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The role of nitric oxide in choleste...

Jung, Jae Yeon.

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The role of nitric oxide in cholesteatoma-induced bone resorption.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The role of nitric oxide in cholesteatoma-induced bone resorption./
作者:	Jung, Jae Yeon.
面頁冊數:	118 p.
附註:	Source: Dissertation Abstracts International, Volume: 64-06, Section: B, page: 2479.
Contained By:	Dissertation Abstracts International64-06B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3095526

The role of nitric oxide in cholesteatoma-induced bone resorption.
Jung, Jae Yeon.

The role of nitric oxide in cholesteatoma-induced bone resorption. - 118 p.

Source: Dissertation Abstracts International, Volume: 64-06, Section: B, page: 2479.

Thesis (Ph.D.)--Washington University, 2003.

Cholesteatoma develops as a result of abnormal epithelial cell migration and proliferation in the middle ear. The expanding mass of keratin debris and inflammatory cells results in the recruitment, development and activation of osteoclasts. Progressive erosion of the surrounding bony structures leads to hearing loss, vestibular dysfunction and possible intracranial complications.Subjects--Topical Terms:

1017686
Biology, Cell.

The role of nitric oxide in cholesteatoma-induced bone resorption.
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245 1 4 $a The role of nitric oxide in cholesteatoma-induced bone resorption.
300 $a 118 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-06, Section: B, page: 2479.
500 $a Chair: Richard A. Chole.
502 $a Thesis (Ph.D.)--Washington University, 2003.
520 $a Cholesteatoma develops as a result of abnormal epithelial cell migration and proliferation in the middle ear. The expanding mass of keratin debris and inflammatory cells results in the recruitment, development and activation of osteoclasts. Progressive erosion of the surrounding bony structures leads to hearing loss, vestibular dysfunction and possible intracranial complications.
520 $a Osteoclasts are highly specialized multinucleated cells with complex regulatory mechanisms. Recent studies demonstrate that nitric oxide (NO) is an important mediator of bone resorption in pathologic and physiologic pathways. Nitric oxide is a short lived, neutral free gas, which has been demonstrated to be a local mediator of neurotransmission, immune function, and vasoregulation. It is generated by the enzyme nitric oxide synthase, of which there are three known isoforms, NOS I, NOS II, and NOS III. NOS I and NOS III are expressed constitutively, are regulated by the calcium/calmodulin system, and generate low levels of nitric oxide (nanomolar). NOS II is inducible in most cell types studied, is differentially regulated by various cytokines, and generates high levels of nitric oxide (micromolar).
520 $a Isolated osteoclasts expressed NOS I constitutively and NOS II after cytokine stimulation. NOS III was not expressed in isolated osteoclasts. In order to investigate the role of NOS isoforms in osteoclast development and activity, mice with targeted deletions of NOS were obtained and their phenotypes examined both in vitro and in vivo.
520 $a In vitro, NOS I -/- osteoclasts demonstrated increased size but decreased resorption when plated on dentine. Consistent with this result, nanomolar concentrations of nitric oxide donors enhanced osteoclast activity. In vivo, NOS I-/- mice had fewer osteoclasts than wild type in a model of cholesteatoma induced bone resorption. In a co-culture system, stromal cells derived from NOS I -/- mice had reduced ability to support osteoclast development. These data suggest that the in vivo results may be explained by a defect of stromal cell function rather than osteoclast development or activity.
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791 $a Ph.D.
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