Macrophage/Microglia-specific Protein Iba1 Enhances Membrane Ruffling and Rac Activation via Phospholipase C-γ-dependent Pathway

Kanazawa, Hiroko; Ohsawa, Keiko; Sasaki, Yo; Kohsaka, Shinichi; Imai, Yoshinori

doi:10.1074/jbc.m109218200

Cited by 163 publications

(114 citation statements)

References 40 publications

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“…Vibratome sections were immunostained for microtubule-associated protein-2 (MAP2), and the percentage of area occupied by immunoreactive neuronal structures of defined signal intensity was determined by computer-aided image analysis as described previously (Buttini et al, 1999;Van Uden et al, 2002). Vibratome sections were immunostained with an anti-Iba-1 antibody (1 g/ml; Wako) to detect activated microglia (Kanazawa et al, 2002) or with an anti-glial fibrillary acid protein (GFAP) antibody (2 g/ml; Chemicon, Temecula, CA) to detect activated astrocytes. The extent of neuritic dystrophy and its relationship to amyloid deposits in the brains of hAPP/Sod2 ϩ/ϩ and hAPP/Sod2 ϩ/Ϫ mice were assessed in doubleimmunolabeled sections as described previously Rockenstein et al, 2001).…”

Section: Methodsmentioning

confidence: 99%

Reduction in Mitochondrial Superoxide Dismutase Modulates Alzheimer's Disease-Like Pathology and Accelerates the Onset of Behavioral Changes in Human Amyloid Precursor Protein Transgenic Mice

Esposito¹,

Raber²,

Kekonius³

et al. 2006

J. Neurosci.

233

166

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Alzheimer's disease (AD) is associated with accumulations of amyloid-␤ (A␤) peptides, oxidative damage, mitochondrial dysfunction, neurodegeneration, and dementia. The mitochondrial antioxidant manganese superoxide dismutase-2 (Sod2) might protect against these alterations. To test this hypothesis, we inactivated one Sod2 allele (Sod2 ϩ/Ϫ ) in human amyloid precursor protein (hAPP) transgenic mice, reducing Sod2 activity to ϳ50% of that in Sod2 wild-type (Sod2 ϩ/ϩ ) mice. A reduction in Sod2 activity did not obviously impair mice without hAPP/A␤ expression. In hAPP mice, however, it accelerated the onset of behavioral alterations and of deficits in prepulse inhibition of acoustic startle, a measure of sensorimotor gating. In these mice, it also worsened hAPP/A␤-dependent depletion of microtubule-associated protein 2, a marker of neuronal dendrites. Sod2 reduction decreased amyloid plaques in the brain parenchyma but promoted the development of cerebrovascular amyloidosis, gliosis, and plaque-independent neuritic dystrophy. Sod2 reduction also increased the DNA binding activity of the transcription factor nuclear factor B. These results suggest that Sod2 protects the aging brain against hAPP/A␤-induced impairments. Whereas reductions in Sod2 would be expected to trigger or exacerbate neuronal and vascular pathology in AD, increasing Sod2 activity might be of therapeutic benefit.

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Section: Methodsmentioning

confidence: 99%

Reduction in Mitochondrial Superoxide Dismutase Modulates Alzheimer's Disease-Like Pathology and Accelerates the Onset of Behavioral Changes in Human Amyloid Precursor Protein Transgenic Mice

Esposito¹,

Raber²,

Kekonius³

et al. 2006

J. Neurosci.

233

166

View full text Add to dashboard Cite

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“…Iba1, which is highly and specifically expressed in microglia and macrophage, 16) and is involved in RacGTPase-dependent membrane ruffling and phagocytosis. 27) By immunohistochemical analyses, anti-Iba1 antibody was found to specifically recognize ramified microglia in normal rat brain, and Iba1 protein was strongly upregulated in activated microglia. 28) Therefore, Iba1 may play significant roles in the regulation of some immunological and pathophysiological functions of microglia, and serve as a novel marker for detecting the activation of microglia.…”

Section: Effect Of Ginsenoside Rg 3 On Microglia Activation In the mentioning

confidence: 99%

Ginsenoside Rg<sub>3</sub> Attenuates Microglia Activation Following Systemic Lipopolysaccharide Treatment in Mice

Park

Choi

Sohn

et al. 2012

Biological & Pharmaceutical Bulletin

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“…Anti-IBA1 (ionized calcium binding adapter molecule 1) is a rabbit polyclonal antibody that detects a 17 kDa EF hand protein that is expressed by microglia and macrophages (Kanazawa et al, 2002;Ohsawa et al, 2000). The immunogen for this antibody is the cterminus of IBA1 (N -PTGPPAKKAISELP-C).…”

Section: Antibody Characterizationmentioning

confidence: 99%

Alterations in sulfated chondroitin glycosaminoglycans following controlled cortical impact injury in mice

Katagiri

Susarla

et al. 2012

J of Comparative Neurology

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Chondroitin sulfate proteoglycans (CSPGs) play a pivotal role in many neuronal growth mechanisms including axon guidance and the modulation of repair processes following injury to the spinal cord or brain. Many actions of CSPGs in the central nervous system (CNS) are governed by the specific sulfation pattern on the glycosaminoglycan (GAG) chains attached to CSPG core proteins. To elucidate the role of CSPGs and sulfated GAG chains following traumatic brain injury (TBI), controlled cortical impact injury of mild to moderate severity was performed over the left sensory motor cortex in mice. Using immunoblotting and immunostaining, we found that TBI resulted in an increase in the CSPGs neurocan and NG2 expression in a tight band surrounding the injury core, which overlapped with the presence of 4-sulfated CS GAGs but not with 6-sulfated GAGs. This increase was observed as early as 7 days post injury (dpi), and persisted up to 28 dpi. Labeling with markers against microglia/macrophages, NG2 + cells, fibroblasts and astrocytes showed that these cells were all localized in the area, suggesting multiple origins of chondroitin-4-sultate increase. TBI also caused a decrease in the expression of aggrecan and phosphacan in the pericontusional cortex with a concomitant reduction in the number of perineuronal nets. In summary, we describe a dual response in CSPGs where they may be actively involved in complex repair processes following TBI. INDEXING TERMSChondroitin sulfate proteoglycan; traumatic brain injury; extracellular matrix; perineuronal nets

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Macrophage/Microglia-specific Protein Iba1 Enhances Membrane Ruffling and Rac Activation via Phospholipase C-γ-dependent Pathway

Abstract: Iba1 is a macrophage/microglia-specific calcium-binding protein that is involved in RacGTPase-dependent membrane ruffling and phagocytosis. In this study, we introduced Iba1 into Swiss 3T3 fibroblasts and demonstrated the enhancement of platelet-derived growth factor (

Cited by 163 publications

References 40 publications

Reduction in Mitochondrial Superoxide Dismutase Modulates Alzheimer's Disease-Like Pathology and Accelerates the Onset of Behavioral Changes in Human Amyloid Precursor Protein Transgenic Mice

Reduction in Mitochondrial Superoxide Dismutase Modulates Alzheimer's Disease-Like Pathology and Accelerates the Onset of Behavioral Changes in Human Amyloid Precursor Protein Transgenic Mice

Ginsenoside Rg<sub>3</sub> Attenuates Microglia Activation Following Systemic Lipopolysaccharide Treatment in Mice

Alterations in sulfated chondroitin glycosaminoglycans following controlled cortical impact injury in mice

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