東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Consequences of differential macroph...

Longbrake, Erin Elisabeth.

FindBook

Google Book

Amazon

博客來

Consequences of differential macrophage activation after spinal cord trauma.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Consequences of differential macrophage activation after spinal cord trauma./
作者:	Longbrake, Erin Elisabeth.
面頁冊數:	192 p.
附註:	Adviser: Phillip G. Popovich.
Contained By:	Dissertation Abstracts International68-04B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3260170

Consequences of differential macrophage activation after spinal cord trauma.
Longbrake, Erin Elisabeth.

Consequences of differential macrophage activation after spinal cord trauma. - 192 p.

Adviser: Phillip G. Popovich.

Thesis (Ph.D.)--The Ohio State University, 2007.

Spinal cord injury (SCI) elicits an immediate and robust microglial response augmented by subsequent infiltration of monocyte derived macrophages. Collectively referred to as CNS macrophages, these cells have been postulated to play both detrimental and protective roles after CNS trauma. An appreciation of macrophage heterogeneity and plasticity suggests that they do both; however concrete evidence supporting this hypothesis is limited. This is, perhaps, not surprising since CNS trauma elicits a dynamic, complex microenvironment within which it is extremely difficult to dissect out precise mechanisms of macrophage-mediated injury or repair.Subjects--Topical Terms:

1017686
Biology, Cell.

Consequences of differential macrophage activation after spinal cord trauma.
LDR:04223nam 2200313 a 45 001 939269
005 20110512
008 110512s2007 ||||||||||||||||| ||eng d
035 $a (UMI)AAI3260170
035 $a AAI3260170
040 $a UMI $c UMI
100 1 $a Longbrake, Erin Elisabeth. $3 1263265
245 1 0 $a Consequences of differential macrophage activation after spinal cord trauma.
300 $a 192 p.
500 $a Adviser: Phillip G. Popovich.
500 $a Source: Dissertation Abstracts International, Volume: 68-04, Section: B, page: 2021.
502 $a Thesis (Ph.D.)--The Ohio State University, 2007.
520 $a Spinal cord injury (SCI) elicits an immediate and robust microglial response augmented by subsequent infiltration of monocyte derived macrophages. Collectively referred to as CNS macrophages, these cells have been postulated to play both detrimental and protective roles after CNS trauma. An appreciation of macrophage heterogeneity and plasticity suggests that they do both; however concrete evidence supporting this hypothesis is limited. This is, perhaps, not surprising since CNS trauma elicits a dynamic, complex microenvironment within which it is extremely difficult to dissect out precise mechanisms of macrophage-mediated injury or repair.
520 $a Relevant in vitro models should yield insight into the potential of each CNS macrophage population to promote neuroprotection or neurotoxicity and identify effector pathways for future manipulation in vivo. For such models to be relevant, they must accurately mimic critical components of the in vivo situation. For example, if cultured cells fail to accurately represent those present in vivo , the subsequent findings are fatally flawed. Although many have used in vitro models to draw conclusions about the contribution of monocyte-derived macrophages to SCI, no one has actually characterized these cells; thus the accuracy of these conclusions remains questionable.
520 $a To develop a physiologically meaningful model for SCI-elicited, monocyte derived macrophages, we first defined the inductive potential of these cells in vivo. Specifically, we used laser capture microdissection and real time PCR to build a molecular profile for hematogenous macrophages at the onset and peak of their response to SCI. We combined these data with findings from chimeric animals to describe a comprehensive phenotype for hematogenous SCI macrophages. We then compared this phenotype to that of three commonly-studied primary macrophage populations in vitro. Resident peritoneal, elicited peritoneal, and bone marrow derived macrophages (BMDM) were not interchangeable; each population exhibited unique characteristics. Of these macrophage subtypes, only cultured BMDM adequately modeled hematogenous SCI macrophages. Further studies utilizing BMDM will allow researchers to dissect the effects of the trauma-elicited inflammatory milieu on hematogenous macrophages.
520 $a A second limitation to the study of macrophages after CNS trauma is that although microglia and monocyte derived macrophages have unique lineages and may play distinct roles after injury, these cells are morphologically identical. The only marker routinely used to differentiate microglia from peripheral macrophages is CD45; however, since both populations express this marker (albeit at different levels), the usefulness of this technique is limited. Recently, it was observed that fractalkine receptor, CX3CR1, might be differentially regulated between microglia and macrophages; others confirmed that although microglia express CX3CR1, at least some populations of peripheral macrophages do not.
520 $a We hypothesized that CX3CR1 expression might differentiate microglia from peripherally derived CNS macrophages. Accordingly, we confirmed that CX3CR1 is ubiquitously expressed by resting microglia but is present on only a subpopulation of CNS macrophages after SCI. (Abstract shortened by UMI.)
590 $a School code: 0168.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Immunology. $3 1017716
690 $a 0379
690 $a 0982
710 2 $a The Ohio State University. $3 718944
773 0 $t Dissertation Abstracts International $g 68-04B.
790 $a 0168
790 1 0 $a Popovich, Phillip G., $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3260170