Induction of heme oxygenase-1 is involved in carbon monoxide-mediated central cardiovascular regulation

Wan Chen Lo, Pei Jung Lu, Wen Yu Ho, Michael Hsiao, Ching Jiunn Tseng

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Carbon monoxide (CO) has been identified as an endogenous biological messenger in the brain. Heme oxygenase (HO) catalyzes the metabolism of heme to CO and biliverdin. Previously, we have shown the involvement of CO in central cardiovascular regulation, baroreflex modulation, and glutaminergic neurotransmission in the nucleus tractus solitarii (NTS) of rats. In this study, we examined which HO isoform could be induced after hemin injection in the NTS. We also investigated their in situ distributions in the NTS after induction. Male Sprague-Dawley rats were anesthetized with urethane, and blood pressure was monitored intra-arterially. Unilateral microinjection of hemin (1 nmol), a heme molecule cleaved by HO to yield CO, produced significant decrease in blood pressure and heart rate. These cardiovascular effects of hemin were attenuated by prior administration of HO inhibitor zinc protoporphyrin IX (ZnPPIX). Microinjection of hemin into NTS resulted in significant induction of HO-1 protein expression in situ. Pretreatment of ZnPPIX significantly inhibited the HO-1 induction after hemin injection. No significant changes of HO-2 expression were found after hemin injection and ZnPPIX pretreatment. The in situ inductions of the HO-1 protein expression were further confirmed to be in glial cells and neurons after hemin injections into the NTS. These results indicated HO-1 but not HO-2 might be responsible for the generation of CO and contribute to central control of cardiovascular effects.

Original languageEnglish
Pages (from-to)8-16
Number of pages9
JournalJournal of Pharmacology and Experimental Therapeutics
Volume318
Issue number1
DOIs
Publication statusPublished - 2006 Jun 27

Fingerprint

Hemin
Heme Oxygenase-1
Carbon Monoxide
Solitary Nucleus
Heme Oxygenase (Decyclizing)
Injections
Microinjections
Heme
Biliverdine
Blood Pressure
Baroreflex
Urethane
Synaptic Transmission
Neuroglia
Sprague Dawley Rats
Protein Isoforms
Proteins
Heart Rate
Neurons
Brain

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

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title = "Induction of heme oxygenase-1 is involved in carbon monoxide-mediated central cardiovascular regulation",
abstract = "Carbon monoxide (CO) has been identified as an endogenous biological messenger in the brain. Heme oxygenase (HO) catalyzes the metabolism of heme to CO and biliverdin. Previously, we have shown the involvement of CO in central cardiovascular regulation, baroreflex modulation, and glutaminergic neurotransmission in the nucleus tractus solitarii (NTS) of rats. In this study, we examined which HO isoform could be induced after hemin injection in the NTS. We also investigated their in situ distributions in the NTS after induction. Male Sprague-Dawley rats were anesthetized with urethane, and blood pressure was monitored intra-arterially. Unilateral microinjection of hemin (1 nmol), a heme molecule cleaved by HO to yield CO, produced significant decrease in blood pressure and heart rate. These cardiovascular effects of hemin were attenuated by prior administration of HO inhibitor zinc protoporphyrin IX (ZnPPIX). Microinjection of hemin into NTS resulted in significant induction of HO-1 protein expression in situ. Pretreatment of ZnPPIX significantly inhibited the HO-1 induction after hemin injection. No significant changes of HO-2 expression were found after hemin injection and ZnPPIX pretreatment. The in situ inductions of the HO-1 protein expression were further confirmed to be in glial cells and neurons after hemin injections into the NTS. These results indicated HO-1 but not HO-2 might be responsible for the generation of CO and contribute to central control of cardiovascular effects.",
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Induction of heme oxygenase-1 is involved in carbon monoxide-mediated central cardiovascular regulation. / Lo, Wan Chen; Lu, Pei Jung; Ho, Wen Yu; Hsiao, Michael; Tseng, Ching Jiunn.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 318, No. 1, 27.06.2006, p. 8-16.

Research output: Contribution to journalArticle

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