Genome expression profiling and network analysis of nitrite therapy during chronic ischemia: possible mechanisms and interesting molecules
Open accessAbstract
Sodium nitrite is widely recognized to be a highly effective NO donor for the treatment of several ischemic tissue disorders. However, mechanisms by which nitrite confers cytoprotection during ischemic disorders remain largely unknown. In this study, we used genome expression profiling approaches to evaluate changes in gene expression in the hind-limb ischemia model using vehicle or sodium nitrite therapy. Sodium nitrite significantly restored ischemic tissue perfusion by day 3 post-ligation which returned to normal by day 7. Genesifter analysis of Affymetrix GeneChip data revealed a significant down-regulation of gene expression profiles at day 3, whereas gene expression profiles were predominantly up-regulated at day 7. Ingenuity network analysis of gene expression profiles at day 3 showed a strong decrease in gene expression from networks associated with immune functions such as acute inflammatory responses, antigen presentation, and humoral immune responses while networks containing increased gene expression profiles were associated with cardiovascular, skeletal, and muscle system development and function. Network analysis of day 7 gene array data revealed predominant up-regulation of genes associated with cell survival, tissue morphology, connective tissue function, skeletal and muscular system development, and lymphoid tissue structure and development. These data suggest that sodium nitrite elicits potent anti-inflammatory and pro-angiogenic gene responses at early time points which is later followed by up-regulation of genes associated with tissue repair and homeostasis.
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Nitrite anion is a reversible metabolite of NO that facilitates endogenous signaling responses differentially affecting gene expression.
“However, nitrite anion has emerged as a reversible metabolite of NO that facilitates endogenous signaling responses differentially affecting gene expression [3, 4], serves as a diagnostic marker of cardiovascular health, and acts as a potential therapeutic agent for several disease states.”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [3]
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“However, nitrite anion has emerged as a reversible metabolite of NO that facilitates endogenous signaling responses differentially affecting gene expression [3, 4], serves as a diagnostic marker of cardiovascular health, and acts as a potential therapeutic agent for several disease states.”
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“Using a genomewide gene expression profile approach, we found a large spectrum of genes regulating vascular remodeling, immune responses, and tissue repair that were altered by sodium nitrite treatment only in ischemic tissue, further highlighting tissue specific and broad spectrum molecular effects of nitrite therapy…”
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“For example, sodium nitrite therapy quickly downregulates the serotonin receptor 2B, which could augment vasodilation responses that may influence shear-mediated vascular remodeling responses (22).”
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“Furthermore, nitrite may contribute to other more chronic aspects of regulating blood flow, including angiogenesis (Kumar et al. 2008, Pattillo et al. 2010).”
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“Suggesting that nitrites mechanism of action in the revascularization process represents a multifactorial gene related mechanism (Pattillo et al. 2010; Pattillo et al. 2011).”
Background
- Authors
- Pattillo, C. B., Fang, K., Pardue, S., & Kevil, C. G.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- Corresponding author
- Kevil, Christopher G.
- Venue
- Nitric Oxide
- Publisher
- Elsevier BV
- Published
- 2010-02
- Volume
- 22
- Issue
- 2
- Pages
- 168-179
- ISSN
- 1089-8603 (ISSN-L)
- PMC
- PMC4599788
- OpenAlex
- W2074512969
- Cited by
- 15
- References
- 48
- Citations by year
- 2020: 1 · 2019: 1 · 2017: 1 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 3
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nitric Oxide (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-80482, HL-94021, F32HL094021, R01HL080482)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK043785, DK-43785)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- sodium nitrite, nitrite therapy, hindlimb ischemia, gene expression profiling, anti-inflammatory response, angiogenesis, tissue perfusion, tissue repair, cytoprotection, nitric oxide donors
- MeSH terms
- Animals, Chronic Disease, Disease Models, Animal, Ischemia, Male, Mice, Inbred C57BL, Sodium Nitrite, Gene Expression Profiling, Mice, Gene Regulatory Networks
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