Beta adrenoceptor regulation of macrophage arginase activity

Andrew C. Bernard, Elizabeth Fitzpatrick, Mary E. Maley, Gloria L. Gellin, Betty J. Tsuei, Warwick A. Arden, Bernard R. Boulanger, Paul A. Kearney, Juan B. Ochoa

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Background. Arginase, which metabolizes L-arginine within the urea cycle, is essential for production of polyamines and affects production of nitric oxide by depletion of L-arginine, the common substrate for both arginase and nitric oxide synthase. Having shown that trauma increases splenic macrophage arginase activity, we seek to define the mechanisms for this. RAW macrophage arginase activity and expression are increased by 8- bromo-cAMP in vitro. We hypothesize that since catecholamines increase cAMP, trauma-induced splenic arginase activity may be mediated by post-injury catecholamine release. Methods. RAW 264.7 macrophage arginase activity was measured in vitro in response to 4 catecholamines with or without propranolol or lipopolysaccharide (LPS). C57BL/6 mice underwent laparotomy as a model of moderate trauma after propranolol treatment, with and without intraperitoneal Escherichia coli LPS administration as a simulated pro-inflammatory stimulus. Results. Macrophage arginase activity increased in vitro in response to catecholamines or LPS (P <. 05). Propranolol pretreatment blocked macrophage arginase activity induced by epinephrine (10 μmol/L) in vitro (P <. 05). Trauma or LPS alone increased splenic arginase activity in vivo (P <. 05). Propranolol did not alter LPS-induced splenic arginase activity but did significantly reduce trauma-induced splenic arginase activity (P < .05). Conclusions. Catecholamines alone increase macrophage arginase activity through β-adrenoceptor activation. Increased splenic arginase activity induced by moderate trauma is decreased by β-adrenoceptor blockade, suggesting that trauma-induced arginase activity is partly mediated by endogenous catecholamines.

Original languageEnglish (US)
Pages (from-to)412-418
Number of pages7
JournalSurgery
Volume127
Issue number4
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

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Arginase
Adrenergic Receptors
Macrophages
Catecholamines
Lipopolysaccharides
Wounds and Injuries
Propranolol
Arginine
8-Bromo Cyclic Adenosine Monophosphate
Polyamines
Inbred C57BL Mouse
Nitric Oxide Synthase
Laparotomy
Epinephrine

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Bernard, A. C., Fitzpatrick, E., Maley, M. E., Gellin, G. L., Tsuei, B. J., Arden, W. A., ... Ochoa, J. B. (2000). Beta adrenoceptor regulation of macrophage arginase activity. Surgery, 127(4), 412-418. https://doi.org/10.1067/msy.2000.104115

Beta adrenoceptor regulation of macrophage arginase activity. / Bernard, Andrew C.; Fitzpatrick, Elizabeth; Maley, Mary E.; Gellin, Gloria L.; Tsuei, Betty J.; Arden, Warwick A.; Boulanger, Bernard R.; Kearney, Paul A.; Ochoa, Juan B.

In: Surgery, Vol. 127, No. 4, 01.01.2000, p. 412-418.

Research output: Contribution to journalArticle

Bernard, AC, Fitzpatrick, E, Maley, ME, Gellin, GL, Tsuei, BJ, Arden, WA, Boulanger, BR, Kearney, PA & Ochoa, JB 2000, 'Beta adrenoceptor regulation of macrophage arginase activity', Surgery, vol. 127, no. 4, pp. 412-418. https://doi.org/10.1067/msy.2000.104115
Bernard AC, Fitzpatrick E, Maley ME, Gellin GL, Tsuei BJ, Arden WA et al. Beta adrenoceptor regulation of macrophage arginase activity. Surgery. 2000 Jan 1;127(4):412-418. https://doi.org/10.1067/msy.2000.104115
Bernard, Andrew C. ; Fitzpatrick, Elizabeth ; Maley, Mary E. ; Gellin, Gloria L. ; Tsuei, Betty J. ; Arden, Warwick A. ; Boulanger, Bernard R. ; Kearney, Paul A. ; Ochoa, Juan B. / Beta adrenoceptor regulation of macrophage arginase activity. In: Surgery. 2000 ; Vol. 127, No. 4. pp. 412-418.
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abstract = "Background. Arginase, which metabolizes L-arginine within the urea cycle, is essential for production of polyamines and affects production of nitric oxide by depletion of L-arginine, the common substrate for both arginase and nitric oxide synthase. Having shown that trauma increases splenic macrophage arginase activity, we seek to define the mechanisms for this. RAW macrophage arginase activity and expression are increased by 8- bromo-cAMP in vitro. We hypothesize that since catecholamines increase cAMP, trauma-induced splenic arginase activity may be mediated by post-injury catecholamine release. Methods. RAW 264.7 macrophage arginase activity was measured in vitro in response to 4 catecholamines with or without propranolol or lipopolysaccharide (LPS). C57BL/6 mice underwent laparotomy as a model of moderate trauma after propranolol treatment, with and without intraperitoneal Escherichia coli LPS administration as a simulated pro-inflammatory stimulus. Results. Macrophage arginase activity increased in vitro in response to catecholamines or LPS (P <. 05). Propranolol pretreatment blocked macrophage arginase activity induced by epinephrine (10 μmol/L) in vitro (P <. 05). Trauma or LPS alone increased splenic arginase activity in vivo (P <. 05). Propranolol did not alter LPS-induced splenic arginase activity but did significantly reduce trauma-induced splenic arginase activity (P < .05). Conclusions. Catecholamines alone increase macrophage arginase activity through β-adrenoceptor activation. Increased splenic arginase activity induced by moderate trauma is decreased by β-adrenoceptor blockade, suggesting that trauma-induced arginase activity is partly mediated by endogenous catecholamines.",
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AU - Fitzpatrick, Elizabeth

AU - Maley, Mary E.

AU - Gellin, Gloria L.

AU - Tsuei, Betty J.

AU - Arden, Warwick A.

AU - Boulanger, Bernard R.

AU - Kearney, Paul A.

AU - Ochoa, Juan B.

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N2 - Background. Arginase, which metabolizes L-arginine within the urea cycle, is essential for production of polyamines and affects production of nitric oxide by depletion of L-arginine, the common substrate for both arginase and nitric oxide synthase. Having shown that trauma increases splenic macrophage arginase activity, we seek to define the mechanisms for this. RAW macrophage arginase activity and expression are increased by 8- bromo-cAMP in vitro. We hypothesize that since catecholamines increase cAMP, trauma-induced splenic arginase activity may be mediated by post-injury catecholamine release. Methods. RAW 264.7 macrophage arginase activity was measured in vitro in response to 4 catecholamines with or without propranolol or lipopolysaccharide (LPS). C57BL/6 mice underwent laparotomy as a model of moderate trauma after propranolol treatment, with and without intraperitoneal Escherichia coli LPS administration as a simulated pro-inflammatory stimulus. Results. Macrophage arginase activity increased in vitro in response to catecholamines or LPS (P <. 05). Propranolol pretreatment blocked macrophage arginase activity induced by epinephrine (10 μmol/L) in vitro (P <. 05). Trauma or LPS alone increased splenic arginase activity in vivo (P <. 05). Propranolol did not alter LPS-induced splenic arginase activity but did significantly reduce trauma-induced splenic arginase activity (P < .05). Conclusions. Catecholamines alone increase macrophage arginase activity through β-adrenoceptor activation. Increased splenic arginase activity induced by moderate trauma is decreased by β-adrenoceptor blockade, suggesting that trauma-induced arginase activity is partly mediated by endogenous catecholamines.

AB - Background. Arginase, which metabolizes L-arginine within the urea cycle, is essential for production of polyamines and affects production of nitric oxide by depletion of L-arginine, the common substrate for both arginase and nitric oxide synthase. Having shown that trauma increases splenic macrophage arginase activity, we seek to define the mechanisms for this. RAW macrophage arginase activity and expression are increased by 8- bromo-cAMP in vitro. We hypothesize that since catecholamines increase cAMP, trauma-induced splenic arginase activity may be mediated by post-injury catecholamine release. Methods. RAW 264.7 macrophage arginase activity was measured in vitro in response to 4 catecholamines with or without propranolol or lipopolysaccharide (LPS). C57BL/6 mice underwent laparotomy as a model of moderate trauma after propranolol treatment, with and without intraperitoneal Escherichia coli LPS administration as a simulated pro-inflammatory stimulus. Results. Macrophage arginase activity increased in vitro in response to catecholamines or LPS (P <. 05). Propranolol pretreatment blocked macrophage arginase activity induced by epinephrine (10 μmol/L) in vitro (P <. 05). Trauma or LPS alone increased splenic arginase activity in vivo (P <. 05). Propranolol did not alter LPS-induced splenic arginase activity but did significantly reduce trauma-induced splenic arginase activity (P < .05). Conclusions. Catecholamines alone increase macrophage arginase activity through β-adrenoceptor activation. Increased splenic arginase activity induced by moderate trauma is decreased by β-adrenoceptor blockade, suggesting that trauma-induced arginase activity is partly mediated by endogenous catecholamines.

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