PubMed · 14380474
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K H AUER. 1955. Bronchitis Circumscripta Non Specifica.. https://pubmed.ncbi.nlm.nih.gov/14380474/
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Post-transcriptional regulation represents a major mechanism by which eukaryotic gene expression is regulated through cis-trans interactions that serve as signals for rapid alterations of messenger RNA (mRNA) stability. Regulation of urokinase-type plasminogen activator receptor (uPAR) mRNA involves the interaction of a uPAR mRNA coding region sequence with a 50 kD uPAR mRNA binding protein. We purified this protein from human bronchial epithelial (Beas2B) cells and identified it as phosphoglycerate kinase (PGK). We cloned PGK cDNA by polymerase chain reaction and expressed the recombinant PGK protein, which specifically bound the uPAR mRNA coding region by gel mobility shift and Northwestern blotting. We also confirmed a direct interaction of PGK protein with uPAR mRNA by immunoprecipitation. Overexpression of PGK in uPAR-overproducing H157 lung carcinoma cells resulted in decreased cytoplasmic uPAR mRNA and cell surface uPAR protein expression. Reduced uPAR mRNA expression involved decreased stability of the uPAR mRNA. Decline in 3H-thymidine incorporation and migration occurred in H157 cells transfected with PGK cDNA. These results demonstrate that PGK regulates uPAR expression at the post-transcriptional level.
1. In the human airway epithelium, VIP/PACAP receptors are distributed in nerve fibers and in epithelial cells but their role in transepithelial ion transport have not been reported. Here, we show that human bronchial epithelial Calu-3 cells expressed the VPAC(1) receptor subtype which shares similar high affinity for VIP and PACAP-27. 2. The stoichiometric binding parameters characterizing the (125)I-VIP and (125)I-PACAP-27 binding to these receptors were determined. 3. We found that VIP (EC(50) approximately 7.6 nM) and PACAP-27 (EC(50) approximately 10 nM) stimulated glibenclamide-sensitive and DIDS-insensitive iodide efflux in Calu-3 cells. 4. The protein kinase A (PKA) inhibitor, H-89 and the protein kinase C (PKC) inhibitor, chelerythrine chloride prevented activation by both peptides demonstrating that PKA and PKC are part of the signaling pathway. This profile corresponds to the pharmacological signature of CFTR. 5. In the cystic fibrosis airway epithelial IB3-1 cell lacking functional CFTR but expressing VPAC(1) receptors, neither VIP, PACAP-27 nor forskolin stimulated chloride transport. 6. Ussing chamber experiments demonstrated stimulation of CFTR-dependent short-circuit currents by VIP or PACAP-27 applied to the basolateral but not to the apical side of Calu-3 cells monolayers. 7. This study shows the stimulation in human bronchial epithelial cells of CFTR-dependent chloride secretion following activation by VIP and PACAP-27 of basolateral VPAC(1) receptors.
The Reid index is an instrument for the evaluation of chronic bronchitis. The thickness of the mucosa and of its gland layer are measured and the relationship is expressed as a gland/wall ratio. Specimens were obtained from 124 autopsies from the German National Study on SIDS (GeSID). The cases were divided into three groups: group 1 typical SIDS ( n=47), group 2 SIDS with signs of mild inflammation of the respiratory tract ( n=50) and group 3 unnatural death controls ( n=23). The Reid index was measured in sections from the trachea, bifurcation/main bronchi and bronchioli (staining HE and PAS). The Reid index was remarkably constant throughout the different levels of the respiratory tract (standard deviation range 0.06-0.10). A comparison of the three groups did not show statistically significant differences. Group 1: mean Reid index trachea 0.37, bifurcation/main bronchi 0.38, bronchioli 0.39. Group 2: mean Reid index trachea 0.40, bifurcation/main bronchi 0.38, bronchioli 0.38. Group 3: mean Reid index trachea 0.39, bifurcation/main bronchi 0.38, bronchioli 0.41. It can be concluded that the dimensions of bronchial glands do not vary in cases of SIDS as compared to controls. This demonstrates that the Reid index has no significance in the vast majority of SIDS cases and that acute inflammation commonly does not produce an elevated Reid index. In addition, the Reid index was confirmed to be a valid instrument to study the respiratory tract including the trachea due to its stability and it was found that the Reid index is age-dependent: compared to adults, the ratios in infants were higher.