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Cell Signal. 2013 Dec;25(12):2374-82. doi: 10.1016/j.cellsig.2013.07.029. Epub 2013 Aug 3.

Nitrosyl-cobinamide (NO-Cbi), a new nitric oxide donor, improves wound healing through cGMP/cGMP-dependent protein kinase.

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1
University of California Irvine, Irvine, CA, United States. Electronic address: rspitler@uci.edu.

Abstract

Nitric oxide (NO) donors have been shown to improve wound healing, but the mechanism is not well defined. Here we show that the novel NO donor nitrosyl-cobinamide (NO-Cbi) improved in vitro wound healing in several cell types, including an established line of lung epithelial cells and primary human lung fibroblasts. On a molar basis, NO-Cbi was more effective than two other NO donors, with the effective NO-Cbi concentration ranging from 3 to 10μM, depending on the cell type. Improved wound healing was secondary to increased cell migration and not cell proliferation. The wound healing effect of NO-Cbi was mediated by cGMP, mainly through cGMP-dependent protein kinase type I (PKGI), as determined using pharmacological inhibitors and activators, and siRNAs targeting PKG type I and II. Moreover, we found that Src and ERK were two downstream mediators of NO-Cbi's effect. We conclude that NO-Cbi is a potent inducer of cell migration and wound closure, acting via cGMP, PKG, Src, and extracellular signal regulated kinase (ERK).

KEYWORDS:

Cell migration; ERK; NO; NO-Cbi; Nitric oxide; PDE; PKG; SNP; Src; Wound healing; cGMP-dependent protein kinase; extracellular signal regulated kinase; nitrosyl-cobinamide; phosphodiesterase; sodium nitroprusside

PMID:
23920342
DOI:
10.1016/j.cellsig.2013.07.029
[Indexed for MEDLINE]
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