Evidence map›Paper›PMID 26637635›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Angiotensin-(1-7)/mas inhibits apoptosis in alveolar epithelial cells through upregulation of MAP kinase phosphatase-2.

Indiwari Gopallawa, Bruce D Uhal

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. COVID-19 in Patients with Hypertension.Advances in experimental medicine and biology · 2021
    Article
  9. Angiotensin Converting Enzyme-2 (ACE-2) role in disease and future in research.Journal of lung, pulmonary & respiratory research · 2021
    Article
  10. Review
  11. Article
  12. ACE2, Much More Than Just a Receptor for SARS-COV-2.Frontiers in cellular and infection microbiology · 2020
    Article
  13. COVID-19 Usurps Host Regulatory Networks.Frontiers in pharmacology · 2020
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Indiwari GopallawaDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan; and.
Bruce D UhalDepartment of Physiology, Michigan State University, East Lansing, Michigan uhal@msu.edu.
Michigan State University · US

Funding

CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR01HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1996 to 2012
$2.9M
CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR29HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1990 to 1994
–
NHLBI NIH HHS HL-45136NHLBI NIH HHS R01 HL045136
6 · The paper itself

Abstract

Earlier work from this laboratory showed that autocrine generation of angiotensin II and c-Jun-NH2-terminal kinase phosphorylation (p-JNK) are both required events in alveolar epithelial cell (AEC) apoptosis. Although earlier data showed that angiotensin-(1-7) [ANG-(1-7)] protects against AEC apoptosis, the pathways by which ANG-(1-7)/mas activation prevent JNK phosphorylation and apoptosis are poorly understood. Therefore, in the current study, it was theorized that ANG-(1-7) activates a mitogen-activated protein kinase phosphatase (MKP) and thereby reduces JNK phosphorylation to inhibit apoptosis and promote cell survival. This hypothesis was evaluated in the human A549 and mouse MLE12 AEC lines and primary cultures of human AECs. Cells were transfected with small-interfering RNAs, antisense oligonucleotides, or inhibitors specific for MKP-2 or mas, and were then assayed for phospho-JNK, caspase-9, loss of mitochondrial membrane potential, and nuclear fragmentation. Silencing of MKP-2 significantly prevented the blockade of all apoptotic markers by ANG-(1-7). Knockdown or blockade of mas receptor by antisense oligonucleotides or by the receptor antagonist A779, respectively, caused significant decreases in MKP-2, and simultaneously increased the apoptotic markers of caspase-9 activation and nuclear fragmentation. These data show that the ANG-(1-7)/mas pathway constitutively prevents JNK phosphorylation and apoptosis of AECs by maintaining activation of the JNK-selective phosphatase MKP-2, and further demonstrate the critical role of the ANG-(1-7) receptor mas in AEC survival.

Indexed as

Alveolar Epithelial CellsAngiotensin IApoptosisCell SurvivalDual-Specificity PhosphatasesEpithelial CellsHumansJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase PhosphatasesPeptide FragmentsPhosphorylationPulmonary AlveoliSignal TransductionUp-RegulationAngiotensin Iangiotensin I (1-7)Dual-Specificity PhosphatasesDUSP4 protein, humanJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase PhosphatasesPeptide Fragmentsangiotensin peptidesc-Jun-NH2-terminal kinase phosphorylationmitogen-activated protein kinase phosphatasetype II pneumocyte

Identifiers

PMID26637635
PMCPMC4888557
OpenAlexW2224952942

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.