Hypoxia/reoxygenation-induced increased activity and expression of PTP-1B in neonatal rat cardiomyocytes are mediated by nitric oxide / 中华心血管病杂志
Zhonghua xinxueguanbing zazhi
; (12): 735-737, 2008.
Article
in Zh
| WPRIM
| ID: wpr-355901
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To explore if the hypoxia/reoxygenation-induced increased activity and expression of PTP-1B in neonatal rat cardiomyocytes are mediated by nitric oxide (NO).</p><p><b>METHODS</b>Neonatal rat cardiomyocytes were isolated and randomly divided into 4 groups: normal group (N group); hypoxia/reoxygenation group (H/R group); N(omega)-nitro-l-arginine methylester treated group (L-NAME group); hypoxia/reoxygenation plus L-NAME group (L-NA + H/R group). PTP-1B activity in cardiomyocytes was determined spectrophotometrically at 405 nm, PTP-1B expression in cardiomyocytes was detected by Western blot.NO and LDH concentrations in cell medium were also assayed.</p><p><b>RESULTS</b>PTP-1B activity and expression in cardiomyocytes was significantly higher in the H/R group as compared to the N group and this increase could be blocked by cotreatment with L-NAME. As compared to H/R group, nitric oxide and LDH concentrations in cell medium were significantly decreased in the L-NA + H/R group (NO concentration: H/R group, 368% +/- 13% and L-NA + H/R group, 61% +/- 7%, P < 0.005; LDH concentration: H/R group, 41.2 +/- 6.7 and L-NA + H/R group, 23.6 +/- 4.8, P < 0.05).</p><p><b>CONCLUSIONS</b>This study showed that pretreatment with L-NAME, a non-selective inhibitor of NOS, prevented the hypoxia/reoxygenation-induced increase in PTP-1B activity and expression in cardiomyocytes, suggesting PTP-1B activation during hypoxia/reoxygenation was mediated by nitric oxide.</p>
Full text:
1
Database:
WPRIM
Main subject:
Pharmacology
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Cell Hypoxia
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Cells, Cultured
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NG-Nitroarginine Methyl Ester
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Cell Biology
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Myocytes, Cardiac
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Metabolism
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Nitric Oxide
Limits:
Animals
Language:
Zh
Journal:
Zhonghua xinxueguanbing zazhi
Year:
2008
Document type:
Article