ArticleMolecular medicine (Cambridge, Mass.)
Peripheral administration of human adrenomedullin and its binding protein attenuates stroke-induced apoptosis and brain injury in rats.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Clinical Potential of Adrenomedullin Signaling in the Cardiovascular System.Circulation research · 2023Review
- Sustained Activation of CLR/RAMP Receptors by Gel-Forming Agonists.International journal of molecular sciences · 2022Article
- Translational studies of adrenomedullin and related peptides regarding cardiovascular diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Adrenomedullin: an important participant in neurological diseases.Neural regeneration research · 2020Review
- Combination of adrenomedullin with its binding protein accelerates cutaneous wound healing.PloS one · 2015Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Stroke is a leading cause of death and the primary medical cause of acquired adult disability worldwide. The progressive brain injury after acute stroke is partly mediated by ischemia-elicited inflammatory responses. The vasoactive hormone adrenomedullin (AM), upregulated under various inflammatory conditions, counterbalances inflammatory responses. However, regulation of AM activity in ischemic stroke remains largely unknown. Recent studies have demonstrated the presence of a specific AM binding protein (that is, AMBP-1) in mammalian blood. AMBP-1 potentiates AM biological activities. Using a rat model of focal cerebral ischemia induced by permanent middle cerebral artery occlusion (MCAO), we found that plasma levels of AM increased significantly, whereas plasma levels of AMBP-1 decreased significantly after stroke. When given peripherally early after MCAO, exogenous human AM in combination with human AMBP-1 reduced brain infarct volume 24 and 72 h after MCAO, an effect not observed after the treatment by human AM or human AMBP-1 alone. Furthermore, treatment of human AM/AMBP-1 reduced neuron apoptosis and morphological damage, inhibited neutrophil infiltration in the brain and decreased serum levels of S100B and lactate. Thus, human AM/AMBP-1 has the ability to reduce stroke-induced brain injury in rats. AM/AMBP-1 can be developed as a novel therapeutic agent for patients with ischemic stroke.
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