ATP and NO dually control migration of microglia to nerve lesions

Duan, Yuanli; Sahley, Christie L.; Muller, Kenneth J.

doi:10.1002/dneu.20689

Cited by 60 publications

(72 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NO's action on the migratory behavior of leech microglia may be mediated by cGMP (228). The leech microglia also has sensitivity to ATP and its analogs, which induce migratory movement; effects of purines were antagonized by reactive blue 2, suggesting the role for P2 purinoceptors (229).…”

Section: Evolutionary Origins Of Microgliamentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,138

2,981

View full text Add to dashboard Cite

Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

show abstract

Section: Evolutionary Origins Of Microgliamentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,138

2,981

View full text Add to dashboard Cite

show abstract

“…Using a similar acute brain slice preparation in rats, Kurpius et al [31] also demonstrated that following tissue slicing, which inevitably induces neuronal injury, microglia cells are able to “home” rapidly to neuron-rich regions presumably by sensing endogenously released neuronal purinergic signals. Subsequently, ATP-induced microglial chemokinesis has been confirmed in the mouse spinal cord [19, 32] and retina [21] as well as in other animal models including the zebrafish [33] and leech [34] indicating the widespread existence of this signaling mechanism. The specific receptors involved in purine-induced chemotaxis have also been identified.…”

Section: The Neuron-to-microglia Communication Axismentioning

confidence: 99%

Bidirectional Microglia-Neuron Communication in the Healthy Brain

2013

View full text Add to dashboard Cite

Unlike other resident neural cells that are of neuroectodermal origin, microglia are resident neural cells of mesodermal origin. Traditionally recognized for their immune functions during disease, new roles are being attributed to these cells in the development and maintenance of the central nervous system (CNS) including specific communication with neurons. In this review, we highlight some of the recent findings on the bidirectional interaction between neurons and microglia. We discuss these interactions along two lines. First, we review data that suggest that microglial activity is modulated by neuronal signals, focusing on evidence that (i) neurons are capable of regulating microglial activation state and influence basal microglial activities; (ii) classic neurotransmitters affect microglial behavior; (iii) chemotactic signals attract microglia during acute neuronal injury. Next, we discuss some of the recent data on how microglia signal to neurons. Signaling mechanisms include (i) direct physical contact of microglial processes with neuronal elements; (ii) microglial regulation of neuronal synapse and circuit by fractalkine, complement, and DAP12 signaling. In addition, we discuss the use of microglial depletion strategies in studying the role of microglia in neuronal development and synaptic physiology. Deciphering the mechanisms of bidirectional microglial-neuronal communication provides novel insights in understanding microglial function in both the healthy and diseased brain.

show abstract

“…These observations suggested that increases in NO level may incur potentially tumor promoting side effects under certain conditions in the neoplastic cells. These and related studies demonstrated a role for NO as a positive regulator of cellular migration and proliferation in both normal and neoplastic cells (Duan et al, 2009; Lu et al, 2015; Yongsanguanchai et al, 2015). …”

Section: Introductionmentioning

confidence: 89%

Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration

Fuseler

Valarmathi

2016

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Nitric oxide (NO) is a small free-radical gas molecule, which is highly diffusible and can activate a wide range of downstream effectors, with rapid and widespread cellular effects. NO is a versatile signaling mediator with a plethora of cellular functions. For example, NO has been shown to regulate actin, the microfilament, dependent cellular functions, and also acts as a putative stem cell differentiation-inducing agent. In this study, using a wound-healing model of cellular migration, we have explored the effect of exogenous NO on the kinetics of movement and morphological changes in postnatal bone marrow-derived mesenchymal stem cells (MSCs). Cellular migration kinetics and morphological changes of the migrating MSCs were measured in the presence of an NO donor (S-Nitroso-N-Acetyl-D,L-Penicillamine, SNAP), especially, to track the dynamics of single-cell responses. Two experimental conditions were assessed, in which SNAP (200 μM) was applied to the MSCs. In the first experimental group (SN-1), SNAP was applied immediately following wound formation, and migration kinetics were determined for 24 h. In the second experimental group (SN-2), MSCs were pretreated for 7 days with SNAP prior to wound formation and the determination of migration kinetics. The generated displacement curves were further analyzed by non-linear regression analysis. The migration displacement of the controls and NO treated MSCs (SN-1 and SN-2) was best described by a two parameter exponential functions expressing difference constant coefficients. Additionally, changes in the fractal dimension (D) of migrating MSCs were correlated with their displacement kinetics for all the three groups. Overall, these data suggest that NO may evidently function as a stop migration signal by disordering the cytoskeletal elements required for cell movement and proliferation of MSCs.

show abstract

ATP and NO dually control migration of microglia to nerve lesions

Cited by 60 publications

References 51 publications

Physiology of Microglia

Physiology of Microglia

Bidirectional Microglia-Neuron Communication in the Healthy Brain

Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration

Contact Info

Product

Resources

About