PubMed · 14906122
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1951-12-31. [Renal function test].. https://pubmed.ncbi.nlm.nih.gov/14906122/
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Mortalin/mtHsp70 (mitochondrial Hsp70) and HSP60 (heat-shock protein 60) are heat-shock proteins that reside in multiple subcellular compartments, with mitochondria being the predominant one. In the present study, we demonstrate that the two proteins interact both in vivo and in vitro, and that the N-terminal region of mortalin is involved in these interactions. Suppression of HSP60 expression by shRNA (short hairpin RNA) plasmids caused the growth arrest of cancer cells similar to that obtained by suppression of mortalin expression by ribozymes. An overexpression of mortalin, but not of HSP60, extended the in vitro lifespan of normal fibroblasts (TIG-1). Taken together, this study for the first time delineates: (i) molecular interactions of HSP60 with mortalin; (ii) their co- and exclusive localizations in vivo; (iii) their involvement in tumorigenesis; and (iv) their functional distinction in pathways involved in senescence.
Interleukin-1 receptor antagonist (IL-1Ra) inhibits the classical biological effects of interleukin (IL)-1 by preventing its binding to IL-1 receptors. There are, however, four different isoforms of IL-1Ra, of which three are intracellular (icIL-1Ra1, 2, 3). Due to their localization, icIL-1Ras cannot interact with cell surface IL-1 receptors and have been suggested to carry out specific functions inside cells. The recent description of nuclear effects of the IL-1alpha precursor (preIL-1alpha) led to the hypothesis that icIL-1Ra variants might antagonize the intracellular actions of preIL-1alpha. The aim of this study was to investigate effects of preIL-1alpha and icIL-1Ra1 in stably transfected SaOS-2 cells. Expression of preIL-1alpha significantly decreased cell growth and this effect was not reversed by addition of exogenous IL-1Ra, suggesting an intracellular mode of action. Transfection of SaOS-2 cells with icIL-1Ra1 did not affect their growth. Furthermore, co-expression of icIL-1Ra1 did not reverse the growth inhibitory effect of preIL-1alpha. In contrast, the production of IL-6 induced by preIL-1alpha was decreased in icIL-1Ra1 co-transfected cells. In conclusion, expression of preIL-1alpha decreased the growth of SaOS-2 cells, likely by an intracellular mechanism. Co-expression of icIL-1Ra1 did not antagonize this effect, indicating that intracellular effects of preIL-1alpha are not necessarily susceptible to inhibition by icIL-1Ra1.
Despite binding to receptors distinct from those of type I interferons (IFNs), human interleukins-28A, -28B and -29 (IL-28A, IL-28B and IL-29; alternatively named IFN lambda-2 {IFN-lambda2}, IFN-lambda3 and IFN-lambda1, respectively, or collectively, type III IFNs), a small family of three structurally-related cytokines, are, like IFNs, known to induce antiviral activity. To further biologically characterize IL-28A and IL-29, we compared their activities with those of IFNs in a range of human cell lines. We found that they induced antiviral activity in fewer cell lines and more weakly than IFNs; also IL-28A was less active than IL-29. Additionally, we showed IL-28A and IL-29 induced reporter genes--protein MxA promoter linked to luciferase, or interferon stimulated response element (ISRE) linked to secreted alkaline phosphatase (SEAP)--more weakly than IFN. Antiproliferative activity was induced by IFNs in most cell lines, but only in one human glioblastoma cell line, LN319, was dose-dependent IL-29-growth inhibition demonstrable. Polymerase chain reaction (PCR) quantification of messenger (m) RNA of IL-28/29 receptor subunits, IL-28Ralpha and IL-10Rbeta, indicated variable expression levels; although their expression was highest in the responsive LN319 cell line, lower but significant expression of both mRNAs was found in relatively unresponsive cell lines. In conclusion, we found IL-28A and IL-29 act similarly to IFNs, but are less effective generally and have activity in a more limited range of cell lines.