RGD Reference Report - Glutamine reduces myocardial cell apoptosis in a rat model of sepsis by promoting expression of heat shock protein 90. - Rat Genome Database

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Glutamine reduces myocardial cell apoptosis in a rat model of sepsis by promoting expression of heat shock protein 90.

Authors: Li, Wanxia  Tao, Shaoyu  Wu, Qinghua  Wu, Tao  Tao, Ran  Fan, Jun 
Citation: Li W, etal., J Surg Res. 2017 Dec;220:247-254. doi: 10.1016/j.jss.2017.06.090. Epub 2017 Aug 5.
RGD ID: 13782295
Pubmed: PMID:29180187   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jss.2017.06.090   (Journal Full-text)


BACKGROUND: Myocardial cell injury and cardiac myocyte apoptosis are associated with sepsis. Glutamine (Gln) has been reported to repair myocardial cell injury. The aim of this study was to explore the role of Gln on cardiac myocytes in a cecal ligation and puncture (CLP) model of sepsis in Wistar rats.
MATERIALS AND METHODS: Following induction of sepsis in a CLP rat model, viral encoding heat shock protein 90 (Hsp90) gene and Hsp90dsDNA were designed to express and knockdown Hsp90, respectively. Rat cardiac tissues were examined histologically, and apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, Hsp90, p53 upregulated modulator of apoptosis, and p53 was measured by western blotting and real-time polymerase chain reaction. Caspase-3, caspase-8, and caspase-9 were detected by enzyme-linked immunosorbent assay.
RESULTS: Rat cardiac myocyte damage induced by CLP was reduced by Gln treatment and Hsp90 overexpression, and these changes were reversed by Hsp90 knockdown. Bcl-2 expression, Bcl-2-associated X protein, p53, p53 upregulated modulator of apoptosis, caspase-8, caspase-9, and caspase-3 activities were significantly upregulated in the CLP model, which were reduced by Gln treatment and Hsp90 overexpression.
CONCLUSIONS: Gln reduced apoptosis of cardiac myocytes in a rat model of sepsis, by promoting Hsp90 expression. Further studies are needed to determine the possible therapeutic action of Gln in sepsis in human tissue.



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Original Reference(s)
CASP3HumanSepsis treatmentISOCasp3 (Rattus norvegicus) RGD 
CASP8HumanSepsis treatmentISOCasp8 (Rattus norvegicus) RGD 
CASP9HumanSepsis treatmentISOCasp9 (Rattus norvegicus) RGD 
Casp3RatSepsis treatmentIEP  RGD 
Casp3MouseSepsis treatmentISOCasp3 (Rattus norvegicus) RGD 
Casp8RatSepsis treatmentIEP  RGD 
Casp8MouseSepsis treatmentISOCasp8 (Rattus norvegicus) RGD 
Casp9RatSepsis treatmentIEP  RGD 
Casp9MouseSepsis treatmentISOCasp9 (Rattus norvegicus) RGD 
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Genes (Rattus norvegicus)
Casp3  (caspase 3) Casp8  (caspase 8) Casp9  (caspase 9)

Genes (Mus musculus)
Casp3  (caspase 3) Casp8  (caspase 8) Casp9  (caspase 9)

Genes (Homo sapiens)
CASP3  (caspase 3) CASP8  (caspase 8) CASP9  (caspase 9)