UV irradiation-induced interleukin-1 and basic fibroblast growth factor synthesis and release mediate part of the UV response.

نویسندگان

  • M Krämer
  • C Sachsenmaier
  • P Herrlich
  • H J Rahmsdorf
چکیده

UV irradiated cells release into the culture medium factors that induce, when given to nonirradiated cells, the transcription of several UV-inducible genes (collagenase I, human immunodeficiency virus type 1, metallothionein IIA). We identify here the active factors released from UV-treated HeLa cells, as interleukin 1 alpha and basic fibroblast growth factor. UV irradiation leads to increased mRNA levels for both factors and to their enhanced synthesis. Experiments with the drug suramin, which inhibits growth factor-growth factor receptor interactions and with antibodies directed against interleukin 1 alpha and basic fibroblast growth factor, suggest that growth factors do not only transduce the UV-induced signal to nonirradiated cells but act on the producer cell thus establishing an obligatory growth factor loop for at least part of the UV response.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Effect of Low–Level Helium-Neon Laser Irradiation on the Release of Interleukin 6 and Basic Fibroblast Growth Factor from Cultured Human Fibroblasts in High Glucose Medium

Purpose: Low level laser therapy is suggested as a new therapeutic method in diabetic wound healing. This survey aimed to evaluate the effects of low level laser on human fibroblasts cultured in high glucose cultures. Materials and Methods: The human skin fibroblasts were cultured under standard condition. The cells were cultured in high glucose culture medium (15mM/L) for a week and two weeks ...

متن کامل

Prevention of the ultraviolet B-mediated skin photoaging by a nuclear factor kappaB inhibitor, parthenolide.

The skin photoaging is characterized by keratinocyte hyperproliferation and degradation of collagen fibers, causing skin wrinkling and laxity and melanocyte proliferation that leads to pigmentation. UV is considered to be a major cause of such skin changes. It is well established that nuclear factor kappaB (NF-kappaB) is activated upon UV irradiation and induces various genes including interleu...

متن کامل

Reactive oxygen species mediate TNF-α-induced inflammatory response in bone marrow mesenchymal cells

Objective(s): It is generally believed that the inflammatory response in bone marrow mesenchymal stem cells (BMSCs) transplantation leads to poor survival and unsatisfactory effects, and is mainly mediated by cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α). In this study, we explored the mechanisms underlying the TNF-α-induced inflammatory ...

متن کامل

The Epidermal Growth Factor Receptor Increases Cytokine Production and Cutaneous Inflammation in Response to Ultraviolet Irradiation

The epidermal growth factor receptor (EGFR) is activated in cutaneous keratinocytes upon ultraviolet (UV) exposure and has been implicated in ultraviolet-(UV-)induced inflammation and skin tumorigenesis. Egfr mutant mice and EGFR inhibitors were used to investigate the hypothesis that EGFR activation augments inflammation following UV irradiation. Topical treatment of mouse skin with the EGFR i...

متن کامل

Involvement of Fas receptor and not tumor necrosis factor-alpha receptor in ultraviolet-induced activation of acid sphingomyelinase.

Fas receptor and tumor necrosis factor receptor-1 (TNFR1) mediate the activation of acid sphingomyelinase (ASMase), which catalyzes the hydrolysis of sphingomyelin to ceramide. Ceramide acts as a second messenger in mediating cell growth, differentiation, stress response, and apoptosis. Ultraviolet (UV) irradiation induces Fas receptor and TNFR1 aggregation. However, the roles of Fas receptor a...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The Journal of biological chemistry

دوره 268 9  شماره 

صفحات  -

تاریخ انتشار 1993