ArticleAmerican journal of physiology. Heart and circulatory physiology2013
A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia.
Article in American journal of physiology. Heart and circulatory physiology, 2013. 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, 16 citations in OpenAlex.
- Sterile inflammation induces vasculopathy and chronic lung injury in murine sickle cell disease.Free radical biology & medicine · 2024Article
- Rational Drug Design of Peptide-Based Therapies for Sickle Cell Disease.Molecules (Basel, Switzerland) · 2019Review
- Plasma proteomic changes during therapeutic hypothermia in resuscitated patients after cardiac arrest.Experimental and therapeutic medicine · 2019Article
- P-selectin drives complement attack on endothelium during intravascular hemolysis in TLR-4/heme-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Hematological indicators in pygmy wood mouse Apodemus uralensis (Muridae, Rodentia) populations as markers of the environmental radiation exposure: East Urals radioactive trace (Russia).Environmental science and pollution research international · 2018Article
- Inflammation in sickle cell disease.Clinical hemorheology and microcirculation · 2018Article
- Intravascular hemolysis and the pathophysiology of sickle cell disease.The Journal of clinical investigation · 2017Review
- Sustained treatment of sickle cell mice with haptoglobin increases HO-1 and H-ferritin expression and decreases iron deposition in the kidney without improvement in kidney function.British journal of haematology · 2016Article
- Higher minor hemoglobin A2 levels in multiple sclerosis patients correlate with lesser disease severity.Neuropsychiatric disease and treatment · 2016Article
- Dietary supplementation with docosahexanoic acid (DHA) increases red blood cell membrane flexibility in mice with sickle cell disease.Blood cells, molecules & diseases · 2015Article
- Anion exchange HPLC isolation of high-density lipoprotein (HDL) and on-line estimation of proinflammatory HDL.PloS one · 2014Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Hemolysis can saturate the hemoglobin (Hb)/heme scavenging system, resulting in increased circulating cell-free Hb (CF-Hb) in hereditary and acquired hemolytic disease. While recent studies have suggested a central role for intravascular hemolysis and CF-Hb in the development of vascular dysfunction, this concept has stimulated considerable debate. This highlights the importance of determining the contribution of CF-Hb to vascular complications associated with hemolysis. Therefore, a novel Hb-binding peptide was synthesized and linked to a small fragment of apolipoprotein E (amino acids 141-150) to facilitate endocytic clearance. Plasma clearance of hE-Hb-b10 displayed a rapid phase t(1/2) of 16 min and slow phase t(1/2) of 10 h, trafficking primarily through the liver. Peptide hE-Hb-B10 decreased CF-Hb in mice treated with phenylhydrazine, a model of acute hemolysis. Administration of hE-Hb-B10 also attenuated CF-Hb in two models of chronic hemolysis: Berkeley sickle cell disease (SS) mice and mice with severe hereditary spherocytosis (HS). The hemolytic rate was unaltered in either chronic hemolysis model, supporting the conclusion that hE-Hb-B10 promotes CF-Hb clearance without affecting erythrocyte lysis. Interestingly, hE-Hb-B10 also decreased plasma ALT activity in SS and HS mice. Although acetylcholine-mediated facialis artery vasodilation was not improved by hE-Hb-B10 treatment, the peptide shifted vascular response in favor of NO-dependent vasodilation in SS mice. Taken together, these data demonstrate that hE-Hb-B10 decreases CF-Hb with a concomitant reduction in liver injury and changes in vascular response. Therefore, hE-Hb-B10 can be used to investigate the different roles of CF-Hb in hemolytic pathology and may have therapeutic benefit in the treatment of CF-Hb-mediated tissue damage.
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