PubMed · 3207454
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R Lewin. 1988-12-09. Caution continues over transplants.. https://doi.org/10.1126/science.3207454
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The expression of transcripts for type 1 interleukin-1 receptors (IL-1R1) were investigated utilizing reverse transcription-polymerase chain reaction (RT-PCR) techniques in male C57BL/6 mice. First, we measured IL-1R1 mRNA 1, 2, 6, and 12 h after a single injection of endotoxin lipopolysaccharide (LPS; 30 microg/mouse). IL-1R1 mRNA was measured in relevant tissues utilizing semiquantitative RT-PCR. IL-1R1 mRNA levels were significantly increased 2 and 6 h after one LPS injection group in comparison with the saline injection group in the hippocampus and testis. Next, we investigated the effect of repeated injections of LPS on IL-1R1 expression. LPS or saline were injected at 24-h intervals for 4 consecutive days. The mice were divided into four groups: (1) LPS injections for 4 days and LPS injection on day 5 (LPS-LPS); (2) LPS injections for 4 days and saline injection on day 5 (LPS-saline); (3) saline injections for 4 days and LPS injection on day 5 (saline-LPS); (4) saline injections for 4 days and saline injection on day 5 (saline-saline). The mice were sacrificed by decapitation 2 h after the last injection. In the hippocampus and pituitary gland, significant increases of IL-1R1 mRNA levels were observed in the saline-LPS group, however, the increases were attenuated in LPS-LPS group. IL-1R1 mRNA levels in the hypothalamus were unchanged in all four groups. In the adrenal gland and testis, IL-1R1 mRNA levels were significantly increased in the LPS-LPS group as well as saline-LPS group. These data demonstrate differential regulation of IL-1R1 mRNA by one and repeated endotoxin treatment and suggest the importance of the cytokines in mediating the effects of infectious challenge on brain, endocrine and immune function during endotoxemia.
Agouti-related protein (AGRP) is a naturally occurring antagonist of melanocortin action. It is expressed mainly in the arcuate nucleus where it plays an important role in the hypothalamic control of feeding and energy homeostasis by antagonism of central melanocortin 4 receptors in mammals. Besides in the brain, the melanocortin 4 receptor is expressed in numerous peripheral tissues in the chicken. To examine whether or not the peripheral melanocortin 4 receptor signaling could be regulated by AGRP, we cloned and localized the expression of the AGRP gene in the chicken. The chicken AGRP gene was found to encode a 154 or 165 amino acid protein, depending on the usage of two alternative translation initiation sites. The coding sequence consisted of three exons, like that of mammalian species. The C-terminal cysteine-rich region of the predicted AGRP displayed high levels of identity to mammalian counterparts (78-84%) and all 10 cysteine residues conferring functional conformation of AGRP were conserved; however, other regions showed apparently no homology, suggesting that biological activities of AGRP are located in its C-terminal region. RT-PCR analysis detected the AGRP mRNA in all tissues examined: the brain, adrenal gland, heart, liver, spleen, gonads, kidney, uropygial gland, skeletal muscle and adipose tissues. Interestingly, the skin also expressed the AGRP mRNA, where Agouti, another melanocortin receptor antagonist regulating hair pigmentation, is expressed in rodents. Most of those AGRP-expressing tissues have been demonstrated to express melanocortin 4 receptors and/or other subtypes of melanocortin receptor whose mammalian counterparts can bind AGRP. These results imply the possibility that some peripheral melanocortin systems could be regulated by the functional interaction between melanocortins and AGRP at melanocortin receptors in the chicken.
Plasma levels of high density lipoprotein (HDL) cholesterol and its major protein component apolipoprotein (apo) A-I are significantly reduced in both acute and chronic inflammatory conditions, but the basis for this phenomenon is not well understood. We hypothesized that secretory phospholipase A(2) (sPLA(2)), an acute phase protein that has been found in association with HDL, promotes HDL catabolism. A series of HDL metabolic studies were performed in transgenic mice that specifically overexpress human sPLA(2) but have no evidence of local or systemic inflammation. We found that HDL isolated from these mice have a significantly lower phospholipid and cholesteryl ester and significantly greater triglyceride content. The fractional catabolic rate (FCR) of (125)I-HDL was significantly faster in sPLA(2) transgenic mice (4.08 +/- 0.01 pools/day) compared with control wild-type littermates (2.16 +/- 0.48 pools/day). (125)I-HDL isolated from sPLA(2) transgenic mice was catabolized significantly faster than (131)I-HDL isolated from wild-type mice after injection in wild-type mice (p < 0.001). Injection of (125)I-tyramine-cellobiose-HDL demonstrated significantly greater degradation of HDL apolipoproteins in the kidneys of sPLA(2) transgenic mice compared with control mice (p < 0.05). The fractional catabolic rate of [(3)H]cholesteryl ether HDL was significantly faster in sPLA(2)-overexpressing mice (6.48 +/- 0.24 pools/day) compared with controls (4.80 +/- 0.72 pools/day). Uptake of [(3)H] cholesteryl ether into the livers and adrenals of sPLA(2) transgenic mice was significantly enhanced compared with control mice. In summary, these data demonstrate that overexpression of sPLA(2) alone in the absence of inflammation causes profound alterations of HDL metabolism in vivo and are consistent with the hypothesis that sPLA(2) may promote HDL catabolism in acute and chronic inflammatory conditions.