Antigen-Retrieval Procedure for Bromodeoxyuridine Immunolabeling with Concurrent Labeling of Nuclear DNA and Antigens Damaged by HCl Pretreatment

Tang, Xiaobing; Falls, Douglas L.; Li, Xuekun; Lane, Tracy; Luskin, Marla B.

doi:10.1523/jneurosci.5048-06.2007

Cited by 106 publications

(108 citation statements)

References 13 publications

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“…Pregnant mice were injected intraperitoneally with BrdU (200 mg/kg of body weight) and sacrificed after 3 h. 29,30) For proliferation analysis, 20 μm thick, serial, coronal sections were prepared from E14 mice. Sections were treated with 2 M HCl at 40°C for 20 min and neutralized with 40 mM sodium borate buffer (pH 8.5) before staining with anti-BrdU antibody.…”

Section: Labeling With Bromodeoxyuridine (Brdu)mentioning

confidence: 99%

“…2,29) BrdU, a thymidine analog, is detected as the proliferation marker by immunohistochemistry, which is a common method for labeling cells in the S-phase of the cell cycle. 30,36,37) Three hours after injection of BrdU at E14, the BrdU-positive cells were analyzed in the SVZ and OB by immunohistology. The number of BrdU-positive cells in the ATF5 -/-OB is reduced significantly compared to the ATF5 +/+ OB (Fig.…”

Section: Decrease In the Interneurons In Atf5mentioning

confidence: 99%

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Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Umemura

Tsunematsu

Shimizu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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Activating transcription factor 5 (ATF5) is a stress response transcription factor of the cAMP-responsive element-binding/ATF family. Earlier, we reported that ATF5 expression is up-regulated in response to stress, such as amino acid limitation or arsenite exposure. Although ATF5 is widely expressed in the brain and the olfactory epithelium, the role of ATF5 is not fully understood. Here, the olfactory bulbs (OBs) of ATF5-deficient mice are smaller than those of wild-type mice. Histological analysis reveals the disturbed laminar structure of the OB, showing the thinner olfactory nerve layer, and a reduced number of interneurons. This is mainly due to the reduced number of bromodeoxyuridine-positive proliferating cells in the subventricular zone, where the interneuron progenitors are formed and migrate to the OBs. Moreover, the olfaction-related aggressive behavior of ATF5-deficient mice is reduced compared to wild-type mice. Our data suggest that ATF5 plays a crucial role in mouse OB development via interneuron.

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Section: Labeling With Bromodeoxyuridine (Brdu)mentioning

confidence: 99%

Section: Decrease In the Interneurons In Atf5mentioning

confidence: 99%

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Umemura

Tsunematsu

Shimizu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…Slides were imaged for CD31-positive vasculature and then processed to enable BrdUrd detection (citrate buffer, pH 6, at 120 C for 10 minutes at 20 psi; ref. 37). BrdUrd adducts were detected using a 1:500 dilution of monoclonal rat anti-BrdUrd (clone BU1/75) followed by 1:500 dilution of anti-rat Alexa 488 and hypoxia was detected via bound pimonidazole adducts using a 1:500 polyclonal rabbit-anti-pimonidazole (Hypoxyprobe) and a 1:500 Alexa 750 anti-rabbit secondary.…”

Section: Camptothecin Media Stability and Cellular Accumulationmentioning

confidence: 99%

Tissue Penetration and Activity of Camptothecins in Solid Tumor Xenografts

Kyle¹,

Baker

Gandolfo³

et al. 2014

Molecular Cancer Therapeutics

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The ability of a panel of camptothecin derivatives to access the tumor compartment was evaluated to determine the mechanisms by which the architecture of solid tumors may act to limit their activity. Microregional localization and activity of members of the camptothecin class of topoisomerase I targeting agents, including topotecan, irinotecan, and irinophore C, a lipid-based nanoparticulate formulation of irinotecan, were evaluated over time in HCT116 and HT29 colorectal tumor xenografts. Using native drug fluorescence, their distributions in tissue cryosections were related to the underlying tumor vasculature, tumor cell proliferation, and apoptosis. Topotecan exhibited a relatively uniform tumor distribution; in tissue 100 mm away from vessels, it reached 94% AE 5% of levels seen around blood vessels, whereas irinotecan and irinophore C were found to reach only 41% AE 10% and 5% AE 2%, respectively. Surprisingly, all three agents were able to initially inhibit proliferation uniformly throughout the tumors, and it was their rate of washout (topotecan > irinotecan > irinophore C) that correlated with activity. To explain this discrepancy, we looked at SN38, the active metabolite of irinotecan, and found it to penetrate tissue similarly to topotecan. Hence, the poor access to the tumor compartment of irinotecan and irinophore C could be offset by their systemic conversion to SN38. It was concluded that all three agents were effective at reaching tumor cells, and that despite the poor access to the extravascular compartment of irinophore C, its extended plasma exposure and systemic conversion to the diffusible metabolite SN38 enabled it to effectively target solid tumors.

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“…Sections (12 m) were obtained using a cryostat (Leica) and submitted to antigen retrieval by steam in 10 mM citrate buffer (pH 6), at 90-95°C for 5-15 minutes (Tang et al, 2007). Primary antibodies, diluted in PBS containing 0.3% Triton X-100, 10% lactoproteins and 1% BSA, were incubated overnight.…”

Section: Immunohistochemistrymentioning

confidence: 99%

p57KIP2 regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex

et al. 2012

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SUMMARYDuring cerebral cortex development, precise control of precursor cell cycle length and cell cycle exit is required for balanced precursor pool expansion and layer-specific neurogenesis. Here, we defined the roles of cyclin-dependent kinase inhibitor (CKI) p57 KIP2 , an important regulator of G1 phase, using deletion mutant mice. Mutant mice displayed macroencephaly associated with cortical hyperplasia during late embryogenesis and postnatal development. Embryonically, proliferation of radial glial cells (RGC) and intermediate precursors (IPC) was increased, expanding both populations, with greater effect on IPCs. Furthermore, cell cycle re-entry was increased during early corticogenesis, whereas cell cycle exit was augmented at middle stage. Consequently, neurogenesis was reduced early, whereas it was enhanced during later development. In agreement, the timetable of early neurogenesis, indicated by birthdating analysis, was delayed. Cell cycle dynamics analyses in mutants indicated that p57 KIP2 regulates cell cycle length in both RGCs and IPCs. By contrast, related CKI p27 KIP1 controlled IPC proliferation exclusively. Furthermore, p57KIP2 deficiency markedly increased RGC and IPC divisions at E14.5, whereas p27 KIP1 increased IPC proliferation at E16.5. Consequently, loss of p57 KIP2 increased primarily layer 5-6 neuron production, whereas loss of p27 KIP1 increased neurons specifically in layers 2-5. In conclusion, our observations suggest that p57 KIP2 and p27 KIP1 control neuronal output for distinct cortical layers by regulating different stages of precursor proliferation, and support a model in which IPCs contribute to both lower and upper layer neuron generation.

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Antigen-Retrieval Procedure for Bromodeoxyuridine Immunolabeling with Concurrent Labeling of Nuclear DNA and Antigens Damaged by HCl Pretreatment

Cited by 106 publications

References 13 publications

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Activating transcription factor 5 is required for mouse olfactory bulb development via interneuron

Tissue Penetration and Activity of Camptothecins in Solid Tumor Xenografts

p57KIP2 regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex

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