Evidence map›Paper›PMID 25056347›Full record

ArticleAmerican journal of physiology. Renal physiology2014

Expression of a novel stress-inducible protein, sestrin 2, in rat glomerular parietal epithelial cells.

Hiroko Hamatani, Keiju Hiromura, Toru Sakairi, Satoshi Takahashi, Mitsuharu Watanabe, Akito Maeshima, Takamoto Ohse, Jeffery W Pippin, Stuart J Shankland, Yoshihisa Nojima

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The role of sirolimus in proteinuria in diabetic nephropathy rats.Iranian journal of basic medical sciences · 2017
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Sestrin 2: a regulator of the glomerular parietal epithelial cell phenotype.American journal of physiology. Renal physiology · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Hiroko HamataniDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan;
Keiju HiromuraDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan; hiromura@gunma-u.ac.jp.
Toru SakairiDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan;
Satoshi TakahashiDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan;
Mitsuharu WatanabeDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan;
Akito MaeshimaDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan;
Takamoto OhseDivision of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan; and.
Jeffery W PippinDivision of Nephrology, University of Washington, Seattle, Washington.
Stuart J ShanklandDivision of Nephrology, University of Washington, Seattle, Washington.
Yoshihisa NojimaDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Japan;
Gunma University · JPUniversity of Washington · USThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sestrin 2, initially identified as a p53 target protein, accumulates in cells exposed to stress and inhibits mammalian target of rapamycin (mTOR) signaling. In normal rat kidneys, sestrin 2 was selectively expressed in parietal epithelial cells (PECs), identified by the marker protein gene product 9.5. In adriamycin nephropathy, sestrin 2 expression decreased in PECs on day 14, together with increased expression of phosphorylated S6 ribosomal protein (P-S6RP), a downstream target of mTOR. Sestrin 2 expression was markedly decreased on day 42, coinciding with glomerulosclerosis and severe periglomerular fibrosis. In puromycin aminonucleoside nephropathy, decreased sestrin 2 expression, increased P-S6RP expression, and periglomerular fibrosis were observed on day 9, when massive proteinuria developed. These changes were transient and nearly normalized by day 28. In crescentic glomerulonephritis, sestrin 2 expression was not detected in cellular crescents, whereas P-S6RP increased. In conditionally immortalized cultured PECs, the forced downregulation of sestrin 2 by short hairpin RNA resulted in increased expression of P-S6RP and increased apoptosis. These data suggest that sestrin 2 is involved in PEC homeostasis by regulating the activity of mTOR. In addition, sestrin 2 could be a novel marker of PECs, and decreased expression of sestrin 2 might be a marker of PEC injury.

Indexed as

AnimalsCells, CulturedDown-RegulationDoxorubicinEpithelial CellsHyaluronan ReceptorsKidney DiseasesKidney GlomerulusMaleMiceNuclear ProteinsPuromycin AminonucleosideRatsRats, Inbred WKYRats, WistarRibosomal Protein S6DoxorubicinHyaluronan ReceptorsmTOR protein, ratNuclear ProteinsPuromycin AminonucleosideRibosomal Protein S6RNA, Small InterferingSesn2 protein, ratSestrinsTOR Serine-Threonine Kinasesglomerular parietal epithelial cellsmammalian target of rapamycinsestrin 2

Identifiers

PMID25056347
PMCPMC4166732
OpenAlexW1984621232

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.