scholarly journals Annexin A3 as a Marker Protein for Microglia in the Central Nervous System of Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Zengli Zhang ◽  
Zhengyiqi Li ◽  
Zhi Ma ◽  
Meiling Deng ◽  
Manyu Xing ◽  
...  

The parenchymal microglia possess different morphological characteristics in cerebral physiological and pathological conditions; thus, visualizing these cells is useful as a means of further investigating parenchymal microglial function. Annexin A3 (ANXA3) is expressed in microglia, but it is unknown whether it can be used as a marker protein for microglia and its physiological function. Here, we compared the distribution and morphology of parenchymal microglia labeled by ANXA3, cluster of differentiation 11b (CD11b), and ionized calcium-binding adaptor molecule 1 (Iba1) and measured the expression of ANXA3 in nonparenchymal macrophages (meningeal and perivascular macrophages). We also investigated the spatiotemporal expression of ANXA3, CD11b, and Iba1 in vivo and in vitro and the cellular function of ANXA3 in microglia. We demonstrated that ANXA3-positive cells were abundant and evenly distributed throughout the whole brain tissue and spinal cord of adult rats. The morphology and distribution of ANXA3-labeled microglia were quite similar to those labeled by the microglial-specific markers CD11b and Iba1 in the central nervous system (CNS). ANXA3 was expressed in the cytoplasm of microglia, and its expression was significantly increased in activated microglia. ANXA3 was almost undetectable in the nonparenchymal macrophages. Meanwhile, the protein and mRNA expression levels of ANXA3 in different regions of the CNS were different from those of CD11b and Iba1. Moreover, knockdown of ANXA3 inhibited the proliferation and migration of microglia, while overexpression of ANXA3 enhanced these activities. This study confirms that ANXA3 may be a novel marker for parenchymal microglia in the CNS of adult rats and enriches our understanding of ANXA3 from expression patterns to physiological function.

1990 ◽  
Vol 258 (5) ◽  
pp. E894-E897 ◽  
Author(s):  
G. C. Tombaugh ◽  
R. M. Sapolsky

Glucocorticoids enhance the neurotoxic potential of several insults to the rat hippocampus that involve overactivation of glutamatergic synapses. These hormones also stimulate the synthesis of glutamine synthetase (GS) in peripheral tissue. Because this enzyme helps regulate glutamate metabolism in the central nervous system, glucocorticoid induction of GS in the brain may underlie the observed synergy. We have measured GS activity in the hippocampus and skeletal muscle (plantaris) of adult rats after bilateral adrenalectomy (ADX), corticosterone (Cort) replacement, or stress. No significant changes in GS were observed in hippocampal tissue, whereas muscle GS was significantly elevated after Cort treatment or stress and was reduced after ADX. These results suggest that Cort-induced shifts in GS activity probably do not explain Cort neurotoxicity, although the stress-induced rise in muscle GS may be relevant to certain types of myopathy.


Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 441-450 ◽  
Author(s):  
K. Blochlinger ◽  
L.Y. Jan ◽  
Y.N. Jan

The cut locus is both necessary and sufficient to specify the identity of a class of sensory organs in Drosophila embryos. It is also expressed in and required for the development of a number of other embryonic tissues, such as the central nervous system, the Malpighian tubules and the tracheal system. We here describe the expression of cut in the precursors of adult sensory organs. We also show that cut is expressed in cells of the prospective wing margin and correlate the wing margin phenotype caused by two cut mutations with altered cut expression patterns. Finally, we observe cut-expressing cells in other adult tissues, including Malpighian tubules, muscles, the central nervous system and ovarian follicle cells.


2017 ◽  
Vol 55 (7) ◽  
pp. 5548-5556 ◽  
Author(s):  
Giuseppe Bertozzi ◽  
Francesco Sessa ◽  
Giuseppe Davide Albano ◽  
Gabriele Sani ◽  
Francesca Maglietta ◽  
...  

1996 ◽  
Vol 286 (3) ◽  
pp. 357-364 ◽  
Author(s):  
Mark Veldman ◽  
Yueqiao Huang ◽  
John Jellies ◽  
Kristen M. Johansen ◽  
Jørgen Johansen

2016 ◽  
Vol 2 ◽  
pp. 205521731663099 ◽  
Author(s):  
Bert A ’t Hart ◽  
Robert Weissert

Background Myelin oligodendrocyte glycoprotein (MOG) is a candidate primary target of the autoimmune attack on the central nervous system (CNS) in multiple sclerosis (MS). However, the physiological function of MOG has been unclear for a long time. Objective We propose that MOG has a central role in the regulation of tolerance and autoimmunity. Conclusion The interaction of MOG with DC-SIGN, an innate antigen receptor of myeloid antigen-presenting cells (m-APCs), present inside the CNS (microglia) or in draining lymph nodes (dendritic cells; DCs), keeps these cells in an immature/tolerogenic state. We postulate that this tolerogenic mechanism may be disturbed in MS by unknown factors.


2019 ◽  
Author(s):  
Brittany A. Mersman ◽  
Sonia N. Jolly ◽  
Zhenguo Lin ◽  
Fenglian Xu

AbstractConnections between neurons called synapses are the key components underlying all nervous system functions of animals and humans. However, important genetic information on the formation and plasticity of one type, the electrical (gap junction-mediated) synapse, is severely understudied, especially in invertebrates. In the present study, we set forth to identify and characterize the gap junction-encoding gene innexin in the central nervous system (CNS) of the mollusc pond snail Lymnaea stagnalis (L. stagnalis). With PCR, 3’ and 5’ RACE, and BLAST searches, we identified eight innexin genes in the L. stagnalis nervous system named Lst Inx1-8. Phylogenetic analysis revealed that the L. stagnalis innexin genes originated from a single copy in the common ancestor of molluscan species by multiple gene duplication events and have been maintained in L. stagnalis since they were generated. The paralogous innexin genes demonstrate distinct expression patterns among tissues. In addition, one paralog, Lst Inx1, exhibits heterogeneity in cells and ganglia, suggesting the occurrence of functional diversification after gene duplication. These results introduce possibilities to study an intriguing potential relationship between innexin paralog expression and cell-specific functional outputs such as heterogenic ability to form channels and exhibit synapse plasticity. The L. stagnalis CNS contains large neurons and a functionally defined network for behaviors; with the introduction of L. stagnalis in the gap junction field, we are providing novel opportunities to combine genetic research with direct investigation of functional outcomes at the cellular, synaptic, and behavioral levels.Summary StatementBy characterizing the gap junction gene innexin in Lymnaea stagnalis, we open opportunities for novel studies on the regulation, plasticity, and evolutionary function of electrical synapses throughout the animal kingdom.


2020 ◽  
Author(s):  
Ting-Ting Luo ◽  
Chun-Qiu Dai ◽  
Jia-Qi Wang ◽  
Zheng-Mei Wang ◽  
Yi Yang ◽  
...  

Abstract Objectives: Drp1 is widely expressed in the mouse central nervous system and plays a role in inducing the mitochondrial fission process. Many diseases are associated with Drp1 and mitochondria. However, since the exact distribution of Drp1 has not been specifically observed, it is difficult to determine the impact of anti-Drp1 molecules on the human body. Clarifying the specific Drp1 distribution could be a good approach to targeted treatment or prognosis. Methods: We visualized the distribution of Drp1 in different brain regions and explicated the relationship between Drp1 and mitochondria. GAD67-GFP knock-in mice were utilized to detect the expression patterns of Drp1 in GABAergic neurons. We also further analyzed Drp1 expression in human malignant glioma tissue. Results : Drp1 was widely but heterogeneously distributed in the central nervous system. Further observation indicated that Drp1 was highly and heterogeneously expressed in inhibitory neurons. Under transmission electron microscopy, the distribution of Drp1 was higher in dendrites than other areas in neurons, and only a small amount of Drp1 was localized in mitochondria. In human malignant glioma, the fluorescence intensity of Drp1 increased from grade I-III, while grade IV showed a declining trend. Conclusion: In this study, we observed a wide heterogeneous distribution of Drp1 in the central nervous system, which might be related to the occurrence and development of neurologic disease. We hope that the relationship between Drp1 and mitochondria may will to therapeutic guidance in the clinic.


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