Beta Blockade Protection of Bone Marrow Following Trauma: The Role of G-CSF

Baranski, Gregg M; Offin, Michael; Elhassan, Ihab; Sifri, Ziad C.; Hannoush, Edward J.; Alzate, Walter D.; Livingston, Dee; Mohr, Alicia M.

doi:10.1016/j.jss.2010.11.331

Cited by 3 publications

(4 citation statements)

References 22 publications

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“…In a murine burn sepsis model, chemical sympathectomy abrogated the effects of granulocyte and macrophage colony-stimulating factors in promoting expansion of hematopoietic progenitors (47). G-CSF is a potent stimulator of hematopoietic progenitor mobilization (26,27), and has been associated with increased progenitor mobilization after severe trauma (45,48). In addition to effects on hematopoietic progenitor mobilization, G-CSF potentiates granulopoiesis, which may occur at the expense of erythropoiesis (28,29).…”

Section: Discussionmentioning

confidence: 99%

The Postinjury Inflammatory State and the Bone Marrow Response to Anemia

Loftus¹,

Mira²,

Miller³

et al. 2018

Am J Respir Crit Care Med

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Section: Discussionmentioning

confidence: 99%

The Postinjury Inflammatory State and the Bone Marrow Response to Anemia

Loftus¹,

Mira²,

Miller³

et al. 2018

Am J Respir Crit Care Med

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“…This process appears to be necessary for wound healing and tissue repair, but prolonged HPC mobilization and loss of these progenitor cells from the bone marrow is also associated with bone marrow dysfunction and anemia (3,4). Activation of the granulocyte colony-stimulating factor (G-CSF)/stromal cell derived factor-1 (SDF-1) axis hones HPCs to the site of injury (5,6). Early mobilization of HPCs following traumatic injury and hemorrhagic shock has been associated with elevation of plasma G-CSF 24 hours after injury, and exogenous administration of G-CSF and SDF-1 to rats subjected to traumatic injury and hemorrhagic shock has been shown to increase HPC mobilization to injured tissue five days after injury (5,6).…”

Section: Introductionmentioning

confidence: 99%

Modulation of the HGF/c-Met Axis Impacts Prolonged Hematopoietic Progenitor Mobilization Following Trauma and Chronic Stress

Loftus

Kannan²,

Mira³

et al. 2020

Shock

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Background: Trauma and hemorrhagic shock trigger mobilization of hematopoietic progenitor cells (HPC) from bone marrow to peripheral blood. Hepatocyte growth factor (HGF), tyrosineprotein 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.Methods: Sprague-Dawley rats were randomized to undergo three models of injury and stress: lung contusion (LC), LC plus hemorrhagic shock (LCHS), or LCHS plus chronic restraint stress for 2h 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. %HPC in peripheral blood was measured by flow cytometry.Results: Propranolol 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). Conclusions:Severe 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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“…17,18 Baranski et al showed that peripheral blood HPCs and plasma levels of G-CSF were increased in both HS and lung contusion hemorrhagic shock (LC/HS) patients. 19 Elevated levels of G-CSF were reported in trauma, burns, and sepsis patients. [20][21][22] 5.…”

Section: G-csf and Mobilization Of Hematopoietic Progenitor Cellsmentioning

confidence: 99%

“…23 A recent study reported that SDF-1 maintains the HPCs connection between the bone marrow and the periphery. 19 The role of SDF-1 is to provide HPCs from bone marrow to injured tissue. HPCs help in healing of injured tissues by differentiating within the healing tissues.…”

Section: G-csf and Mobilization Of Hematopoietic Progenitor Cellsmentioning

confidence: 99%

Impaired hematopoietic progenitor cells in trauma hemorrhagic shock

Kumar

Bhoi

2016

Journal of Clinical Orthopaedics and Trauma

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Hemorrhagic shock (HS) is the major cause of death during trauma. Mortality due to HS is about 50%. Dysfunction of hematopoietic progenitor cells (HPCs) has been observed during severe trauma and HS. HS induces the elevation of cytokines, granulocyte-colony stimulating factor (G-CSF), peripheral blood HPCs, and circulating catecholamines, and decreases the expression of erythropoietin receptor connected with suppression of HPCs. Impaired HPCs may lead to persistent anemia and risk of susceptibility to infection, sepsis, and MOF. There is a need to reactivate impaired HPCs during trauma hemorrhagic shock.

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Beta Blockade Protection of Bone Marrow Following Trauma: The Role of G-CSF

Cited by 3 publications

References 22 publications

The Postinjury Inflammatory State and the Bone Marrow Response to Anemia

The Postinjury Inflammatory State and the Bone Marrow Response to Anemia

Modulation of the HGF/c-Met Axis Impacts Prolonged Hematopoietic Progenitor Mobilization Following Trauma and Chronic Stress

Impaired hematopoietic progenitor cells in trauma hemorrhagic shock

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