Contribution of melanogenic proteins to the heterogeneous pigmentation of human melanocytes

1993 ◽  
Vol 106 (4) ◽  
pp. 1323-1331 ◽  
Author(s):  
Z. Abdel-Malek ◽  
V. Swope ◽  
C. Collins ◽  
R. Boissy ◽  
H. Zhao ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Tyrosinase Activity ◽  
Melanin Content ◽  
Necrosis Factor Alpha ◽  
Dopachrome Tautomerase ◽  
Human Melanocytes ◽  
Factor Alpha ◽  
Tyrosinase Enzyme ◽  
Necrosis Factor ◽  
Tyrosinase Related Protein

Human melanocytes from individuals with different skin types, as well as from the skin of the same individual, are heterogeneous in their melanin content. This heterogeneity may be attributed to differences in the activity and expression of the three melanogenic proteins: tyrosinase and tyrosinase-related proteins 1 and 2 (gp75 and DOPAchrome tautomerase, respectively), which in turn are affected by certain regulatory factors. Established melanocyte strains that exhibited intrinsic melanogenic heterogeneity could be separated into subpopulations according to density and melanin content by Percoll density gradient centrifugation. The least melanotic subpopulation consisted of melanocytes that contained an active tyrosinase enzyme and a low amount of melanin. Tyrosinase activity and the quantities of tyrosinase enzyme, tyrosinase-related protein-1 and DOPAchrome tautomerase gradually increased with increased melanin content and Percoll density of the isolated melanocyte subpopulations. We have found a direct correlation between melanin content, tyrosinase activity and the expression of the three melanogenic proteins in melanocyte strains established from different skin types. Addition of the two epidermal cytokines, tumor necrosis factor-alpha or interleukin-1 alpha, to cultures of human melanocytes from different skin types caused decreased proliferation, tyrosinase activity and expression of tyrosinase, tyrosinase-related protein-1 and DOPAchrome tautomerase. Similar results were obtained when Percoll-derived melanocyte subpopulations were treated with tumor necrosis factor-alpha and interleukin-1 alpha. These results indicate that the variation in melanin content in human melanocytes is due to differences in the activity and expression of the melanogenic proteins, which are influenced by autocrine and paracrine factors.

Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 1026-1031 ◽  
Author(s):  
K. Yamada ◽  
N. Takane ◽  
S. Otabe ◽  
C. Inada ◽  
M. Inoue ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Beta Cell ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Differential effects of cytokines on thermosensitive neurons in guinea pig preoptic area slices

1991 ◽  
Vol 261 (5) ◽  
pp. R1096-R1103 ◽  
Author(s):  
M. Shibata ◽  
C. M. Blatteis
Keyword(s):  
Guinea Pig ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor Alpha ◽  
Firing Rates ◽  
Artificial Cerebrospinal Fluid ◽  
Cold Sensitive ◽  
Factor Alpha ◽  
Necrosis Factor

This study was undertaken to determine whether the reported different courses of the febrile responses to the cytokines interleukin-1 beta (IL-1), interferon-alpha 2 (IFN), and tumor necrosis factor-alpha (TNF) might have neuroelectrophysiological correlates. The reactions of individual thermosensitive neurons in the preoptic area (POA) were evaluated by recording their extracellular single-unit firing rates (FR) in slices of guinea pig POA perfused with artificial cerebrospinal fluid (aCSF), human recombinant IL-1 (50-500 ng), IFN (1,000-8,000 U), and TNF (400-5,000 ng) (all doses per min/ml aCSF); thermosensitivity was assessed by FR responses to changes of perfusate temperature (32-42 degrees C). Overall, these cytokines depressed the FR of warm-sensitive units and excited those of cold-sensitive units, in agreement with expectations. However, the responses of individual neurons treated with two or all three cytokines were dissimilar: 61% of the units tested reacted differentially to two or three cytokines, 32% exhibited identical responses, and 7% had no response to any cytokine. These results support the possibility that IL-1, IFN, and TNF may affect not the same but rather distinct neurons functionally connected to common pyrogenic effectors. Thus they suggest that differential neuronal substrates may be utilized by each cytokine to exert its pyrogenic effect.

scholarly journals Inflammatory cytokines induce synthesis and secretion of gro protein and a neutrophil chemotactic factor but not β2-microglobulin in human synovial cells and fibroblasts

1989 ◽  
Vol 259 (2) ◽  
pp. 585-588 ◽  
Author(s):  
E E Golds ◽  
P Mason ◽  
P Nyirkos
Keyword(s):  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Chemotactic Factor ◽  
Synovial Cells ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Neutrophil Chemotactic Factor ◽  
Factor Alpha ◽  
Beta 2 Microglobulin ◽  
Necrosis Factor

Exposure of human synovial cells and fibroblasts in monolayer culture to interleukin 1 results in prominent secretion of proteins with Mr values of 6000 and 7000. By N-terminal sequence analysis, the Mr-6000 protein is identified as the protein encoded by a recently described gro mRNA. The Mr-7000 protein is identical to a neutrophil chemotactic factor released from monocytes. Stimulation of normal human fibroblasts with tumour necrosis factor alpha also results in expression and secretion of these two proteins. In addition to these cytokine-induced proteins, we have identified beta 2-microglobulin as an Mr-8000 protein constitutively secreted by synovial cells.

The Role of Nuclear Factor-kappaB and Melanogenesis in Tumor Necrosis Factor-Alpha-Induced Apoptosis of Normal Human Melanocytes

2002 ◽  
Vol 15 (5) ◽  
pp. 321-329 ◽  
Author(s):  
Jing Shang ◽  
Jürgen Eberle ◽  
Christoph C. Geilen ◽  
Amir M. Hossini ◽  
Lothar F. Fecker ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Nuclear Factor Kappab ◽  
Nuclear Factor ◽  
Necrosis Factor Alpha ◽  
Human Melanocytes ◽  
Normal Human ◽  
Factor Alpha ◽  
Induced Apoptosis ◽  
Necrosis Factor

NF-IL6 and AP-1 cooperatively modulate the activation of the TSG-6 gene by tumor necrosis factor alpha and interleukin-1

1994 ◽  
Vol 14 (10) ◽  
pp. 6561-6569
Author(s):  
L Klampfer ◽  
T H Lee ◽  
W Hsu ◽  
J Vilcek ◽  
S Chen-Kiang
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) activate transcription of the TSG-6 gene in normal human fibroblasts through a promoter region (-165 to -58) that encompasses an AP-1 and a NF-IL6 site. We show by deletion analysis and substitution mutagenesis that both sites are necessary for activation by TNF-alpha. Activation by IL-1 requires the NF-IL6 site and is enhanced by the AP-1 site. These results suggest that the NF-IL6 and AP-1 family transcription factors functionally cooperate to mediate TNF-alpha and IL-1 signals. Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the AP-1 site, and NF-IL6 activates the native TSG-6 promoter. Activation by NF-IL6 requires an intact NF-IL6 site and is modulated by the ratio of activator to inhibitor NF-IL6 isoforms that are translated from different in-frame AUGs. However, the inhibitor isoform can also bind to the AP-1 site and repress AP-1 site-mediated transcription. The finding that the inhibitor isoform antagonizes activation of the native TSG-6 promoter by IL-1 and TNF-alpha suggests that NF-IL6 has a physiologic role in these cytokine responses. Thus, the functionally distinct NF-IL6 isoforms cooperate with Fos and Jun to positively and negatively regulate the native TSG-6 promoter by TNF-alpha and IL-1.

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