Evidence map›Paper›PMID 28528353›Full record

ArticleInternational urology and nephrology2017

Adrenomedullin ameliorates podocyte injury induced by puromycin aminonucleoside in vitro and in vivo through modulation of Rho GTPases.

Nan Dong, Lixia Meng, Ruqun Xue, Meng Yu, Zhonghua Zhao, Xueguang Liu

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In one paragraph

Article in International urology and nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  5. Lack of serum- and glucocorticoid-inducible kinase 3 leads to podocyte dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    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

6 authors at 2 institutions in 1 country.

Nan DongDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 131 Dongan Road, Shanghai, 200032, China.
Lixia MengDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 131 Dongan Road, Shanghai, 200032, China.
Ruqun XueDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 131 Dongan Road, Shanghai, 200032, China.
Meng YuDepartment of Clinical Medicine, Fudan University, 131 Dongan Road, Shanghai, 200032, China.
Zhonghua ZhaoDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 131 Dongan Road, Shanghai, 200032, China.
Xueguang LiuDepartment of Pathology, School of Basic Medical Sciences, Fudan University, 131 Dongan Road, Shanghai, 200032, China. glxg69@shmu.edu.cn.ORCID http://orcid.org/0000-0002-5615-0337
Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePodocyte injury is a key event in proteinuric kidney disease and eventually glomerular scarring. While adrenomedullin (AM), a potent vasodilatory peptide, has been reported to confer renoprotection in several experimental models of kidney diseases, its effect on injured podocytes and the related mechanism is still largely unknown.

methodsEmploying Western blotting analysis, immunoprecipitation and immunofluorescence, we investigated the effects of AM on the expressions of podocyte cytoskeletal proteins and Rho-family small GTPases (Rho GTPases) in puromycin aminonucleoside (PAN)-induced podocyte injury, both in cultured podocytes and in PAN nephrosis rats. Urinary protein excretion and the morphologic changes of kidney in PAN nephrosis rats were evaluated. Glutathione-S-transferase pull-down assay was applied for Rho GTPases activity.

resultsPAN induced massive albuminuria and morphologic injury, which were significantly mitigated by AM administration. AM significantly antagonized not only the PAN-decreased expressions of synaptopodin, nephrin, CD2AP and podocin, but also the PAN-disrupted interactions between synaptopodin-RhoA, nephrin-CD2AP, and CD2AP-Rac1-cortactin. These effects of AM in cultured podocytes were mostly significantly blocked by H89, a PKA inhibitor. AM dramatically upregulated the PAN-induced Rho GTPases protein expressions and their activities. PAN increased the expressions of endogenous AM and its receptor RAMP2 which was furthermore upregulated by AM administration.

conclusionsAM alleviated podocyte injury induced by PAN both in cell culture and in PAN nephrosis. The beneficial effects of AM on podocytes can be attributable to direct modulation of podocyte cytoskeletal proteins and Rho GTPases, mainly via a PKA-dependent pathway.

Indexed as

Adaptor Proteins, Signal TransducingAdrenomedullinAlbuminuriaAnimalscdc42 GTP-Binding ProteinCell LineCortactinCytoskeletal ProteinsIntracellular Signaling Peptides and ProteinsKidney GlomerulusMaleMembrane ProteinsMiceMicrofilament ProteinsNephrosisNeuropeptidesAdaptor Proteins, Signal TransducingAdrenomedullinCD2-associated proteincdc42 GTP-Binding ProteinCdc42 protein, mouseCortactinCttn protein, mouseCytoskeletal ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsnephrinNeuropeptidesNPHS2 proteinPuromycin Aminonucleosiderac1 GTP-Binding ProteinRac1 protein, mouseRamp2 protein, ratReceptor Activity-Modifying Protein 2rhoA GTP-Binding ProteinRhoA protein, mouserho GTP-Binding ProteinsSynpo protein, ratVasodilator AgentsAdrenomedullinPodocytePuromycin aminonucleoside nephrosis ratsRho GTPases

Identifiers

PMID28528353
OpenAlexW2615601559

What OpenQuestion holds

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Registered trials

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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.