansKidney GlomerulusMiceMice, TransgenicMicroRNAsAPOL1 protein, humanApolipoprotein L1MicroRNAsMIRN193 microRNA, human

Identifiers

PMID30201495
PMCPMC6222279
OpenAlexW2889882659

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.