engleski

Endoplasmic reticulum-resident heat shock protein gp96 as an innate sensor of damage induced by tissue remodelling, stress and bacterial peptidoglycan

Since tissue disintegration after injury leads in the endoplasmic reticulum (ER) to activation of ER stress response, in this study we analysed the expression of ER resident heat shock protein gp96 in the liver: 1) in conditions of normal growth, induced by partial hepatectomy, 2) in psychosocial stress without the tissue lesions and 3) after the treatment with bacterial peptidoglycan-monomer linked with zinc. The data showed that all procedures might induce fast cytoplasmic overexpression of gp96 protein in hepatocytes, suggesting that during the disturbance of morphostasis, or activation of neuro-endocrino-immune circuit and Toll like receptors the liver cells cope with ER stress by an adaptive protective response, in which gp96, as a natural adjuvant, regulates the protein folding and degradation and participates in the induction of adaptive and innate immune responses.

gp96; liver; partial hepatectomy; stress; peptidoglycan monomer

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