Turnover of resident microglia in the normal adult mouse brain

Lawson, L.J.; Perry, V.H.; Gordon, Siamon

doi:10.1016/0306-4522(92)90500-2

Cited by 606 publications

(408 citation statements)

References 30 publications

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“…Because MHC I are not constitutively expressed in normal rat brains (Flaris et al, 1993), it was necessary to induce upregulation of these molecules to disclose the presence of labeled cells. Di erences in the induced expression of MHC I and the slow turnover of microglial cells in the adult brain (Lawson et al, 1992) may explain why Matsumoto and Ikuta (1985) found no labeled rami®ed microglia, whereas Hickey and co-workers (Hickey and Kimura, 1988;Hickey et al, 1992) did identify a few rami®ed microglia of donor origin.…”

Section: Origin From Primitive Hemopoietic Cellsmentioning

confidence: 99%

“…In the quail many microglial precursors enter the nervous parenchyma during the last week of incubation NavascueÂ s et al, 1995), and they appear for the ®rst time within the rodent nervous system during the end of embryonic life and ®rst days of postnatal life (Perry et al, 1985;Milligan et al, 1991a;Perry and Gordon, 1991). The entry of microglial precursors during embryonic or early postnatal life, together with proliferation of such cells within the CNS (Dalmau, 1997;Dalmau et al, 1997a), should provide enough precursors to produce the mature microglial population, which shows slow turnover in the adult (Lawson et al, 1992). In the adult, new microglial cells appear presumably through mechanisms di erent from those involved in the early migration of precursors, and will therefore not be discussed here.…”

Section: Invasion Of the Developing Cns By Microglial Precursorsmentioning

confidence: 99%

“…Microglia show proliferative activity in the normal adult brain (Lawson et al, 1992) which greatly increases when microglia activate in injured brain (Streit et al, 1988;Reid et al, 1993;Amat et al, 1996). Brain macrophages and immature microglia in the developing CNS also have mitotic activity, as revealed by the uptake of labeled nucleotides or by the presence of proliferating cell nuclear antigen (PCNA) (Mander and Morris, 1996;Cossmann et al, 1997;Dalmau, 1997;MarõÂ n-Teva et al, 1998).…”

Section: Proliferationmentioning

confidence: 99%

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The origin and differentiation of microglial cells during development

Cuadros

Navascués

1998

Progress in Neurobiology

266

175

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AbstractÐSome authors claim that microglia originate from the neuroepithelium, although most now believe that microglial cells are of mesodermal origin, and probably belong to the monocyte/macrophage cell line. These cells must enter the developing central nervous system (CNS) from the blood stream, the ventricular space or the meninges. Afterward microglial cells are distributed more or less homogeneously through the entire nervous parenchyma. Stereotyped patterns of migration have been recognized during development, in which long-distance tangential migration precedes radial migration of individual cells. Microglial cells moving through the nervous parenchyma are ameboid microglia, which apparently di erentiate into rami®ed microglia after reaching their de®nitive location. This is supported by the presence of cells showing intermediate features between those of ameboid and rami®ed microglia. The factors that control the invasion of the nervous parenchyma, migration within the developing CNS and di erentiation of microglial cells are not well known. These phenomena apparently depend on environmental factors such as soluble or cell-surface bound molecules and components of the extracellular matrix. Microglial cells within the developing CNS are involved in clearing cell debris and withdrawing misdirected or transitory axons, and presumably support cell survival and neurite growth. #

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Section: Origin From Primitive Hemopoietic Cellsmentioning

confidence: 99%

Section: Invasion Of the Developing Cns By Microglial Precursorsmentioning

confidence: 99%

Section: Proliferationmentioning

confidence: 99%

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The origin and differentiation of microglial cells during development

Cuadros

Navascués

1998

Progress in Neurobiology

266

175

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“…Under physiological conditions, there is negligible infiltration of peripheral monocytes to the brain parenchyma and the microglia population is likely sustained by self‐renewal (Ajami et al ., 2007). Although, there have been previous studies aiming to understand the cycling rate of microglia (Lawson et al ., 1992), the contribution of microglia proliferation to sustain the population in the brain during organismal lifespan remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Enhanced microglial pro‐inflammatory response to lipopolysaccharide correlates with brain infiltration and blood–brain barrier dysregulation in a mouse model of telomere shortening

et al. 2015

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SummaryMicroglia are a proliferative population of resident brain macrophages that under physiological conditions self‐renew independent of hematopoiesis. Microglia are innate immune cells actively surveying the brain and are the earliest responders to injury. During aging, microglia elicit an enhanced innate immune response also referred to as ‘priming’. To date, it remains unknown whether telomere shortening affects the proliferative capacity and induces priming of microglia. We addressed this issue using early (first‐generation G1 mTerc−/−)‐ and late‐generation (third‐generation G3 and G4 mTerc−/−) telomerase‐deficient mice, which carry a homozygous deletion for the telomerase RNA component gene (mTerc). Late‐generation mTerc−/− microglia show telomere shortening and decreased proliferation efficiency. Under physiological conditions, gene expression and functionality of G3 mTerc−/− microglia are comparable with microglia derived from G1 mTerc−/− mice despite changes in morphology. However, after intraperitoneal injection of bacterial lipopolysaccharide (LPS), G3 mTerc−/− microglia mice show an enhanced pro‐inflammatory response. Nevertheless, this enhanced inflammatory response was not accompanied by an increased expression of genes known to be associated with age‐associated microglia priming. The increased inflammatory response in microglia correlates closely with increased peripheral inflammation, a loss of blood–brain barrier integrity, and infiltration of immune cells in the brain parenchyma in this mouse model of telomere shortening.

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“…Moreover, the ability of BMM to cross BBB was also investigated (Lawson et al 1992;Kurkowska-Jastrzebska et al 1999a, b;Streit et al 1999;Male and Rezaie 2001;Simard and Rivest 2004) In particular, it was demonstrated that monocytes infiltrate the brain in the 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD (KurkowskaJastrzebska et al 1999a, b;Kokovay and Cunningham 2005).…”

Section: Cells and Nanomaterials Hybrids For Clinical Neurosciencementioning

confidence: 99%

Novel Nanomaterials for Clinical Neuroscience

Gilmore

Xiang

Quan

et al. 2008

J Neuroimmune Pharmacol

203

119

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Neurodegenerative disorders including Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, and stroke are rapidly increasing as population ages. The field of nanomedicine is rapidly expanding and promises revolutionary advances to the diagnosis and treatment of devastating human diseases. This paper provides an overview of novel nanomaterials that have potential to improve diagnosis and therapy of neurodegenerative disorders. Examples include liposomes, nanoparticles, polymeric micelles, block ionomer complexes, nanogels, and dendrimers that have been tested clinically or in experimental models for delivery of drugs, genes, and imaging agents. More recently discovered nanotubes and nanofibers are evaluated as promising scaffolds for neuroregeneration. Novel experimental neuroprotective strategies also include nanomaterials, such as fullerenes, which have antioxidant properties to eliminate reactive oxygen species in the brain to mitigate oxidative stress. Novel technologies to enable these materials to cross the blood brain barrier will allow efficient systemic delivery of therapeutic and diagnostic agents to the brain. Furthermore, by combining such nanomaterials with cell-based delivery strategies, the outcomes of neurodegenerative disorders can be greatly improved.

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Turnover of resident microglia in the normal adult mouse brain

Cited by 606 publications

References 30 publications

The origin and differentiation of microglial cells during development

The origin and differentiation of microglial cells during development

Enhanced microglial pro‐inflammatory response to lipopolysaccharide correlates with brain infiltration and blood–brain barrier dysregulation in a mouse model of telomere shortening

Novel Nanomaterials for Clinical Neuroscience

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