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Investigating Intercellular Signalin...

Vitucci, Eva Christina Maria,

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Investigating Intercellular Signaling between the Alveolar Epithelium and Microvascular Endothelium with an Organotypic Model of the Alveolar Capillary Region /

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Investigating Intercellular Signaling between the Alveolar Epithelium and Microvascular Endothelium with an Organotypic Model of the Alveolar Capillary Region // Eva Christina Maria Vitucci.
作者:	Vitucci, Eva Christina Maria,
面頁冊數:	1 electronic resource (201 pages)
附註:	Source: Dissertations Abstracts International, Volume: 84-07, Section: B.
Contained By:	Dissertations Abstracts International84-07B.
標題:	Toxicology. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29327091
ISBN:	9798363514043

Investigating Intercellular Signaling between the Alveolar Epithelium and Microvascular Endothelium with an Organotypic Model of the Alveolar Capillary Region /
Vitucci, Eva Christina Maria,

Investigating Intercellular Signaling between the Alveolar Epithelium and Microvascular Endothelium with an Organotypic Model of the Alveolar Capillary Region /Eva Christina Maria Vitucci. - 1 electronic resource (201 pages)

Source: Dissertations Abstracts International, Volume: 84-07, Section: B.

The alveolar capillary region (ACR) of the lung is a large, susceptible target of inhaled materials. As the interface of the respiratory and cardiovascular region, deposited material in the ACR induces adverse respiratory and cardiovascular effects. Despite the susceptibility and significance of this region, our understanding of the cellular and molecular mechanisms activated in the ACR upon deposition of various materials is poorly understood. A limitation in accessible and reflective in vitro models of the ACR is a main contributor to this gap in understanding. Thus, we developed a novel, organotypic in vitro model of the ACR to improve our understanding of the mechanisms involved in driving adverse health effects following exposure to inhaled toxicants, such as air pollutants. Through using this model, we have identified a novel mechanism of intercellular communication between the alveolar epithelium and microvascular endothelium of the ACR following exposure to diesel exhaust particulates (DEP). In addition, our data suggest the microvascular endothelium of the ACR may play a significant role in mediating pulmonary and systemic inflammation, and in promoting a pro-thrombotic hemodynamic shift following exposure to DEP. Endothelial pro-inflammatory and pro-thrombotic activation are common indicators of endothelial dysfunction, a precursor to the development of cardiovascular disease. In addition, unregulated pulmonary inflammation is a precursor to the development of respiratory disease. Furthermore, we show the protein content of extracellular vesicles secreted from our model is affected by exposure to biomass smoke and is affiliated with adverse respiratory and cardiovascular signaling mechanisms. Respiratory and cardiovascular diseases are associated with exposure to air pollution, such as DEP and biomass. Thus, we suggest the microvascular endothelium of the ACR plays a significant role in mediating inhalation exposure responses and that extracellular vesicles may be important mechanisms of perpetuating intercellular exposure responses to inhaled materials.

English

ISBN: 9798363514043Subjects--Topical Terms:

556884
Toxicology.
Subjects--Index Terms:

Alveoli

Investigating Intercellular Signaling between the Alveolar Epithelium and Microvascular Endothelium with an Organotypic Model of the Alveolar Capillary Region /
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245 1 0 $a Investigating Intercellular Signaling between the Alveolar Epithelium and Microvascular Endothelium with an Organotypic Model of the Alveolar Capillary Region / $c Eva Christina Maria Vitucci.
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520 $a The alveolar capillary region (ACR) of the lung is a large, susceptible target of inhaled materials. As the interface of the respiratory and cardiovascular region, deposited material in the ACR induces adverse respiratory and cardiovascular effects. Despite the susceptibility and significance of this region, our understanding of the cellular and molecular mechanisms activated in the ACR upon deposition of various materials is poorly understood. A limitation in accessible and reflective in vitro models of the ACR is a main contributor to this gap in understanding. Thus, we developed a novel, organotypic in vitro model of the ACR to improve our understanding of the mechanisms involved in driving adverse health effects following exposure to inhaled toxicants, such as air pollutants. Through using this model, we have identified a novel mechanism of intercellular communication between the alveolar epithelium and microvascular endothelium of the ACR following exposure to diesel exhaust particulates (DEP). In addition, our data suggest the microvascular endothelium of the ACR may play a significant role in mediating pulmonary and systemic inflammation, and in promoting a pro-thrombotic hemodynamic shift following exposure to DEP. Endothelial pro-inflammatory and pro-thrombotic activation are common indicators of endothelial dysfunction, a precursor to the development of cardiovascular disease. In addition, unregulated pulmonary inflammation is a precursor to the development of respiratory disease. Furthermore, we show the protein content of extracellular vesicles secreted from our model is affected by exposure to biomass smoke and is affiliated with adverse respiratory and cardiovascular signaling mechanisms. Respiratory and cardiovascular diseases are associated with exposure to air pollution, such as DEP and biomass. Thus, we suggest the microvascular endothelium of the ACR plays a significant role in mediating inhalation exposure responses and that extracellular vesicles may be important mechanisms of perpetuating intercellular exposure responses to inhaled materials.
546 $a English
590 $a School code: 0153
650 4 $a Toxicology. $3 556884
650 4 $a Molecular biology. $3 517296
653 $a Alveoli
653 $a Endothelial
653 $a Inhalation toxicology
653 $a Intercellular signaling
653 $a Organotypic modeling
690 $a 0383
690 $a 0307
710 2 $a The University of North Carolina at Chapel Hill. $b Toxicology. $e degree granting institution. $3 3823856
720 1 $a McCullough, Shaun D. $e degree supervisor.
773 0 $t Dissertations Abstracts International $g 84-07B.
790 $a 0153
791 $a Ph.D.
792 $a 2022
856 4 0 $u https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29327091