previously observed in the Y11C mutant of ribosomal protein L10 (homolog of E. coli L16) located at the base of the aa-tRNA accommodation corridor, and in the É2922C (E. coli U2554) 25S rRNA mutant located in the peptidyltransferase center (50, 51) . The observation that mutations located in three very different and topologically distinct regions of the large subunit conferred similar structural effects suggest that this kissing loop interaction plays an important role in ribosome function. Its location on the cytoplasmic face of the ribosome where deacylated tRNA leaves the molecule implies that the interaction between the terminal loops of Helices 88 and 22 may be involved in gating this deacylated tRNA exit corridor open and closed. This is consistent with the model of allosteric coordination between the A-and E-sites (52, 53) , which would indicate that the defects conferred by all of these mutants on aa-tRNA binding might impair this E-site gating function. The decreased lability of C2531 and G2534 in ES31 is similarly intriguing, raising more questions than answers. No function is currently associated with this expansion segment, but recent cryo-EM analysis shows it to be located on a solvent accessible surface of the large subunit (4) . Perhaps this site is also involved in A-site/ E-site coordination. Alternatively, it may be a site for recognition of defective ribosomes by the nonfunctional ribosome decay apparatus. Involvement of microRNAs in physiological and pathological processes in the lung To date, at least 900 different microRNA (miRNA) genes have been discovered in the human genome. These short, single-stranded RNA molecules originate from larger precursor molecules that fold to produce hairpin structures, which are subsequently processed by ribonucleases Drosha/Pasha and Dicer to form mature miRNAs. MiRNAs play role in the posttranscriptional regulation of about one third of human genes, mainly via degradation of target mRNAs. Whereas the target mRNAs are often involved in the regulation of diverse physiological processes ranging from developmental timing to apoptosis, miRNAs have a strong potential to regulate fundamental biological processes also in the lung compartment. However, the knowledge of the role of miRNAs in physiological and pathological conditions in the lung is still limited. This review, therefore, summarizes current knowledge of the mechanism, function of miRNAs and their contribution to lung development and homeostasis. Besides the involvement of miRNAs in pulmonary physiological conditions, there is evidence that abnormal miRNA expression may lead to pathological processes and development of various pulmonary diseases. Next, the review describes current state-of-art on the miRNA expression profiles in smoking-related diseases including lung cancerogenesis, in immune system mediated pulmonary diseases and fibrotic processes in the lung. From the current research it is evident that miRNAs may play role in the posttranscriptional regulation of key genes in human pulmonary diseases. Further studies are, therefore, necessary to explore miRNA expression profiles and their association with target mRNAs in human pulmonary diseases. A. miRNA definition, biology and function Discovery of microRNA (miRNA) lin-4 was the first short non-coding RNA discovered in 1993 as a regulator of developmental timing in Caenorhabditis elegans [1] . The first non-coding RNA identified in humans was let-7, which has been found involved in the control of developmental timing in humans and animals [2, 3] . Soon it became evident that these short non-coding RNAs are a part of much larger class of non-coding RNAs and the term microRNA (miRNA) was introduced [4] . To date, more than 900 miRNAs in Homo sapiens have been identified (940 in miRBase v15).