Calcium-Binding Protein Iba-1/AIF-1 in Rat Brain Cells

Кирик, О. В.; Sukhorukova, E. G.; Коржевский, Д. Э.

doi:10.1007/s11055-011-9391-z

Cited by 11 publications

(6 citation statements)

References 9 publications

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“…In our study, immunohistochemistry and immunofluorescence staining indicated that Iba‐1, OX‐6, and CD68 were expressed in epiplexus cells of sham‐operated rats. OX‐6 recognizes major histocompatibility complex II (MHC II) antigens as an activated macrophage marker in rat brains, while Iba‐1 is a macrophage marker in many sites in brain, including the choroid plexus in rat . An interesting phenomenon was that most OX‐6‐positive epiplexus cells were different from Iba‐1‐positive epiplexus cells, with only a small portion colocalizing on immunofluorescence staining.…”

Section: Discussionmentioning

confidence: 99%

“…OX-6 recognizes major histocompatibility complex II (MHC II) antigens as an activated macrophage marker in rat brains, while Iba-1 is a macrophage marker in many sites in brain, including the choroid plexus in rat. 21,22 An interesting phenomenon was that most OX-6-positive epiplexus cells were different from Iba-1-positive epiplexus cells, with only a small portion colocalizing on immunofluorescence staining. The role of these subsets of epiplexus cells requires further investigation.…”

Section: Cd68-positive Cells Increased After Intraventricular Thrommentioning

confidence: 99%

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Activation of epiplexus macrophages in hydrocephalus caused by subarachnoid hemorrhage and thrombin

et al. 2019

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Aims We have found that hydrocephalus development in spontaneously hypertensive rats was associated with activation of epiplexus cells. The current study examined whether epiplexus cell activation occurs in a rat subarachnoid hemorrhage (SAH), whether activation would be greater in a subset of rats that developed hydrocephalus and the potential role of thrombin in epiplexus cell activation. Methods There were two parts in this study. First, an endovascular perforation was performed in rats to induce SAH. Second, rats received an intraventricular infusion of either thrombin or saline. Magnetic resonance imaging was used to measure the ventricular volumes. Immunofluorescence and immunohistochemistry were used to study epiplexus cell activation. Results Iba‐1, OX‐6, and CD68 were expressed in the epiplexus cells of the choroid plexus in sham‐operated rats. SAH increased Iba‐1 and CD68 immunoreactivity in epiplexus cells in addition to an increase in Iba‐1‐positive cell soma size. Those effects were greater in rats that developed hydrocephalus. Intraventricular thrombin mimicked the effects of SAH on epiplexus cell activation and hydrocephalus. Conclusion This study supports the concept that epiplexus cell activation is associated with hydrocephalus development. Epiplexus cell activation may be in response to thrombin production after hemorrhage, and it may be a therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Section: Cd68-positive Cells Increased After Intraventricular Thrommentioning

confidence: 99%

Activation of epiplexus macrophages in hydrocephalus caused by subarachnoid hemorrhage and thrombin

et al. 2019

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“…Historically, AIF1 has primarily been applied as a marker of microglia of the nervous system in multiple species. 6,8,21,23,41 In contrast, AIF1 has been used infrequently to detect macrophages in other tissues. For example, AIF1 expression has been observed in monocytic cell lines 20 and in activated macrophages after cardiac transplantation of rats and humans.…”

Section: Discussionmentioning

confidence: 99%

Allograft Inflammatory Factor 1 as an Immunohistochemical Marker for Macrophages in Multiple Tissues and Laboratory Animal Species

et al. 2018

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Allograft inflammatory factor 1 (AIF1) is a commonly used marker for microglia in the brains of humans and some animal models but has had limited applications elsewhere. We sought to determine whether AIF1 can be used as a macrophage marker across common laboratory animal species and tissues. We studied tissues (that is, spleen, liver, and lung) with defined macrophage populations by using an AIF1 immunostaining technique previously validated in human tissue. Tissues were collected from various mouse strains ( = 20), rat strains ( = 15), pigs ( = 4), ferrets ( = 4), and humans ( = 4, lung only). All samples of liver had scattered immunostaining in interstitial cells, consistent with resident tissue macrophages (Kupffer cells). Spleen samples had cellular immunostaining of macrophages in both the red and white pulp compartments, but the red pulp had more immunostained cellular aggregates and, in some species, increased immunostaining intensity compared with white pulp. In lung, alveolar macrophages had weak to moderate staining, whereas interstitial and perivascular macrophages demonstrated moderate to robust staining. Incidental lesions and tissue changes were detected in some sections, including a tumor, inducible bronchus-associated lymphoid tissue, and inflammatory lesions that demonstrated AIF1 immunostaining of macrophages. Finally, we compared AIF1 immunostaining of alveolar macrophages between a hypertensive rat model (SHR strain) and a normotensive model (WKY strain). SHR lungs had altered intensity and distribution of immunostaining in activated macrophages compared with macrophages of WKY lungs. Overall, AIF1 immunostaining demonstrated reproducible macrophage staining across multiple species and tissue types. Given the increasing breadth of model species used to study human disease, the use of cross-species markers and techniques can reduce some of the inherent variability within translational research.

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“…Also of note, whether IBA-1 is expressed exclusively by microglia has been recently questioned. For example, one study of rat brain suggested that other types of macrophages also express IBA-1 including meningeal, supra ependymal, and vascular stromal cells (Kirik et al, 2011). Of these, stromal cells may be found in dentate gyrus, and their morphology differs from that of microglia.…”

Section: Discussionmentioning

confidence: 99%

Microglial disruption in young mice with early chronic lead exposure

et al. 2013

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The mechanisms by which early chronic lead (Pb) exposure alter brain development have not been identified. We examined neuroimmune system effects in C57BL/6J mice with Pb exposure, including levels that may be common among children in lower socioeconomic income environments. Pups were exposed via dams’ drinking water from birth to post-natal day 28 to low, high or no Pb conditions. We compared gene expression of neuroinflammatory markers (study 1); and microglial mean cell body volume and mean cell body number in dentate gyrus, and dentate gyrus volume (study 2). Blood Pb levels in exposed animals at sacrifice (post-natal day 28) ranged from 2.66 to 20.31 μg/dL. Only interleukin-6 (IL6) differed between groups and reductions were dose-dependent. Microglia cell body number also differed between groups and reductions were dose-dependent. As compared with controls, microglia cell body volume was greater but highly variable in only low-dose animals; dentate gyri volumes in low- and high-dose animals were reduced. The results did not support a model of increased neuroinflammation. Instead, early chronic exposure to Pb disrupted microglia via damage to, loss of, or lack of proliferation of microglia in the developing brains of Pb-exposed animals.

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Calcium-Binding Protein Iba-1/AIF-1 in Rat Brain Cells

Cited by 11 publications

References 9 publications

Activation of epiplexus macrophages in hydrocephalus caused by subarachnoid hemorrhage and thrombin

Activation of epiplexus macrophages in hydrocephalus caused by subarachnoid hemorrhage and thrombin

Allograft Inflammatory Factor 1 as an Immunohistochemical Marker for Macrophages in Multiple Tissues and Laboratory Animal Species

Microglial disruption in young mice with early chronic lead exposure

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