Second-messenger signaling in lung capillaries

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

In the lung, several endothelial cell (EC) processes are regulated by an increase in EC cytosolic Ca2+. However, the role of EC cytosolic Ca2+ in mediating capillary proinflammatory processes is not clear. Mainly, it is not clear to what extent EC cytosolic Ca2+ increases activate other second messengers, which in turn might play a direct role in initiating proinflammatory responses. We determined this in intact lung capillaries using videomicroscopy and image analysis. We subjected the lungs to stressors including increased vascular pressure and tumor necrosis factor α. Our studies indicate that the primary response to these lung stresses is an increase in EC cytosolic Ca2+. These stresses induce proinflammatory responses in these capillaries, as indicated by the increase in P-selectin expression. However, determination of the signaling pathways underlying the Ca2+-induced P-selectin expression indicates a role for mitochondrial mechanisms. The lung stressors induce cytosolic Ca 2+-dependent increases in mitochondrial Ca2+ and reactive oxygen species, which in turn regulate exocytosis of P-selectin. Hence, mitochondrial reactive oxygen species act as signaling intermediates in Ca 2+-induced P-selectin exocytosis in lung capillaries. Thus, second messengers Ca2+ and mitochondrial reactive oxygen species are critical in the regulation of lung proinflammatory responses.

Original languageEnglish (US)
Title of host publicationCell Signaling in Vascular Inflammation
PublisherHumana Press
Pages147-154
Number of pages8
ISBN (Print)1588295257, 9781588295255
DOIs
StatePublished - Dec 1 2005

Fingerprint

Second Messenger Systems
P-Selectin
Lung
Endothelial Cells
Reactive Oxygen Species
Exocytosis
Video Microscopy
Blood Vessels
Tumor Necrosis Factor-alpha
Pressure

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Parthasarathi, K. (2005). Second-messenger signaling in lung capillaries. In Cell Signaling in Vascular Inflammation (pp. 147-154). Humana Press. https://doi.org/10.1007/978-1-59259-909-7_15

Second-messenger signaling in lung capillaries. / Parthasarathi, Kaushik.

Cell Signaling in Vascular Inflammation. Humana Press, 2005. p. 147-154.

Research output: Chapter in Book/Report/Conference proceedingChapter

Parthasarathi, K 2005, Second-messenger signaling in lung capillaries. in Cell Signaling in Vascular Inflammation. Humana Press, pp. 147-154. https://doi.org/10.1007/978-1-59259-909-7_15
Parthasarathi K. Second-messenger signaling in lung capillaries. In Cell Signaling in Vascular Inflammation. Humana Press. 2005. p. 147-154 https://doi.org/10.1007/978-1-59259-909-7_15
Parthasarathi, Kaushik. / Second-messenger signaling in lung capillaries. Cell Signaling in Vascular Inflammation. Humana Press, 2005. pp. 147-154
@inbook{5b338ce64e7b423facb736dd6f5ff4ec,
title = "Second-messenger signaling in lung capillaries",
abstract = "In the lung, several endothelial cell (EC) processes are regulated by an increase in EC cytosolic Ca2+. However, the role of EC cytosolic Ca2+ in mediating capillary proinflammatory processes is not clear. Mainly, it is not clear to what extent EC cytosolic Ca2+ increases activate other second messengers, which in turn might play a direct role in initiating proinflammatory responses. We determined this in intact lung capillaries using videomicroscopy and image analysis. We subjected the lungs to stressors including increased vascular pressure and tumor necrosis factor α. Our studies indicate that the primary response to these lung stresses is an increase in EC cytosolic Ca2+. These stresses induce proinflammatory responses in these capillaries, as indicated by the increase in P-selectin expression. However, determination of the signaling pathways underlying the Ca2+-induced P-selectin expression indicates a role for mitochondrial mechanisms. The lung stressors induce cytosolic Ca 2+-dependent increases in mitochondrial Ca2+ and reactive oxygen species, which in turn regulate exocytosis of P-selectin. Hence, mitochondrial reactive oxygen species act as signaling intermediates in Ca 2+-induced P-selectin exocytosis in lung capillaries. Thus, second messengers Ca2+ and mitochondrial reactive oxygen species are critical in the regulation of lung proinflammatory responses.",
author = "Kaushik Parthasarathi",
year = "2005",
month = "12",
day = "1",
doi = "10.1007/978-1-59259-909-7_15",
language = "English (US)",
isbn = "1588295257",
pages = "147--154",
booktitle = "Cell Signaling in Vascular Inflammation",
publisher = "Humana Press",
address = "United States",

}

TY - CHAP

T1 - Second-messenger signaling in lung capillaries

AU - Parthasarathi, Kaushik

PY - 2005/12/1

Y1 - 2005/12/1

N2 - In the lung, several endothelial cell (EC) processes are regulated by an increase in EC cytosolic Ca2+. However, the role of EC cytosolic Ca2+ in mediating capillary proinflammatory processes is not clear. Mainly, it is not clear to what extent EC cytosolic Ca2+ increases activate other second messengers, which in turn might play a direct role in initiating proinflammatory responses. We determined this in intact lung capillaries using videomicroscopy and image analysis. We subjected the lungs to stressors including increased vascular pressure and tumor necrosis factor α. Our studies indicate that the primary response to these lung stresses is an increase in EC cytosolic Ca2+. These stresses induce proinflammatory responses in these capillaries, as indicated by the increase in P-selectin expression. However, determination of the signaling pathways underlying the Ca2+-induced P-selectin expression indicates a role for mitochondrial mechanisms. The lung stressors induce cytosolic Ca 2+-dependent increases in mitochondrial Ca2+ and reactive oxygen species, which in turn regulate exocytosis of P-selectin. Hence, mitochondrial reactive oxygen species act as signaling intermediates in Ca 2+-induced P-selectin exocytosis in lung capillaries. Thus, second messengers Ca2+ and mitochondrial reactive oxygen species are critical in the regulation of lung proinflammatory responses.

AB - In the lung, several endothelial cell (EC) processes are regulated by an increase in EC cytosolic Ca2+. However, the role of EC cytosolic Ca2+ in mediating capillary proinflammatory processes is not clear. Mainly, it is not clear to what extent EC cytosolic Ca2+ increases activate other second messengers, which in turn might play a direct role in initiating proinflammatory responses. We determined this in intact lung capillaries using videomicroscopy and image analysis. We subjected the lungs to stressors including increased vascular pressure and tumor necrosis factor α. Our studies indicate that the primary response to these lung stresses is an increase in EC cytosolic Ca2+. These stresses induce proinflammatory responses in these capillaries, as indicated by the increase in P-selectin expression. However, determination of the signaling pathways underlying the Ca2+-induced P-selectin expression indicates a role for mitochondrial mechanisms. The lung stressors induce cytosolic Ca 2+-dependent increases in mitochondrial Ca2+ and reactive oxygen species, which in turn regulate exocytosis of P-selectin. Hence, mitochondrial reactive oxygen species act as signaling intermediates in Ca 2+-induced P-selectin exocytosis in lung capillaries. Thus, second messengers Ca2+ and mitochondrial reactive oxygen species are critical in the regulation of lung proinflammatory responses.

UR - http://www.scopus.com/inward/record.url?scp=84891452944&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84891452944&partnerID=8YFLogxK

U2 - 10.1007/978-1-59259-909-7_15

DO - 10.1007/978-1-59259-909-7_15

M3 - Chapter

AN - SCOPUS:84891452944

SN - 1588295257

SN - 9781588295255

SP - 147

EP - 154

BT - Cell Signaling in Vascular Inflammation

PB - Humana Press

ER -