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Title: Arachidonic acid metabolism in fibroblasts derived from canine myocardium

Abstract

Canine fibroblasts from normal or healing infarcted myocardium were grown in culture. The cells were morphologically indistinguishable, but the doubling time of cells from healing myocardium was 39.6 +/- 3.5 hr whereas that of normals was 24 +/- 3.7 (n=5, p < .025). Fibroblasts incorporated (/sup 3/H)arachidonate (AA) into phospholipids. Calcium ionophore A23187 (10 ..mu..M) caused release and metabolism of (/sup 3/H) AA. A23187 or AA (10..mu..M) induced production of 6-keto PGF1..cap alpha.., PGE2, and a hydroxy metabolite of AA. RIA of 6-keto PGF1..cap alpha.. showed that subconfluent cells from healing myocardium produced 1202 +/- 354 pg/mg protein whereas that of normals was 551 +/- 222 (n=7, p < .025). Histamine and bradykinin also induced AA metabolism but were less potent. They examined the effect of AA released from deteriorating myocytes on AA metabolism by cultured fibroblasts. They confirmed that isolated myocytes labelled with (/sup 3/H)AA released but did not metabolize (/sup 3/H)AA. In coincubations, fibroblasts incorporated myocyte-derived AA. Subsequent stimulation of the fibroblasts with A23187 induced the synthesis of 6-keto PGF1..cap alpha.., PGE2 and a hydroxy metabolite. The fibroblast content of healing myocardium was 35-1000 times that of normal tissue (n=7). Thus even a moderate change in AA metabolism,more » amplified by the AA released from deteriorating myocytes, may be a significant physiologic or pathologic event.« less

Authors:
;
Publication Date:
Research Org.:
Univ. of Utah, Salt Lake City
OSTI Identifier:
6991182
Report Number(s):
CONF-8604222-
Journal ID: CODEN: FEPRA
Resource Type:
Conference
Journal Name:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
Additional Journal Information:
Journal Volume: 45:4; Conference: 70. annual meeting of the Federation of American Society for Experimental Biology, St. Louis, MO, USA, 13 Apr 1986
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; ARACHIDONIC ACID; METABOLISM; MYOCARDIAL INFARCTION; PATHOGENESIS; CATS; FIBROBLASTS; METABOLITES; MYOCARDIUM; PHOSPHOLIPIDS; PROSTAGLANDINS; TRACER TECHNIQUES; TRITIUM COMPOUNDS; ANIMAL CELLS; ANIMALS; BODY; CARBOXYLIC ACIDS; CARDIOVASCULAR DISEASES; CARDIOVASCULAR SYSTEM; CONNECTIVE TISSUE CELLS; DISEASES; ESTERS; HEART; ISOTOPE APPLICATIONS; LABELLED COMPOUNDS; LIPIDS; MAMMALS; MONOCARBOXYLIC ACIDS; MUSCLES; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC PHOSPHORUS COMPOUNDS; ORGANS; SOMATIC CELLS; VERTEBRATES; 550501* - Metabolism- Tracer Techniques; 550901 - Pathology- Tracer Techniques

Citation Formats

Weber, D R, and Prescott, S M. Arachidonic acid metabolism in fibroblasts derived from canine myocardium. United States: N. p., 1986. Web.
Weber, D R, & Prescott, S M. Arachidonic acid metabolism in fibroblasts derived from canine myocardium. United States.
Weber, D R, and Prescott, S M. 1986. "Arachidonic acid metabolism in fibroblasts derived from canine myocardium". United States.
@article{osti_6991182,
title = {Arachidonic acid metabolism in fibroblasts derived from canine myocardium},
author = {Weber, D R and Prescott, S M},
abstractNote = {Canine fibroblasts from normal or healing infarcted myocardium were grown in culture. The cells were morphologically indistinguishable, but the doubling time of cells from healing myocardium was 39.6 +/- 3.5 hr whereas that of normals was 24 +/- 3.7 (n=5, p < .025). Fibroblasts incorporated (/sup 3/H)arachidonate (AA) into phospholipids. Calcium ionophore A23187 (10 ..mu..M) caused release and metabolism of (/sup 3/H) AA. A23187 or AA (10..mu..M) induced production of 6-keto PGF1..cap alpha.., PGE2, and a hydroxy metabolite of AA. RIA of 6-keto PGF1..cap alpha.. showed that subconfluent cells from healing myocardium produced 1202 +/- 354 pg/mg protein whereas that of normals was 551 +/- 222 (n=7, p < .025). Histamine and bradykinin also induced AA metabolism but were less potent. They examined the effect of AA released from deteriorating myocytes on AA metabolism by cultured fibroblasts. They confirmed that isolated myocytes labelled with (/sup 3/H)AA released but did not metabolize (/sup 3/H)AA. In coincubations, fibroblasts incorporated myocyte-derived AA. Subsequent stimulation of the fibroblasts with A23187 induced the synthesis of 6-keto PGF1..cap alpha.., PGE2 and a hydroxy metabolite. The fibroblast content of healing myocardium was 35-1000 times that of normal tissue (n=7). Thus even a moderate change in AA metabolism, amplified by the AA released from deteriorating myocytes, may be a significant physiologic or pathologic event.},
doi = {},
url = {https://www.osti.gov/biblio/6991182}, journal = {Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)},
number = ,
volume = 45:4,
place = {United States},
year = {Wed Mar 05 00:00:00 EST 1986},
month = {Wed Mar 05 00:00:00 EST 1986}
}

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