Skeletal muscle amino acid and myofibrillar protein mRNA response to thermal injury and infection

Y. Fong, J. P. Minei, M. A. Marano, L. L. Moldawer, H. Wei, G. T. Shires, G. T. Shires, S. F. Lowry

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Skeletal muscle changes associated with severe injury were investigated in male Wistar rats subjected to 30% full thickness scald injury (burn) and thermal injury followed by immediate colonization with 108 colony-forming units of Pseudomonas aeruginosa (BI). Freely fed animals (FF) and animals pair fed to the BI animals (PF) served as controls. Thermal injury in conjunction with infection produced a rapid and sustained muscle cellular membrane depolarization (transmembrane potential difference at 12 h after injury: FF 92.1 ± 0.3 and BI 85.2 ± 2.3 mV; P < 0.05). This was followed by body weight loss and skeletal muscle protein wasting (gastrocnemius protein at 7 days: FF 0.35 ± 0.01 and BI 0.16 ± 0.03 g; P < 0.05) and intracellular high-energy phosphate depletion (ATP at 10 days: FF 6.6 ± 0.4 and BI 4.5 ± 0.4 μmol/g tissue; P < 0.05). These body and cellular changes were not accounted for by the anorexia alone. Marked alterations in intracellular free amino acids were also noted in the BI group characterized by increases in levels of all amino acids (total intracellular free amino acids at 7 days: FF 51 ± 7 and BI 91 ± 12 mM; P < 0.05) except intracellular glutamine (at 7 days: FF 6.0 ± 0.2 and BI 2.4 ± 0.6 mM; P < 0.05). A significant decline in total cellular RNA content (RNA at 7 days: FF 4.7 ± 0.6 and BI 2.2 ± 0.2 mg; P < 0.05), as well as a coordinate decrease in mRNA for α-actin and myosin heavy chain were noted in the BI animals. We conclude from our data that 1) early alterations in membrane ionic gradient after burn-infection injury are not due to a cellular energy deficit; 2) infected burn injury produced a muscle protein wasting and intracellular high-energy phosphate depletion not explainable by anorexia alone; and 3) decrease in muscle protein mass is in part due to decrease in myofibrillar protein transcription.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume261
Issue number3 30-3
StatePublished - 1991

Fingerprint

Skeletal Muscle
Hot Temperature
Amino Acids
Messenger RNA
Wounds and Injuries
Infection
Proteins
Muscle Proteins
Anorexia
Phosphates
RNA
Membranes
Myosin Heavy Chains
Glutamine
Burns
Membrane Potentials
Pseudomonas aeruginosa
Wistar Rats
Actins
Weight Loss

Keywords

  • Cytokines
  • Glutamine
  • Membrane function

ASJC Scopus subject areas

  • Physiology

Cite this

Skeletal muscle amino acid and myofibrillar protein mRNA response to thermal injury and infection. / Fong, Y.; Minei, J. P.; Marano, M. A.; Moldawer, L. L.; Wei, H.; Shires, G. T.; Shires, G. T.; Lowry, S. F.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 261, No. 3 30-3, 1991.

Research output: Contribution to journalArticle

Fong, Y. ; Minei, J. P. ; Marano, M. A. ; Moldawer, L. L. ; Wei, H. ; Shires, G. T. ; Shires, G. T. ; Lowry, S. F. / Skeletal muscle amino acid and myofibrillar protein mRNA response to thermal injury and infection. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 1991 ; Vol. 261, No. 3 30-3.
@article{83779f0ea34244a1b9642b96b3d058df,
title = "Skeletal muscle amino acid and myofibrillar protein mRNA response to thermal injury and infection",
abstract = "Skeletal muscle changes associated with severe injury were investigated in male Wistar rats subjected to 30{\%} full thickness scald injury (burn) and thermal injury followed by immediate colonization with 108 colony-forming units of Pseudomonas aeruginosa (BI). Freely fed animals (FF) and animals pair fed to the BI animals (PF) served as controls. Thermal injury in conjunction with infection produced a rapid and sustained muscle cellular membrane depolarization (transmembrane potential difference at 12 h after injury: FF 92.1 ± 0.3 and BI 85.2 ± 2.3 mV; P < 0.05). This was followed by body weight loss and skeletal muscle protein wasting (gastrocnemius protein at 7 days: FF 0.35 ± 0.01 and BI 0.16 ± 0.03 g; P < 0.05) and intracellular high-energy phosphate depletion (ATP at 10 days: FF 6.6 ± 0.4 and BI 4.5 ± 0.4 μmol/g tissue; P < 0.05). These body and cellular changes were not accounted for by the anorexia alone. Marked alterations in intracellular free amino acids were also noted in the BI group characterized by increases in levels of all amino acids (total intracellular free amino acids at 7 days: FF 51 ± 7 and BI 91 ± 12 mM; P < 0.05) except intracellular glutamine (at 7 days: FF 6.0 ± 0.2 and BI 2.4 ± 0.6 mM; P < 0.05). A significant decline in total cellular RNA content (RNA at 7 days: FF 4.7 ± 0.6 and BI 2.2 ± 0.2 mg; P < 0.05), as well as a coordinate decrease in mRNA for α-actin and myosin heavy chain were noted in the BI animals. We conclude from our data that 1) early alterations in membrane ionic gradient after burn-infection injury are not due to a cellular energy deficit; 2) infected burn injury produced a muscle protein wasting and intracellular high-energy phosphate depletion not explainable by anorexia alone; and 3) decrease in muscle protein mass is in part due to decrease in myofibrillar protein transcription.",
keywords = "Cytokines, Glutamine, Membrane function",
author = "Y. Fong and Minei, {J. P.} and Marano, {M. A.} and Moldawer, {L. L.} and H. Wei and Shires, {G. T.} and Shires, {G. T.} and Lowry, {S. F.}",
year = "1991",
language = "English (US)",
volume = "261",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "3 30-3",

}

TY - JOUR

T1 - Skeletal muscle amino acid and myofibrillar protein mRNA response to thermal injury and infection

AU - Fong, Y.

AU - Minei, J. P.

AU - Marano, M. A.

AU - Moldawer, L. L.

AU - Wei, H.

AU - Shires, G. T.

AU - Shires, G. T.

AU - Lowry, S. F.

PY - 1991

Y1 - 1991

N2 - Skeletal muscle changes associated with severe injury were investigated in male Wistar rats subjected to 30% full thickness scald injury (burn) and thermal injury followed by immediate colonization with 108 colony-forming units of Pseudomonas aeruginosa (BI). Freely fed animals (FF) and animals pair fed to the BI animals (PF) served as controls. Thermal injury in conjunction with infection produced a rapid and sustained muscle cellular membrane depolarization (transmembrane potential difference at 12 h after injury: FF 92.1 ± 0.3 and BI 85.2 ± 2.3 mV; P < 0.05). This was followed by body weight loss and skeletal muscle protein wasting (gastrocnemius protein at 7 days: FF 0.35 ± 0.01 and BI 0.16 ± 0.03 g; P < 0.05) and intracellular high-energy phosphate depletion (ATP at 10 days: FF 6.6 ± 0.4 and BI 4.5 ± 0.4 μmol/g tissue; P < 0.05). These body and cellular changes were not accounted for by the anorexia alone. Marked alterations in intracellular free amino acids were also noted in the BI group characterized by increases in levels of all amino acids (total intracellular free amino acids at 7 days: FF 51 ± 7 and BI 91 ± 12 mM; P < 0.05) except intracellular glutamine (at 7 days: FF 6.0 ± 0.2 and BI 2.4 ± 0.6 mM; P < 0.05). A significant decline in total cellular RNA content (RNA at 7 days: FF 4.7 ± 0.6 and BI 2.2 ± 0.2 mg; P < 0.05), as well as a coordinate decrease in mRNA for α-actin and myosin heavy chain were noted in the BI animals. We conclude from our data that 1) early alterations in membrane ionic gradient after burn-infection injury are not due to a cellular energy deficit; 2) infected burn injury produced a muscle protein wasting and intracellular high-energy phosphate depletion not explainable by anorexia alone; and 3) decrease in muscle protein mass is in part due to decrease in myofibrillar protein transcription.

AB - Skeletal muscle changes associated with severe injury were investigated in male Wistar rats subjected to 30% full thickness scald injury (burn) and thermal injury followed by immediate colonization with 108 colony-forming units of Pseudomonas aeruginosa (BI). Freely fed animals (FF) and animals pair fed to the BI animals (PF) served as controls. Thermal injury in conjunction with infection produced a rapid and sustained muscle cellular membrane depolarization (transmembrane potential difference at 12 h after injury: FF 92.1 ± 0.3 and BI 85.2 ± 2.3 mV; P < 0.05). This was followed by body weight loss and skeletal muscle protein wasting (gastrocnemius protein at 7 days: FF 0.35 ± 0.01 and BI 0.16 ± 0.03 g; P < 0.05) and intracellular high-energy phosphate depletion (ATP at 10 days: FF 6.6 ± 0.4 and BI 4.5 ± 0.4 μmol/g tissue; P < 0.05). These body and cellular changes were not accounted for by the anorexia alone. Marked alterations in intracellular free amino acids were also noted in the BI group characterized by increases in levels of all amino acids (total intracellular free amino acids at 7 days: FF 51 ± 7 and BI 91 ± 12 mM; P < 0.05) except intracellular glutamine (at 7 days: FF 6.0 ± 0.2 and BI 2.4 ± 0.6 mM; P < 0.05). A significant decline in total cellular RNA content (RNA at 7 days: FF 4.7 ± 0.6 and BI 2.2 ± 0.2 mg; P < 0.05), as well as a coordinate decrease in mRNA for α-actin and myosin heavy chain were noted in the BI animals. We conclude from our data that 1) early alterations in membrane ionic gradient after burn-infection injury are not due to a cellular energy deficit; 2) infected burn injury produced a muscle protein wasting and intracellular high-energy phosphate depletion not explainable by anorexia alone; and 3) decrease in muscle protein mass is in part due to decrease in myofibrillar protein transcription.

KW - Cytokines

KW - Glutamine

KW - Membrane function

UR - http://www.scopus.com/inward/record.url?scp=0025942171&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025942171&partnerID=8YFLogxK

M3 - Article

C2 - 1716065

AN - SCOPUS:0025942171

VL - 261

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 3 30-3

ER -