HSP90alpha, HSP90beta, and p53 Expression following in Vitro Hyperthermia Exposure in Gestation Day 10 Rat Embryos

Abstract

The studies presented here are aimed at understanding the expression of p53, HSP90alpha, and HSP90beta in gestation day (GD) 10 CD rat embryos. GD 10 rat embryos were exposed in vitro to 37 degrees C or 42 degrees C for 15 min, then cultured at 37 degrees C for 0.5, 1, 3, or 5 h. Immunohistochemistry was performed on formalin-fixed, paraffin embedded, sectioned embryos for p53, HSP90alpha, or HSP90beta expression. p53 expression was minimal in control embryos but was induced with heat exposure. Maximum expression of p53 was observed in rostral tissues, e.g., the optic vesicle, rostral neuroepithelium, and mature (rostral) somites 3 and 5 h after heat exposure. Expression of p53 in the caudal region, such as in mid and caudal neuroepithelium, immature (caudal) somites, and presomitic mesoderm, was moderate compared to rostral areas. No p53 expression was observed in the heart under any condition. The rostral-caudal gradient of p53 expression was not observed for HSP90alpha expression. HSP90alpha was induced in heat-exposed embryos beginning at 1 h, predominantly in neural tube and optic vesicle. Moderate but increased expression was observed in the somites of heat-exposed embryos at 3 and 5 h. Expression of p53 was primarily nuclear while HSP90alpha expression was mostly cytoplasmic. No clear association was observed between heat-induced HSP90alpha and p53 expression. HSP90beta was expressed extensively in control and heat-exposed embryos. Results indicate that heat induces p53 and HSP90alpha expression, but not HSP90beta expression, and that HSP90alpha induction is not likely to be involved in p53 regulation in mammalian embryos.

Hypoglycemia induced changes in cell death and cell proliferation in the organogenesis stage embryonic mouse heart

“…There has not been consistent demonstration of p53 expression in the embryonic heart. There is no immunohistochemical detection of p53 protein in hearts of gd10 rat embryos exposed to normal or hyperthermic conditions in vitro, despite its induction in developing brain, eye, and somites (Dugyala et al, 2002). Chemically induced genotoxic stress in gd8 mouse embryos likewise induces p53 gene expression and apoptosis in neural tissues but not heart (Wubah et al, 1996).…”

“…Expression of p53 has not been consistently demonstrated in the developing heart. No p53 expression was found in hearts of gestation day (gd)10 rat or gd8 mouse embryos under normal or stressed conditions (Wubah et al, 1996; Dugyala et al, 2002). However, p53 expression was demonstrated in the hearts of chick, rat, and human embryos (Miosge et al, 1997; Lichnovsky et al, 1998; Rees et al 1999; Krinka et al, 2001) and in response to hypoxia in chick cardiomyocytes (Chandel et al, 2000).…”

Analysis of gene and protein expression of cytochrome P450 and stress‐associated molecules in rat liver after spaceflight

“…In the present study, accumulation of glycogen and lipid was observed on histology, suggesting that CYP4A1 gene expression was in some part induced by the change in lipid metabolism. Heat shock induces HSP90 and p53 gene expression, 22,23 and cold stress upregulates Cirp and p53 gene expression 24,25 . As to cold response, HSP90 gene expression is not induced during cold stress itself but is induced on rewarming after cold treatment 26 .…”

Hyperthermia inhibits cell proliferation and induces apoptosis: Relative signaling status of P53, S100A4, and Notch in heat sensitive and resistant cell lines

“…Both p53‐dependent and ‐independent mechanisms have been evoked in the induction of apoptosis by hyperthermia [Abe et al, 2001; Dugyala et al, 2002; Guan et al, 2002; Mikheeva et al, 2004; Yasumoto et al, 2003, 2004; Nashimoto et al, 2005]. The mediation of apoptosis by p53 frequently involves activation down stream of Bax [Tamamoto et al, 2003].…”