Tissue-specific expression of the gene coding for human Clara cell 10-kD protein, a phospholipase A2-inhibitory protein.

Peri, Alessandro; Cordella‐Miele, Eleonora; Miele, Lucio; Mukherjee, Anil B.

doi:10.1172/jci116810

Cited by 119 publications

(95 citation statements)

References 46 publications

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“…However, that study only looked at short-term effects. Work in humans is consistent with our observations that CCSP is downregulated in asthma and in areas of mucus metaplasia (2,24,32,46,47). It is interesting that, although IL-13 downregulates CCSP, interferon gamma is known to upregulate CCSP (39).…”

Section: Discussionsupporting

confidence: 89%

Differential expression of chitinases identify subsets of murine airway epithelial cells in allergic inflammation

Homer¹,

Zhu²,

Cohn³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Section: Discussionsupporting

confidence: 89%

Differential expression of chitinases identify subsets of murine airway epithelial cells in allergic inflammation

Homer¹,

Zhu²,

Cohn³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The detection of RT-PCR products was performed as described previously (21). Briefly, cDNAs were subjected to agarose gel electrophoresis and subsequent Southern blot on nylon membranes (Roche Diagnostics).…”

Section: Detection Of Rt-pcr Productsmentioning

confidence: 99%

Expression of cAMP-responsive element binding protein and inducible cAMP early repressor in hyperfunctioning thyroid adenomas

Peri

Luciani

Tonacchera

et al. 2002

European Journal of Endocrinology

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Objective: The pathogenesis of thyroid hyperfunctioning adenomas is still only partially understood and controversy exists about the frequency of gain-of-function mutations of the TSH receptor or G s a gene, which activate the cAMP pathway. The nuclear transcription factors cAMP-responsive element binding protein (CREB) and inducible cAMP early repressor (ICER) are among the final targets of this signalling cascade. Design: In our study we focused on the expression of CREB and ICER genes in the nodular as well as in the extranodular tissue of hyperfunctioning tumours of the thyroid. Methods: RT-PCR and Western blot analysis were performed in a series of 14 patients. The presence of an activating mutation of the TSH receptor or of the G s a gene was ascertained by direct sequencing. Results: The levels of CREB transcripts did not significantly differ in the adenomas and in the normal tissues (CREB/GAPDH, mean optical density^S.E.: 0:98^0:18 vs 0:88^0:27 respectively, P = not significant (N.S.)), although case-to-case variability was observed. The absence of a significant difference between the adenoma and the surrounding normal tissue was maintained after dividing the patients into two groups, according to TSH receptor status. Accordingly, no significant difference in the levels of CREB protein (total and Ser 133 -phosphorylated) was observed between the nodular and the extranodular tissue. In addition, no difference was found in the levels of ICER transcripts (ICER/GAPDH, mean optical density^S.E.: 0:52^0:11; nodule vs 0:36^0:11; normal thyroid, P ¼ N:S:), independently of the TSH receptor gene status (i.e. wild-type or mutated). Conclusions: Our results support the recent hypothesis that the activation of the cAMP pathway in hyperfunctioning adenomas of the thyroid might be counteracted by opposite events and suggest that complex molecular mechanisms might take part in the pathogenesis of hyperfunctioning tumours.

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“…We also demonstrated that UG-knock-out (UG-KO) mice (16) are highly susceptible to lung tumorigenesis by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, a carcinogen in cigarette smoke (20). Previously, we reported that the UG gene is constitutively expressed at a high level in the lung epithelia (21). However, UG expression in both malignant lung tumors originating from lung epithelia as well as in the cell lines derived from these tumors is either drastically suppressed or totally undetectable (22,23).…”

mentioning

confidence: 92%

Lack of an Endogenous Anti-inflammatory Protein in Mice Enhances Colonization of B16F10 Melanoma Cells in the Lungs

Saha

Lee

Zhang

et al. 2010

Journal of Biological Chemistry

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Emerging evidence indicates a link between inflammation and cancer metastasis, but the molecular mechanism(s) remains unclear. Uteroglobin (UG), a potent anti-inflammatory protein, is constitutively expressed in the lungs of virtually all mammals. UG-knock-out (UG-KO) mice, which are susceptible to pulmonary inflammation, and B16F10 melanoma cells, which preferentially metastasize to the lungs, provide the components of a model system to determine how inflammation and metastasis are linked. We report here that B16F10 cells, injected into the tail vein of UG-KO mice, form markedly elevated numbers of tumor colonies in the lungs compared with their wild type littermates. Remarkably, UG-KO mouse lungs overexpress two calcium-binding proteins, S100A8 and S100A9, whereas B16F10 cells express the receptor for advanced glycation end products (RAGE), which is a known receptor for these proteins. Moreover, S100A8 and S100A9 are potent chemoattractants for RAGE-expressing B16F10 cells, and pretreatment of these cells with a blocking antibody to RAGE suppressed migration and invasion. Interestingly, in UG-KO mice S100A8/S100A9 concentrations in blood are lowest in tail vein and highest in the lungs, which most likely guide B16F10 cells to migrate to the lungs. Further, B16F10 cells treated with S100A8 or S100A9 overexpress matrix metalloproteinases, which are known to promote tumor invasion. Most notably, the metastasized B16F10 cells in UG-KO mouse lungs express MMP-2, MMP-9, and MMP-14 as well as furin, a pro-protein convertase that activates MMPs. Taken together, our results suggest that a lack of an anti-inflammatory protein leads to increased pulmonary colonization of melanoma cells and identify RAGE as a potential anti-metastatic drug target.It is estimated that more than 90% of human cancer deaths result from metastasis (1-8), a complex process in which the cells from a primary tumor successfully invade and colonize a distant organ (6 -9). It has long been suspected that a functional relationship exists between inflammation and cancer. Indeed, in 1863, Virchow observed that cancer develops at locations where chronic inflammation is present. This hypothesis is partly based on his assumption that some substances that cause tissue injury and inflammation also enhance cell proliferation (10). Although it is clear now that proliferation alone does not account for cancer, the cause and effect relationship between inflammation and cancer is widely accepted. Nonetheless, many aspects of the molecular and cellular mechanisms that link inflammation, migration, and establishment of tumor colonies in a distant organ remain unresolved (5). Recently, it has been reported that a tumor microenvironment actively contributes to cancer initiation, progression, and metastasis (11, 12). It has also been suggested that reductions in the rates of cancer morbidity and mortality may be achieved by gaining greater understanding of the molecular mechanism(s) of tumor cell migration, invasion, and establishment of colonies (13). In this regard...

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Tissue-specific expression of the gene coding for human Clara cell 10-kD protein, a phospholipase A2-inhibitory protein.

Cited by 119 publications

References 46 publications

Differential expression of chitinases identify subsets of murine airway epithelial cells in allergic inflammation

Differential expression of chitinases identify subsets of murine airway epithelial cells in allergic inflammation

Expression of cAMP-responsive element binding protein and inducible cAMP early repressor in hyperfunctioning thyroid adenomas

Lack of an Endogenous Anti-inflammatory Protein in Mice Enhances Colonization of B16F10 Melanoma Cells in the Lungs

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