ArticleBMC molecular biology2007
Regulation of heme oxygenase-1 mRNA deadenylation and turnover in NIH3T3 cells by nitrosative or alkylation stress.
Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- SIAH2-mediated and organ-specific restriction of HO-1 expression by a dual mechanism.Scientific reports · 2020Article
- Human mesenchymal stem cells improve rat islet functionality under cytokine stress with combined upregulation of heme oxygenase-1 and ferritin.Stem cell research & therapy · 2019Article
- Article
- Role of heme in cardiovascular physiology and disease.Journal of the American Heart Association · 2015Review
- Cleavage by signal peptide peptidase is required for the degradation of selected tail-anchored proteins.The Journal of cell biology · 2014Article
- Involvement of ELAV RNA-binding proteins in the post-transcriptional regulation of HO-1.Frontiers in cellular neuroscience · 2014Article
- Emerging roles of Nrf2 and phase II antioxidant enzymes in neuroprotection.Progress in neurobiology · 2013Review
- Heme oxygenase-1 induction and organic nitrate therapy: beneficial effects on endothelial dysfunction, nitrate tolerance, and vascular oxidative stress.International journal of hypertension · 2012Article
- CREB downregulation in vascular disease: a common response to cardiovascular risk.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Analysis of nitric oxide-stabilized mRNAs in human fibroblasts reveals HuR-dependent heme oxygenase 1 upregulation.Molecular and cellular biology · 2009Article
- The p38 mitogen-activated protein kinase pathway is involved in the regulation of heme oxygenase-1 by acidic extracellular pH in aortic smooth muscle cells.Journal of cellular biochemistry · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHeme oxygenase-1 (HO-1) catalizes heme degradation, and is considered one of the most sensitive indicators of cellular stress. Previous work in human fibroblasts has shown that HO-1 expression is induced by NO, and that transcriptional induction is only partially responsible; instead, the HO-1 mRNA half-life is substantially increased in response to NO. The mechanism of this stabilization remains unknown.
resultsIn NIH3T3 murine fibroblasts, NO exposure increased the half-life of the HO-1 transcript from ~1.6 h to 11 h, while treatments with CdCl2, NaAsO2 or H2O2 increased the half-life only up to 5 h. Although poly(A) tail shortening can be rate-limiting in mRNA degradation, the HO-1 mRNA deadenylation rate in NO-treated cells was ~65% of that in untreated controls. In untreated cells, HO-1 poly(A) removal proceeded until 30-50 nt remained, followed by rapid mRNA decay. In NO-treated cells, HO-1 deadenylation stopped with the mRNA retaining poly(A) tails 30-50 nt long. We hypothesize that NO treatment stops poly(A) tail shortening at the critical 30- to 50-nt length. This is not a general mechanism for the post-transcriptional regulation of HO-1 mRNA. Methyl methane sulfonate also stabilized HO-1 mRNA, but that was associated with an 8-fold decrease in the deadenylation rate compared to that of untreated cells. Another HO-1 inducer, CdCl2, caused a strong increase in the mRNA level without affecting the HO-1 mRNA half-life.
conclusionThe regulation of HO-1 mRNA levels in response to cellular stress can be induced by transcriptional and different post-transcriptional events that act independently, and vary depending on the stress inducer. While NO appears to stabilize HO-1 mRNA by preventing the final steps of deadenylation, methyl methane sulfonate achieves stabilization through the regulation of earlier stages of deadenylation.
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