Estrogen receptors, progesterone receptors and heat-shock 27-kD protein in liver biopsy specimens from patients with hepatitis B virus infection

Abstract

It has been proposed that in the human liver, the estrogen receptor gene may become inappropriately expressed as a consequence of HBV integration, contributing to cell transformation. This study was undertaken to examine estrogen receptor status in patients with hepatitis B virus infection and to analyze the expression of progesterone receptor and of a heat-shock 27,000-D protein (hsp27), both of which are estrogen regulated in estrogen target tissues. Receptor proteins were detected in liver biopsy specimens by immunocytochemistry using antireceptor monoclonal antibodies; a monoclonal antibody was also used to detect hsp27. Estrogen receptor and progesterone receptor were mainly seen in the nuclei of hepatocytes. The presence of hepatitis B virus infection did not always result in elevated estrogen receptor expression, but in general the expression of this receptor protein was higher in hepatitis B virus-positive patients than in patients with the same pathological findings (hepatitis, cirrhosis, hepatocarcinoma) but without hepatitis B virus. This was more clearly seen in the patients with hepatitis. Although estrogen receptor expression was moderate to high in many samples, the expression of the two biochemical markers of estrogen action at postreceptor levels (progesterone receptor and hsp27) was low or absent in most of the liver tissues examined, suggesting that in the liver the interaction of estrogen-estrogen receptor-DNA has characteristics inherent to this tissue.

Expression of heat-shock protein 47 in mouse liver

“…Therefore, these HSPs are important to protect cells from stress condition. The expression of HSPs 25, 60 70, and 90 has been reported in the liver (Ohmori et al 1990;Delhaye et al 1992;Jorge et al 1993;Koskinas et al 1993;Ciocca et al 1991;Broome et al 1993;Benjamin 1993). HSP70 is induced in hepatectomized liver and in proliferating hepatocytes (Ohmori et al 1990).…”

Immunological evidence for the identity between the hsp27 estrogen-regulated heat shock protein and the p29 estrogen receptor-associated protein in breast and endometrial cancer

“…Therefore, it is possible that while estrogen receptors remain in the cytoplasm, the site of protein synthesis, they could also be complexed to another protein of the heat shock family, the hsp27 (p29 estrogen receptor-associated protein). In addition, we believe that the presence of the hsp27/ p29 protein is not a universal method to detect hormone responsive tumors, since the hsp27 heat shock protein is under hormonal control and related to estrogen receptors in certain organs but not in others [8,33,42]. Even in breast cancer, some have reported only a weak association between p29 and estrogen receptors [43].…”

Impact of Female Sex Hormones on Liver Tissue Lactic Acidosis During Ischemia

“…Currently, the mechanisms underlying these ischemic metabolic sex differences leading to greater hepatic tissue lactic acidosis in females are unknown. A potential role for sex hormones is suggested by the presence of functional receptors for sex hormones in hepatocytes (23)(24)(25) and by the recent findings of lower lactate concentrations in perfused rabbit livers subjected to acute normothermic ischemia that were administered the sex hormone prolactin (26). Thus, this study was done to further elucidate the mechanisms for the reported sex differences in the liver's metabolic response to ischemic stress with a focus on the potential role of key sex hormones-estrogen, progesterone, and androgens-in a rat model of warm liver ischemia.…”