Abstract
Metallothionein (MT) has many functions that are modulated by several factors, including ultraviolet (UV) radiation and cytokines. We thought that these diverse functions of MT might reflect the specific regulatory mechanisms of its expression. To understand some of the molecular mechanisms underlying MT expression, we examined the effects of several cytokines and UVB on the promoter activity of the MT gene. First, we introduced the MT promoter construct into the HaCaT keratinocytes and treated them with various concentrations of interleukin-1α (IL-1α) and IL-6. The addition of IL-1α and IL-6 led to an increase in the promoter activity of the MT gene. UVB is known to induce MT expression in epidermal keratinocytes, and IL-6 is a possible mediator of MT induction by UV radiation. Therefore, we investigated whether UVB could induce MT promoter activity. Our results showed, interestingly, that UVB radiation has no or little effect on the promoter activity. This suggested a complex molecular regulation of the MT gene.
Highlights
Metallothionein (MT) is a ubiquitously distributed, cysteine-rich, low molecular weight protein having a high binding capacity for metals such as zinc, copper, and cadmium
To understand some of the molecular mechanisms underlying MT expression, we examined the effects of several cytokines and UVB on the promoter activity of the MT gene
We found that β-thujaplicin induced MT expression in keratinocytes, both in vitro and in vivo, and thereby reduced UVB irradiation-induced apoptosis [6]
Summary
Metallothionein (MT) is a ubiquitously distributed, cysteine-rich, low molecular weight protein having a high binding capacity for metals such as zinc, copper, and cadmium. It plays a role in zinc homeostasis and detoxification of heavy metals [1]. MT induction has protective effects against oxidative stresses such as anticancer drugs and ultraviolet (UV) radiation [3]. MT gene expression is induced by heavy metals and by various stress-inducing agents such as UV [4] and X-ray radiation [5]. We found that β-thujaplicin induced MT expression in keratinocytes, both in vitro and in vivo, and thereby reduced UVB irradiation-induced apoptosis [6]. A number of cytokines, including interferon-α and β, tumor necrosis factor-α, interleukin-1 (IL-1), and IL-6, increase MT expression, suggesting that MT expression involves additional functions, including immunomodulation, cell growth, and cell differentiation [7]
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