Evidence map›Paper›PMID 21205827›Full record

ArticleThe Journal of biological chemistry2011

Caveolae-dependent endocytosis is required for class A macrophage scavenger receptor-mediated apoptosis in macrophages.

Xu-Dong Zhu, Yan Zhuang, Jing-Jing Ben, Ling-Ling Qian, Han-Peng Huang, Hui Bai, Jia-Hao Sha, Zhi-Gang He, Qi Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 119 citations in OpenAlex.

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  18. PepFect14 Signaling and Transfection.Methods in molecular biology (Clifton, N.J.) · 2022
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  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 3 countries.

Xu-Dong ZhuFrom the Institute of Reproductive Medicine and; Atherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and.
Yan ZhuangAtherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and.
Jing-Jing BenAtherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and.
Ling-Ling QianAtherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and.
Han-Peng HuangAtherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and.
Hui BaiAtherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and.
Jia-Hao ShaFrom the Institute of Reproductive Medicine and.
Zhi-Gang Hethe Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
Qi ChenFrom the Institute of Reproductive Medicine and; Atherosclerosis Research Center, Key Laboratory of Human Functional Genomics, Nanjing Medical University, Nanjing 210029, China and. Electronic address: qichen@njmu.edu.cn.
Nanjing Medical University · CNHarvard University · USInstitute of Reproductive Medicine · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SR-A (class A macrophage scavenger receptor) is a transmembrane receptor that can bind many different ligands, including modified lipoproteins that are relevant to the development of vascular diseases. However, the precise endocytic pathways of SR-A/mediated ligands internalization are not fully characterized. In this study, we show that the SR-A/ligand complex can be endocytosed by both clathrin- and caveolae-dependent pathways. Internalizations of SR-A-lipoprotein (such as acLDL) complexes primarily go through clathrin-dependent endocytosis. In contrast, macrophage apoptosis triggered by SR-A-fucoidan internalization requires caveolae-dependent endocytosis. The caveolae-dependent process activates p38 kinase and JNK signaling, whereas the clathrin-mediated endocytosis elicits ERK signaling. Our results suggest that different SR-A endocytic pathways have distinct functional consequences due to the activation of different signaling cascades in macrophages.

Indexed as

AnimalsAnti-Ulcer AgentsApoptosisCaveolaeCell LineEndocytosisEnzyme ActivationMacrophagesMAP Kinase Kinase 4MAP Kinase Signaling SystemMicep38 Mitogen-Activated Protein KinasesPolysaccharidesScavenger Receptors, Class AAnti-Ulcer AgentsfucoidanMAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesPolysaccharidesScavenger Receptors, Class A

Identifiers

PMID21205827
PMCPMC3048709
OpenAlexW1964180981

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.