Evidence map›Paper›PMID 22288595›Full record

ArticleClinical and experimental immunology2012

Surfactant protein D inhibits lipopolysaccharide-induced monocyte chemoattractant protein-1 expression in human renal tubular epithelial cells: implication for tubulointerstitial fibrosis.

F Hu, W Liang, Z Ren, G Wang, G Ding

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2012. 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
0.2field-weighted citation impact, top 38% 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, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. STING deficiency protects against wasp venom-induced acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Collectins in urinary tract and kidney diseases.International urology and nephrology · 2018
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. 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

5 authors at 3 institutions in 2 countries.

F HuDivision of Nephrology, Department of Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
W Liang
Z Ren
G Wang
G Ding
Wuhan University · CNRenmin Hospital of Wuhan University · CNSUNY Upstate Medical University · US

Funding

Mechanisms of 5'UTR splicing of human surfactant protein (SP)-A1 and SP-A2R21HL096007 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI WANG, GUIRONG · 2010 to 2011
$427k
NHLBI NIH HHS HL096007NHLBI NIH HHS R21 HL096007
6 · The paper itself

Abstract

Surfactant protein D (SP-D), a member of the C-type lectin (collectin) protein family, plays a critical role in innate host defence against various microbial pathogens and in the modulation of inflammatory responses in the lung. However, little is known about its expression and biological function in the kidney. In this work, we studied SP-D expression in human kidney and cultured human renal proximal tubular epithelial cells (HK-2), and examined the effect of SP-D on proinflammatory cytokine production after lipopolysaccharide (LPS) stimulus. We observed the expression of both SP-D mRNA and protein in human kidney and in-vitro HK-2 cells by immunohistochemistry, Western blot analysis, reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR. To explore the potential role of SP-D in the pathogenesis of tubulointerstitial fibrosis in kidney infection, we examined the production of monocyte chemoattractant protein-1 (MCP-1) in HK-2 cells after LPS treatment. Results showed that the level of MCP-1 in the conditioned medium increased significantly when HK-2 cells were cultured with LPS (>0·1 µg/ml) for 8 h. Of interest, LPS treatment inhibited SP-D expression in HK-2 cells. Furthermore, over-expression of SP-D reduced significantly the LPS-induced expression of MCP-1 in transfected cells. These findings suggest that SP-D in the kidney functions as an anti-inflammatory factor in renal tubular epithelial cells and may modulate tubulointerstitial fibrosis in kidney.

Indexed as

Base SequenceCell LineChemokine CCL2Culture Media, ConditionedEpithelial CellsFibrosisGene ExpressionHumansKidney DiseasesKidney TubulesLipopolysaccharidesPulmonary Surfactant-Associated Protein DRecombinant ProteinsRNA, MessengerTransfectionCCL2 protein, humanChemokine CCL2Culture Media, ConditionedLipopolysaccharidesPulmonary Surfactant-Associated Protein DRecombinant ProteinsRNA, Messenger

Identifiers

PMID22288595
PMCPMC3374284
OpenAlexW1488660619

What OpenQuestion holds

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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.