ArticleJCI insight2017
Integrin-Kindlin3 requirements for microglial motility in vivo are distinct from those for macrophages.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesis.Cardiovascular research · 2025Article
- YAP Signaling in Glia: Pivotal Roles in Neurological Development, Regeneration and Diseases.Neuroscience bulletin · 2025Review
- Mechanism of Tumor-Platelet Communications in Cancer.Circulation research · 2023Article
- Opposite roles of Kindlin orthologs in cell survival and proliferation.Cell proliferation · 2022Article
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- Kindlin-3 mutation in mesenchymal stem cells results in enhanced chondrogenesis.Experimental cell research · 2021Article
- JAM-A functions as a female microglial tumor suppressor in glioblastoma.Neuro-oncology · 2020Article
- Effects of a Single Head Exposure to GSM-1800 MHz Signals on the Transcriptome Profile in the Rat Cerebral Cortex: Enhanced Gene Responses Under Proinflammatory Conditions.Neurotoxicity research · 2020Article
- Macrophage Migration and Phagocytosis Are Controlled by Kindlin-3's Link to the Cytoskeleton.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Intravital 2-photon imaging reveals distinct morphology and infiltrative properties of glioblastoma-associated macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Site-specific phosphorylation regulates the functions of kindlin-3 in a variety of cells.Life science alliance · 2019Article
- The physiology of foamy phagocytes in multiple sclerosis.Acta neuropathologica communications · 2018Review
- Integrins promote axonal regeneration after injury of the nervous system.Biological reviews of the Cambridge Philosophical Society · 2018Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Microglia play a critical role in the development and homeostasis of the CNS. While mobilization of microglia is critical for a number of pathologies, understanding of the mechanisms of their migration in vivo is limited and often based on similarities to macrophages. Kindlin3 deficiency as well as Kindlin3 mutations of integrin-binding sites abolish both integrin inside-out and outside-in signaling in microglia, thereby resulting in severe deficiencies in cell adhesion, polarization, and migration in vitro, which are similar to the defects observed in macrophages. In contrast, while Kindlin3 mutations impaired macrophage mobilization in vivo, they had no effect either on the population of microglia in the CNS during development or on mobilization of microglia and subsequent microgliosis in a model of multiple sclerosis. At the same time, acute microglial response to laser-induced injury was impaired by the lack of Kindlin3-integrin interactions. Based on 2-photon imaging of microglia in the brain, Kindlin3 is required for elongation of microglial processes toward the injury site and formation of phagosomes in response to brain injury. Thus, while Kindlin3 deficiency in human subjects is not expected to diminish the presence of microglia within CNS, it might delay the recovery process after injury, thereby exacerbating its complications.
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Registered trials
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.