Evidence map›Paper›PMID 25568136›Full record

ArticleAmerican journal of physiology. Renal physiology2015

An angiotensin-(1-7) peptidase in the kidney cortex, proximal tubules, and human HK-2 epithelial cells that is distinct from insulin-degrading enzyme.

Bryan A Wilson, Nildris Cruz-Diaz, Allyson C Marshall, Nancy T Pirro, Yixin Su, TanYa M Gwathmey, James C Rose, Mark C Chappell

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Renin in critically ill patients.Annals of intensive care · 2024
    Review
  2. Article
  3. Review
  4. Endocrine · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Evidence for a mitochondrial angiotensin-(1-7) system in the kidney.American journal of physiology. Renal physiology · 2016
    Article
  11. Biochemical evaluation of the renin-angiotensin system: the good, bad, and absolute?American journal of physiology. Heart and circulatory physiology · 2016
    Review
  12. Review
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Bryan A WilsonHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Cartolina; and.
Nildris Cruz-DiazHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Cartolina; and.
Allyson C MarshallHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Cartolina; and.
Nancy T PirroHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Cartolina; and.
Yixin SuDepartment of Obstetrics and Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Cartolina.
TanYa M GwathmeyHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Cartolina; and.
James C RoseDepartment of Obstetrics and Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Cartolina.
Mark C ChappellHypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Cartolina; and mchappel@wakehealth.edu.
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DELL'ITALIA, LOUIS J. · 1994 to 2019
$34.8M
The Impact of Antenatal Steroid Exposure on the Intrarenal Renin-Angiotensin SystP01HD047584 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMES C. · 2005 to 2016
$13.0M
FETAL ENDOCRINE-CARDIOVASCULAR RELATIONSHIPSR01HD017644 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMES C. · 1985 to 2011
$2.8M
Postdoctoral Research, Instruction, and Mentoring Experience (PRIME)K12GM102773 · NIGMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HOWLETT, ALLYN C · 2013 to 2018
$2.6M
Integrative Lipid Metabolism, Inflammation, and Chronic DiseasesT32HL091797 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PARKS, JOHN S · 2008 to 2017
$1.8M
Novel Angiotensin-(1-7) Endopeptidase in Fetal ProgrammingR21HD084227 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C, ROSE, JAMES C. · 2016 to 2017
$426k
NHLBI NIH HHS HL091797NHLBI NIH HHS HL-51952NHLBI NIH HHS T32 HL091797NICHD NIH HHS HD-017644NICHD NIH HHS HD-047584NICHD NIH HHS P01 HD047584NICHD NIH HHS R21 HD084227NIGMS NIH HHS K12 GM102773NIGMS NIH HHS K12-GM102773
6 · The paper itself

Abstract

Angiotensin 1-7 [ANG-(1-7)] is expressed within the kidney and exhibits renoprotective actions that antagonize the inflammatory, fibrotic, and pro-oxidant effects of ANG II. We previously identified an peptidase that preferentially metabolized ANG-(1-7) to ANG-(1-4) in the brain medulla and cerebrospinal fluid (CSF) of sheep (Marshall AC, Pirro NT, Rose JC, Diz DI, Chappell MC. J Neurochem 130: 313-323, 2014); thus the present study established the expression of the peptidase in the kidney. Utilizing a sensitive HPLC-based approach, we demonstrate a peptidase activity that hydrolyzed ANG-(1-7) to ANG-(1-4) in the sheep cortex, isolated tubules, and human HK-2 renal epithelial cells. The peptidase was markedly sensitive to the metallopeptidase inhibitor JMV-390; human HK-2 cells expressed subnanomolar sensitivity (IC50 = 0.5 nM) and the highest specific activity (123 ± 5 fmol·min(-1)·mg(-1)) compared with the tubules (96 ± 12 fmol·min(-1)·mg(-1)) and cortex (107 ± 9 fmol·min(-1)·mg(-1)). The peptidase was purified 41-fold from HK-2 cells; the activity was sensitive to JMV-390, the chelator o-phenanthroline, and the mercury-containing compound p-chloromercuribenzoic acid (PCMB), but not to selective inhibitors against neprilysin, neurolysin and thimet oligopeptidase. Both ANG-(1-7) and its endogenous analog [Ala(1)]-ANG-(1-7) (alamandine) were preferentially hydrolyzed by the peptidase compared with ANG II, [Asp(1)]-ANG II, ANG I, and ANG-(1-12). Although the ANG-(1-7) peptidase and insulin-degrading enzyme (IDE) share similar inhibitor characteristics of a metallothiolendopeptidase, we demonstrate marked differences in substrate specificity, which suggest these peptidases are distinct. We conclude that an ANG-(1-7) peptidase is expressed within the renal proximal tubule and may play a potential role in the renal renin-angiotensin system to regulate ANG-(1-7) tone.

Indexed as

Angiotensin IAnimalsCell LineEpithelial CellsHumansInsulysinKidney CortexKidney Tubules, ProximalPeptide FragmentsPeptide HydrolasesSheepAngiotensin Iangiotensin I (1-7)InsulysinPeptide FragmentsPeptide HydrolasesANG-(1–7)endopeptidaseHK-2 epithelial cellsproximal tubules

Identifiers

PMID25568136
PMCPMC4360035
OpenAlexW2104640396

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.