ArticleShock (Augusta, Ga.)2020
Modulation of the HGF/c-Met Axis Impacts Prolonged Hematopoietic Progenitor Mobilization Following Trauma and Chronic Stress.
Article in Shock (Augusta, Ga.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Experimental study of a novel mouse model of tibial shaft fracture combined with blunt chest trauma.Animal models and experimental medicine · 2025Article
- A rat model of multicompartmental traumatic injury and hemorrhagic shock induces bone marrow dysfunction and profound anemia.Animal models and experimental medicine · 2024Article
- Adrenergic Modulation of Erythropoiesis After Trauma.Frontiers in physiology · 2022Review
- Mediators of Prolonged Hematopoietic Progenitor Cell Mobilization After Severe Trauma.The Journal of surgical research · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
backgroundTrauma and hemorrhagic shock trigger mobilization of hematopoietic progenitor cells (HPC) from bone marrow to peripheral blood. Hepatocyte growth factor (HGF), tyrosine-protein kinase Met (c-Met), matrix metallopeptidase 9 (MMP-9), and corticosterone regulate this mobilization process. We hypothesized that beta-blockade with propranolol and sympathetic outflow inhibition with clonidine following trauma and chronic stress would decrease hematopoietic progenitor cell mobilization.
methodsSprague-Dawley rats were randomized to undergo three models of injury and stress: lung contusion, LC plus hemorrhagic shock (LCHS), or LCHS plus chronic restraint stress for 2 h daily (LCHS/CS). Propranolol and clonidine were administered by daily intraperitoneal injection until sacrifice on day seven. Bone marrow HGF, c-Met, and MMP-9 were measured by real-time PCR. Plasma corticosterone was measured by ELISA. Percentage HPC in peripheral blood was measured by flow cytometry.
resultsPropranolol and clonidine significantly decreased bone marrow MMP-9 expression, plasma corticosterone levels, and HPC mobilization, and significantly increased hemoglobin levels. HPC mobilization was greatest following LCHS/CS (5.4 ± 1.8) and was significantly decreased by propranolol (2.2 ± 0.9, P < 0.001) and clonidine (1.7 ± 0.5, P < 0.001). Hemoglobin (g/dL) was lowest following LCHS/CS (12.3 ± 1.2) and was significantly increased by propranolol (13.7 ± 0.4, P = 0.022) and clonidine (14.1 ± 1.1, P < 0.001).
conclusionsSevere injury was associated with increased bone marrow HGF, c-Met, and MMP-9, circulating corticosterone, HPC mobilization, and persistent anemia. Attenuating the neuroendocrine response to injury and stress with propranolol and clonidine reduced MMP-9 expression, corticosterone levels, HPC mobilization, and the degree of anemia.
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