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7. Ghrelin inhibits skeletal muscle protein breakdown in rats with thermal injury through normalizing elevated expression of E3 ubiquitin ligases MuRF1 and MAFbx

Author

Balasubramaniam, Ambikaipakan, Joshi, Rashika, Su, Chunhua, Friend, Lou Ann, Sheriff, Sulaiman, Kagan, Richard J., and James, J. Howard

Subjects
Gene expression -- Research, Ghrelin -- Health aspects, Ghrelin -- Research, Muscle proteins -- Physiological aspects, Muscle proteins -- Genetic aspects, Muscle proteins -- Research, Rats -- Usage, Rats -- Models, Rattus -- Usage, Rattus -- Models, Muscles -- Physiological aspects, Muscles -- Genetic aspects, Muscles -- Research, Biological sciences
Abstract

We previously determined that ghrelin synthesis was downregulated after burn injury and that exogenous ghrelin retained its ability both to stimulate food intake and to restore plasma growth hormone levels in burned rats. These observations and the finding that anabolic hormones can attenuate skeletal muscle catabolism led us to investigate whether ghrelin could attenuate bum-induced skeletal muscle protein breakdown in rats. These studies were performed in young rats (50-60 g) 24 h after ~30% total body surface area bum injury. Burn injury increased total and myofibrillar protein breakdown in extensor digitorum longus (EDL) muscles assessed by in vitro tyrosine and 3-methyl-histidine release, respectively. Continuous 24-h administration of ghrelin (0.2 mg x [kg.sup.-1] x [h.sup.-1]) significantly inhibited both total and myofibrillar protein breakdown in burned rats. Ghrelin significantly attenuated burn-induced changes in mRNA expression of IGFBP-1 and IGFBP-3 in liver. In EDL, ghrelin attenuated the increases in mRNA expression of the binding proteins, but had no significant effect on reduced expression of IGF-I. Ghrelin markedly reduced the elevated mRNA expression of TNF-[alpha] and IL-6 in EDL muscle that occurred after burn. Moreover, ghrelin normalized plasma glucocorticoid levels, which were elevated after burn. Expression of the muscle-specific ubiquitin-ligating enzyme (E3) ubiquitin ligases MuRF1 and MAFbx were markedly elevated in both EDL and gastrocnemius and were normalized by ghrelin. These results suggest that ghrelin is a powerful anticatabolic compound that reduces skeletal muscle protein breakdown through attenuating multiple burn-induced abnormalities. burn; cachexia; IGF-I; inflammatory cytokines

Published
2009

13. Vibration Does Not Affect Short Term Outcomes Following Traumatic Brain Injury in a Porcine Model

Author

Jung, Andrew D, primary, Morris, Mackenzie C, additional, Veile, Rosalie, additional, Friend, Lou Ann, additional, Stevens-Topie, Sabre, additional, Cox, Daniel D, additional, McGuire, Jennifer L, additional, Foreman, Brandon, additional, Hartings, Jed A, additional, Pritts, Timothy A, additional, Makley, Amy T, additional, and Goodman, Michael D, additional

Published
2020
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16. MICROVESICLES GENERATED FOLLOWING TRAUMATIC BRAIN INJURY INDUCE PLATELET DYSFUNCTION VIA ADP RECEPTOR: Platelet Dysfunction Following TBI

Author

Martin, Grace E, Pugh, Amanda, Moran, Ryan, Veile, Rose, Friend, Lou Ann, Pritts, Timothy A, Makley, Amy T, Caldwell, Charles C, and Goodman, Michael D

Subjects
Male, Mice, Inbred C57BL, Mice, nervous system, Platelet Aggregation, Cell-Derived Microparticles, Receptors, Purinergic P2, Brain Injuries, Traumatic, Animals, Blood Platelet Disorders, Article, Piperazines, nervous system diseases
Abstract

INTRODUCTION: Traumatic brain injury (TBI) can result in an acute coagulopathy including platelet dysfunction that can contribute to ongoing intracranial hemorrhage. Previous studies have shown ADP-induced platelet aggregation to be reduced after TBI. In addition, circulating microvesicles (MVs) are increased following TBI and have been shown to play a role in post-TBI coagulopathy and platelet function. We hypothesized that post-TBI MVs would affect platelet aggregation in a murine head injury model. METHODS: Moderate TBI was performed using a weight-drop method in male C57BL6 mice. Whole blood, plasma, MVs, and MV-poor plasma were isolated from blood collected 10 minutes following TBI and were mixed separately with whole blood from uninjured mice. Platelet aggregation was measured with Multiplate impedance platelet aggregometry in response to adenosine diphosphate (ADP). The ADP P2Y(12) receptor inhibitor, R-138727, was incubated with plasma and MVs from TBI mice, and platelet inhibition was again measured. RESULTS: Whole blood taken from 10 minute post-TBI mice demonstrated diminished ADP-induced platelet aggregation compared to sham mice. When mixed with normal donor blood, post-TBI plasma and MVs induced diminished ADP-induced platelet aggregation compared to sham plasma and sham MVs. By contrast, the addition of post-TBI MV-poor plasma to normal blood did not change ADP-induced platelet aggregation. The observed dysfunction in post-TBI ADP platelet aggregation was prevented by the pretreatment of post-TBI plasma with R-138727. Treatment of post-TBI MVs with R-138727 resulted in similar findings of improved ADP-induced platelet aggregation compared to non-treated post-TBI MVs. CONCLUSION: ADP-induced platelet aggregation is inhibited acutely following TBI in a murine model. This platelet inhibition is reproduced in normal blood by the introduction of post-TBI plasma and MVs. Furthermore, observed platelet dysfunction is prevented when post-TBI plasma and MVs are treated with an inhibitor of the P2Y(12) ADP receptor. Clinically observed post-TBI platelet dysfunction may therefore be partially explained by the presence of the ADP P2Y(12) receptor within post-TBI MVs. LEVEL OF EVIDENCE: III

Published
2019

37. Simulated Aeromedical Evacuation Does Not Affect Systemic Inflammation or Organ Injury in a Murine Model of Hemorrhagic Shock

Author

Makley, Amy T., primary, Belizaire, Ritha, additional, Campion, Eric M., additional, Goodman, Michael D., additional, Sonnier, Dennis I., additional, Friend, Lou Ann, additional, Schuster, Rebecca M., additional, Bailey, Stephanie R., additional, Johannigman, Jay A., additional, Dorlac, Warren C., additional, Lentsch, Alex B., additional, and Pritts, Timothy A., additional

Published
2012
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42. Hypobaric Hypoxia Exacerbates the Neuroinflammatory Response to Traumatic Brain Injury

Author

Goodman, Michael D., primary, Makley, Amy T., additional, Huber, Nathan L., additional, Clarke, Callisia N., additional, Friend, Lou Ann W., additional, Schuster, Rebecca M., additional, Bailey, Stephanie R., additional, Barnes, Stephen L., additional, Dorlac, Warren C., additional, Johannigman, Jay A., additional, Lentsch, Alex B., additional, and Pritts, Timothy A., additional

Published
2011
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43. MURINE BLOOD BANKING

Author

Makley, Amy T., primary, Goodman, Michael D., additional, Friend, Lou Ann W., additional, Johannigman, Jay A., additional, Dorlac, Warren C., additional, Lentsch, Alex B., additional, and Pritts, Timothy A., additional

Published
2010
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