Heat shock protein 25 plays multiple roles during mouse skin development

Abstract

Heat shock protein (Hsp) 25 is a member of the small Hsp family. High levels of Hsp25 can be detected in skin. During adult epidermis differentiation, the concentration of Hsp25 increases as the distance of keratinocytes from the basal layer increases, in parallel with the extent of keratinization. We previously showed that Hsp25, mouse keratin (MK) 5, and MK14 participated in the formation of characteristic ring-shaped aggregates during the differentiation of the PAM212 keratinocyte cell line. We suggested that Hsp25 was involved in the disorganization of the MK5-MK14 keratin network before the establishment of the MK1-MK10 keratin network at the beginning of epidermis stratification. In this study, we have investigated the distribution of Hsp25 and keratins throughout skin development. We demonstrate that the distribution of Hsp25 and MK5 in the epidermis at the beginning of stratification and before keratinization is similar to that observed in PAM212 keratinocytes. These results indicate that there is a strong correlation between the mechanism we described ex vivo and the events taking place in vivo. Moreover, we show that Hsp25 is produced in different cell types in the epidermis and in the hair follicle at different stages of their development. Thus, our results suggest that Hsp25 is involved in more than one process during skin development.

Insights into function and regulation of small heat shock protein 25 (HSPB1) in a mouse model with targeted gene disruption

“…In the spinal cord, clearer hspb1 expression in neuronal cells was observed (data not shown). It is important to note that the expression pattern of the hspb1 reporter in the different tissues described here is consistent with several reports in the literature where HSPB1 expression in mammalian tissues was studied (Abdelwahid et al, 2001;Chen and Brown, 2007;Duverger and Morange, 2005;Wakayama and Iseki, 1998). However, our finding of restricted hspb1 expression in the brain contrasts somewhat with published data that demonstrate abundant HSPB1 expression in the central nervous system of an unstressed embryo, as visualized by immunohistochemistry (Loones et al, 2000).…”

Systematic evaluations of skin damage irradiated by an erbium:YAG laser: Histopathologic analysis, proteomic profiles, and cellular response

“…During the differentiation of keratinocytes, HSP25 participates in the formation of large aggregated structures and seems to be involved in the reorganization of the keratin network. The concentration of HSP25 increases as the distance of keratinocytes from the basal layer increases, in parallel with the extent of keratinization [38]. Both the low and high fluences of the laser resulted in obviously decreased levels of HSP25 protein, indicating the disruption of skin cells within 24 h. Afterwards, HSP25 expression increased in the group treated with 7.5 J/cm 2 at 96 h, whereas HSP25 had markedly decreased in intensity in the group treated with 15 J/cm 2 , resulting from the severe damage to skin cells.…”

Importance of transient receptor potential vanilloid 4 (TRPV4) in epidermal barrier function in human skin keratinocytes

“…Temperature-dependent skin barrier formation could be regulated by TRPV4-or TRPV3-independent factors such as epidermal growth factors and the small heat shock protein family, or other thermosensors such as TRPM8 [10,12,15,31]. Moreover, intracellular Ca 2+ increase, which is a crucial event initiating keratinocyte differentiation, is also induced by other Ca 2+ -permeable channels and Ca 2+ -sensitive receptors [3,13,37].…”