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Leukocyte Common Antigen antibody

RRID:AB_2174426

Antibody ID

AB_2174426

Target Antigen

Mouse Thymus / Spleen The 30-F11 clone has been reported to react with all isoforms and both alloantigens of CD45, which is found on hematopoietic stem cells and all cells of hematopoietic origin, except erythrocytes.

Proper Citation

(BD Biosciences Cat# 550539, RRID:AB_2174426)

Clonality

monoclonal antibody

Comments

Western blot

Clone ID

[30-F11]

Host Organism

rat

Ndrg2 deficiency ameliorates neurodegeneration in experimental autoimmune encephalomyelitis.

  • Le TM
  • J. Neurochem.
  • 2018 Jan 10

Literature context:


Abstract:

N-myc downstream-regulated gene 2 (NDRG2) is a differentiation- and stress-associated molecule that is predominantly expressed in astrocytes in the central nervous system. In this study, we examined the expression and role of NDRG2 in experimental autoimmune encephalomyelitis (EAE), which is an animal model of multiple sclerosis. Western blot and immunohistochemical analysis revealed that the expression of NDRG2 was observed in astrocytes of spinal cord, and was enhanced after EAE induction. A comparative analysis of wild-type and Ndrg2-/- mice revealed that deletion of Ndrg2 ameliorated the clinical symptoms of EAE. Although Ndrg2 deficiency only slightly affected the inflammatory response, based on the results of flow cytometry, qRT-PCR, and immunohistochemistry, it significantly reduced demyelination in the chronic phase, and, more importantly, neurodegeneration both in the acute and chronic phases. Further studies revealed that the expression of astrocytic glutamate transporters, including glutamate aspartate transporter (GLAST) and glutamate transporter 1, was more maintained in the Ndrg2-/- mice compared with wild-type mice after EAE induction. Consistent with these results, studies using cultured astrocytes revealed that Ndrg2 gene silencing increased the expression of GLAST, while NDRG2 over-expression decreased it without altering the expression of glial fibrillary acidic protein. The effect of NDRG2 on GLAST expression was associated with the activation of Akt, but not with the activation of nuclear factor-kappa B. These findings suggest that NDRG2 plays a key role in the pathology of EAE by modulating glutamate metabolism. Cover Image for this Issue: doi: 10.1111/jnc.14173.

Funding information:
  • NCRR NIH HHS - C06 RR015455(United States)

Recruited Monocytes and Type 2 Immunity Promote Lung Regeneration following Pneumonectomy.

  • Lechner AJ
  • Cell Stem Cell
  • 2017 Jul 6

Literature context:


Abstract:

To investigate the role of immune cells in lung regeneration, we used a unilateral pneumonectomy model that promotes the formation of new alveoli in the remaining lobes. Immunofluorescence and single-cell RNA sequencing found CD115+ and CCR2+ monocytes and M2-like macrophages accumulating in the lung during the peak of type 2 alveolar epithelial stem cell (AEC2) proliferation. Genetic loss of function in mice and adoptive transfer studies revealed that bone marrow-derived macrophages (BMDMs) traffic to the lung through a CCL2-CCR2 chemokine axis and are required for optimal lung regeneration, along with Il4ra-expressing leukocytes. Our data suggest that these cells modulate AEC2 proliferation and differentiation. Finally, we provide evidence that group 2 innate lymphoid cells are a source of IL-13, which promotes lung regeneration. Together, our data highlight the potential for immunomodulatory therapies to stimulate alveologenesis in adults.

Funding information:
  • NHLBI NIH HHS - F30 HL131198()
  • NHLBI NIH HHS - R01 HL127002()
  • NHLBI NIH HHS - U01 HL134766()
  • NIGMS NIH HHS - T32 GM007618()

Interferon-λ Mediates Non-redundant Front-Line Antiviral Protection against Influenza Virus Infection without Compromising Host Fitness.

  • Galani IE
  • Immunity
  • 2017 May 16

Literature context:


Abstract:

Lambda interferons (IFNλs) or type III IFNs share homology, expression patterns, signaling cascades, and antiviral functions with type I IFNs. This has complicated the unwinding of their unique non-redundant roles. Through the systematic study of influenza virus infection in mice, we herein show that IFNλs are the first IFNs produced that act at the epithelial barrier to suppress initial viral spread without activating inflammation. If infection progresses, type I IFNs come into play to enhance viral resistance and induce pro-inflammatory responses essential for confronting infection but causing immunopathology. Central to this are neutrophils which respond to both cytokines to upregulate antimicrobial functions but exhibit pro-inflammatory activation only to type I IFNs. Accordingly, Ifnlr1-/- mice display enhanced type I IFN production, neutrophilia, lung injury, and lethality, while therapeutic administration of PEG-IFNλ potently suppresses these effects. IFNλs therefore constitute the front line of antiviral defense in the lung without compromising host fitness.

Funding information:
  • NINDS NIH HHS - T32 NS063391(United States)

Diverse Requirements for Microglial Survival, Specification, and Function Revealed by Defined-Medium Cultures.

  • Bohlen CJ
  • Neuron
  • 2017 May 17

Literature context:


Abstract:

Microglia, the resident macrophages of the CNS, engage in various CNS-specific functions that are critical for development and health. To better study microglia and the properties that distinguish them from other tissue macrophage populations, we have optimized serum-free culture conditions to permit robust survival of highly ramified adult microglia under defined-medium conditions. We find that astrocyte-derived factors prevent microglial death ex vivo and that this activity results from three primary components, CSF-1/IL-34, TGF-β2, and cholesterol. Using microglial cultures that have never been exposed to serum, we demonstrate a dramatic and lasting change in phagocytic capacity after serum exposure. Finally, we find that mature microglia rapidly lose signature gene expression after isolation, and that this loss can be reversed by engrafting cells back into an intact CNS environment. These data indicate that the specialized gene expression profile of mature microglia requires continuous instructive signaling from the intact CNS.

Funding information:
  • NIDA NIH HHS - R01 DA015043()
  • NIMH NIH HHS - K08 MH112120()
  • NIMH NIH HHS - T32 MH019938()

Pericytes of Multiple Organs Do Not Behave as Mesenchymal Stem Cells In Vivo.

  • Guimarães-Camboa N
  • Cell Stem Cell
  • 2017 Mar 2

Literature context:


Abstract:

Pericytes are widely believed to function as mesenchymal stem cells (MSCs), multipotent tissue-resident progenitors with great potential for regenerative medicine. Cultured pericytes isolated from distinct tissues can differentiate into multiple cell types in vitro or following transplantation in vivo. However, the cell fate plasticity of endogenous pericytes in vivo remains unclear. Here, we show that the transcription factor Tbx18 selectively marks pericytes and vascular smooth muscle cells in multiple organs of adult mouse. Fluorescence-activated cell sorting (FACS)-purified Tbx18-expressing cells behaved as MSCs in vitro. However, lineage-tracing experiments using an inducible Tbx18-CreERT2 line revealed that pericytes and vascular smooth muscle cells maintained their identity in aging and diverse pathological settings and did not significantly contribute to other cell lineages. These results challenge the current view of endogenous pericytes as multipotent tissue-resident progenitors and suggest that the plasticity observed in vitro or following transplantation in vivo arises from artificial cell manipulations ex vivo.

Funding information:
  • NCI NIH HHS - R01 CA095287()
  • NHLBI NIH HHS - DP1 HL117649()
  • NHLBI NIH HHS - R01 HL070867()
  • NHLBI NIH HHS - R01 HL119967()
  • NHLBI NIH HHS - R01 HL123747()
  • NHLBI NIH HHS - R01 HL130452()
  • NIH HHS - DP1 OD006428()
  • NINDS NIH HHS - P30 NS047101()

RABL2 Is Required for Hepatic Fatty Acid Homeostasis and Its Dysfunction Leads to Steatosis and a Diabetes-Like State.

  • Yi Lo JC
  • Endocrinology
  • 2016 Dec 12

Literature context:


Abstract:

Fatty liver, or hepatic steatosis, is an alarmingly common pathology in western societies, in large part because if left unheeded, it can lead to life-threatening forms of nonalcoholic fatty liver disease, including nonalcoholic steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. As such, it is essential that we attain a greater understanding of the pathways that control energy partitioning in the liver and ultimately how they are impacted by environmental factors. Here, we define the essential requirement for a member of the Ras-related protein in the brain (RAB)-like (RABL) clade of small GTPases, RABL2, in fatty acid metabolism including in microtubule-associated mitochondrial movement within the liver. RABL2 dysfunction, even in mice fed a low-fat chow diet, leads to retarded hepatic mitochondria movement associated with and a cascading phenotype of interrelated metabolic defects reminiscent of a type 2 diabetic state: hepatic steatosis, insulin resistance, glucose intolerance, and adult onset obesity. RABL2 dysfunction does not, however, alter mitochondrial content, or the inherent respiratory capacity of individual mitochondria per se. Rather, it is associated with a decreased capacity for fatty oxidation in the context of the intact cell, suggesting a complex, and important, role for mitochondrial movement in metabolic health. Our data highlight the importance of RABL2 and mitochondrial dynamics in hepatic fatty acid oxidation and in the achievement of metabolic balance.

Funding information:
  • NINDS NIH HHS - R01 NS042867(United States)

NLRP3 Deficiency Improves Angiotensin II-Induced Hypertension But Not Fetal Growth Restriction During Pregnancy.

  • Shirasuna K
  • Endocrinology
  • 2015 Nov 17

Literature context:


Abstract:

Preeclampsia is a pregnancy-specific syndrome characterized by elevated blood pressure, proteinuria, and intrauterine growth restriction (IUGR). Although sterile inflammation appears to be involved, its pathogenesis remains unclear. Recent evidence indicates that sterile inflammation is mediated through the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasomes, composed of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1. Here we investigated the role of the NLRP3 inflammasomes in the pathogenesis of preeclampsia using Nlrp3(-/-) and Asc(-/-) (Nlrp3 and Asc deficient) pregnant mice. During pregnancy in mice, continuous infusion of high-dose angiotensin II (AngII) induced hypertension, proteinuria, and IUGR, whereas infusion of low-dose AngII caused hypertension alone. AngII-induced hypertension was prevented in Nlrp3(-/-) mice but not in Asc(-/-), indicating that NLRP3 contributes to gestational hypertension independently of ASC-mediated inflammasomes. Although NLRP3 deficiency had no effect on IUGR, it restored the IL-6 up-regulation in the placenta and kidney of AngII-infused mice. Furthermore, treatment with hydralazine prevented the development of gestational hypertension but not IUGR or IL-6 expression in the placenta and kidney. These findings demonstrate that NLRP3 contributes to the development of gestational hypertension independently of the inflammasomes and that IUGR and kidney injury can occur independent of blood pressure elevation during pregnancy.

Funding information:
  • NIMH NIH HHS - R21 MH098506(United States)

The astrocytic lineage marker calmodulin-regulated spectrin-associated protein 1 (Camsap1): phenotypic heterogeneity of newly born Camsap1-expressing cells in injured mouse brain.

  • Yoshioka N
  • J. Comp. Neurol.
  • 2012 Apr 15

Literature context:


Abstract:

Calmodulin-regulated spectrin-associated protein 1 (Camsap1) has been recognized as a new marker for astrocytic lineage cells and is expressed on mature astrocytes in the adult brain (Yamamoto et al. [2009] J. Neurosci. Res. 87:503–513). In the present study, we found that newly born Camsap1-expressing cells exhibited regional heterogeneity in an early phase after stab injury of the mouse brain. In the surrounding area of the lesion site, Camsap1 was expressed on quiescent astrocytes. At 3 days after injury, Camsap1 immunoreactivity was upregulated on glial fibrillary acidic protein-immunoreactive (GFAP-ir) astrocytes. Some of these astrocytes incorporated bromodeoxyuridine (BrdU) together with re-expression of the embryonic cytoskeleton protein nestin. In the neighboring region of the lesion cavity, Camsap1 was expressed on GFAP-negative cells. At 3 days after injury, GFAP-ir astrocytes were absent around the lesion cavity. At this stage, NG2-ir cells immunopositive for Camsap1 and immunonegative for GFAP were distributed in border of the lesion cavity. By 10 days, Camsap1 immunoreactivity was exclusively detected on GFAP-ir reactive astrocytes devoid of NG2 immunoreactivity. BrdU pulse-chase labeling assay suggested the differentiation of Camsap1+/NG2+ cells into Camsap1+/GFAP+ astrocytes. In the subependymal zone of the lateral ventricle, Camsap1-ir cells increased after injury. Camsap1 immunoreactivity was distributed on ependymal and subependymal cells bearing various astrocyte markers, and BrdU incorporation was enhanced on such Camsap1-ir cells after injury. These results suggest that newly born reactive astrocytes are derived from heterogeneous Camsap1-expressing cells in the injured brain.

Funding information:
  • NIDDK NIH HHS - R01 DK084352(United States)

Suppression of fibrotic scar formation promotes axonal regeneration without disturbing blood-brain barrier repair and withdrawal of leukocytes after traumatic brain injury.

  • Yoshioka N
  • J. Comp. Neurol.
  • 2010 Sep 15

Literature context:


Abstract:

The fibrotic scar containing type IV collagen (Col IV) formed in a lesion site is considered as an obstacle to axonal regeneration, because intracerebral injection of 2,2'-dipyridyl (DPY), an inhibitor of Col IV triple-helix formation, suppresses fibrotic scar formation in the lesion site and promotes axonal regeneration. To determine the role of the fibrotic scar on the healing process of injured central nervous system (CNS), the restoration of blood-brain barrier (BBB) and withdrawal of inflammatory leukocytes were examined in mice subjected to unilateral transection of the nigrostriatal dopaminergic pathway and intracerebral DPY injection. At 5 days after injury, destruction of BBB represented by leakage of Evans blue (EB) and widespread infiltration of CD45-immunoreactive leukocytes was observed around the lesion site, whereas reactive astrocytes increased surrounding the BBB-destroyed area. By 2 weeks after injury, the region of EB leakage and the diffusion of leukocytes were restricted to the inside of the fibrotic scar, and reactive astrocytes gathered around the fibrotic scar. In the DPY-treated lesion site, formation of the fibrotic scar was suppressed (84% decrease in Col IV-deposited area), reactive astrocytes occupied the lesion center, and areas of both EB leakage and leukocyte infiltration decreased by 86%. DPY treatment increased the number of regenerated dopaminergic axons by 2.53-fold. These results indicate that suppression of fibrotic scar formation does not disturb the healing process in damaged CNS, and suggest that this strategy is a reliable tool to promote axonal regeneration after traumatic injury in the CNS.

Funding information:
  • NHGRI NIH HHS - R01 HG004744-01(United States)