Journal of epithelial biology & pharmacology最新文献_第2页

Targeting Hypoxia to Augment Mucosal Barrier Function. 以缺氧为目标增强粘膜屏障功能

Journal of epithelial biology & pharmacology Pub Date : 2012-01-01 Epub Date: 2012-01-16 DOI: 10.2174/1875044301205010067

Caleb J Kelly, Sean P Colgan

引用次数: 0

Role of chitotriosidase (chitinase 1) under normal and disease conditions. 几丁质酶1在正常和疾病条件下的作用。

Journal of epithelial biology & pharmacology Pub Date : 2012-01-01 DOI: 10.2174/1875044301205010001

Manasa Kanneganti, Alan Kamba, Emiko Mizoguchi

{"title":"Role of chitotriosidase (chitinase 1) under normal and disease conditions.","authors":"Manasa Kanneganti, Alan Kamba, Emiko Mizoguchi","doi":"10.2174/1875044301205010001","DOIUrl":"https://doi.org/10.2174/1875044301205010001","url":null,"abstract":"Mammalian chitinases belong to the glycosyl hydrolase 18 family based on structural homology and the family includes a large number of bacterial and eukaryotic chitinases. Among the mammalian chitinases, chitotriosidase (CHIT1) and acidic mammalian chitinase (AMCase) are capable of hydrolyzing the β-(1, 4)-linkage between the adjacent N-acetyl glucosamine residues of chitin. CHIT1 is one of the most abundantly secreted proteins, being mainly produced by activated macrophages and epithelial cells. CHIT1 plays a pivotal role in the context of infectious disease including malaria and fungi infections as a host defense towards chitin in pathogen's cell structure and as a diagnostic marker of disease. In contrast, CHI1 released by activated Kupffer cells in liver could induce hepatic fibrosis and cirrhosis. Increased serum levels of CHIT1 were observed in patients with many disorders, including Gaucher's disease, bronchial asthma, and atherosclerosis. Therefore, CHIT1 seems to have dual (regulatory and pathogenic) roles depending on the disease and producing cell types during the inflammatory conditions.","PeriodicalId":88010,"journal":{"name":"Journal of epithelial biology & pharmacology","volume":"5 ","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579558/pdf/nihms-442678.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31356880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 110

Role of Glutamine in Protection of Intestinal Epithelial Tight Junctions. 谷氨酰胺在肠上皮紧密连接保护中的作用。

Journal of epithelial biology & pharmacology Pub Date : 2012-01-01 DOI: 10.2174/1875044301205010047

RadhaKrishna Rao, Geetha Samak

引用次数: 101

Famotidine and Omeprazole Both Induce Gastric Transmucosal Leak 法莫替丁和奥美拉唑均可诱发胃粘膜漏

Journal of epithelial biology & pharmacology Pub Date : 2011-09-23 DOI: 10.2174/1875044301104010007

David S. Rudolph, M. Valenzano, B. Ngo, K. Kearney, Giancarlo Mercogli, J. M. Mullin

{"title":"Famotidine and Omeprazole Both Induce Gastric Transmucosal Leak","authors":"David S. Rudolph, M. Valenzano, B. Ngo, K. Kearney, Giancarlo Mercogli, J. M. Mullin","doi":"10.2174/1875044301104010007","DOIUrl":"https://doi.org/10.2174/1875044301104010007","url":null,"abstract":"Background: Our group has recently published that proton pump inhibitors (PPIs) induce transmucosal, paracellular, bidirectional leakage in the gastric corpus epithelium to a wide range of molecules. Aim: This study was undertaken to determine if H-2 blocker medications also induce such leakage, or whether it is a result of specific inhibition of H + ,K + -ATPase. Methods: At the beginning and end of a dosage regimen of omeprazole or famotidine, healthy volunteers with no history of gastrointestinal disease consumed a (probe) solution of 100 gms of sucrose in 200 cc of water. Subsequently an 8 hr urine specimen was collected. The sucrose concentration in the urine specimen (mg/ml) multiplied by the total urine vol- ume equaled the amount of sucrose (mg) which leaked from the gastric lumen into the bloodstream. Results: Like omeprazole, famotidine was also able to induce significant transmucosal leakage across the mucosal barrier of the upper gastrointestinal tract. Famotidine-induced leakage exhibited a narrower time course than was observed with omeprazole. Conclusions: The fact that both classes of acid suppressive medications induce leak implies that leak results not from di- rect inhibition of the H + ,K + -ATPase, or from a side effect of omeprazole-like molecules, but is more generally related to the overall inhibition of acid secretion. The medical significance of such gastric leak is discussed.","PeriodicalId":88010,"journal":{"name":"Journal of epithelial biology & pharmacology","volume":"4 1","pages":"7-11"},"PeriodicalIF":0.0,"publicationDate":"2011-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68110051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aerosolized BIO-11006, a Novel MARCKS- Related Peptide, Improves Airway Obstruction in a Mouse Model of Mucus Hypersecretion 雾化BIO-11006，一种新的MARCKS相关肽，改善黏液高分泌小鼠模型的气道阻塞

Journal of epithelial biology & pharmacology Pub Date : 2011-04-11 DOI: 10.2174/1875044301104010001

A. Agrawal, Edward C. Murphy, Joungjoa Park, K. Adler, I. Parikh

{"title":"Aerosolized BIO-11006, a Novel MARCKS- Related Peptide, Improves Airway Obstruction in a Mouse Model of Mucus Hypersecretion","authors":"A. Agrawal, Edward C. Murphy, Joungjoa Park, K. Adler, I. Parikh","doi":"10.2174/1875044301104010001","DOIUrl":"https://doi.org/10.2174/1875044301104010001","url":null,"abstract":"Rationale: Mucus hypersecretion has been shown to be an important cause of airway obstruction in COPD and asthma, and has been associated with fatal asthma. Previous in-vitro and in-vivo studies have provided direct evidence that the myristoylated alanine-rich C kinase substrate (MARCKS) is a central regulatory molecule linking secretagogue stimu- lation at the goblet cell surface to mucin granule release. BIO-11006 is a novel, highly soluble, aerosolized peptide that inhibits MARCKS function and results in reduced mucus secretion and improved airway obstruction. BIO-11006 is being tested in Phase 2 clinical studies of COPD. Objective: To determine access of BIO-11006 to the intracellular compartment of normal human bronchial epithelial (NHBE) cells, and assess the effectiveness of BIO-11006 inhalation solution in inhibiting airway obstruction caused by mucus hypersecretion as a function of dose and time. Methods: Biotin labeled BIO-11006 was incubated with NHBE cells and visualized with fluorescein-labeled streptavidin. Ovalbumin-sensitized and challenged mice with airway inflammation and hyperresponsiveness to methacholine (MCh) were treated with aerosolized BIO-11006 solution prior to MCh challenge, and effects on airway obstruction and mucus secretion were measured. Results: A 30-minute aerosol exposure to a 10 mM BIO-11006 solution was maximally effective in inhibiting MCh- induced airway obstruction and mucus hypersecretion. There was a long-lasting effect on inhibition of airway obstruction after a single treatment with BIO-11006 (t 1/2 ~4 hrs). The duration of effect on inhibition of mucin secretion was shorter (t 1/2 ~2 hrs). Conclusion: The pharmacodynamic properties of aerosolized BIO-11006 Inhalation Solution are suitable for therapeutic use. Inhaled BIO-11006 effectively inhibits mucin secretion and improves airway obstruction.","PeriodicalId":88010,"journal":{"name":"Journal of epithelial biology & pharmacology","volume":"4 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2011-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68110042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

High-Level Expression of Golsyn/Syntabulin in Glandular Epithelium and its Role in the Secretory Process~!2010-01-02~!2010-06-13~!2010-08-16~! Golsyn/Syntabulin在腺上皮的高水平表达及其在分泌过程中的作用2010-01-02 2010-06-13 2010-08-16

Journal of epithelial biology & pharmacology Pub Date : 2010-09-03 DOI: 10.2174/1875044301003010049

Ryosuke Oda, E. Funakoshi, K. Ozaki, K. Ogita, N. Shimizu, Fumiaki Ito

引用次数: 0

Application of Probes in Live Cell Imaging~!2010-01-03~!2010-05-09~!2010-08-16~! 探针在活细胞成像中的应用2010-01-03 2010-05-09 2010-08-16

Journal of epithelial biology & pharmacology Pub Date : 2010-09-03 DOI: 10.2174/1875044301003010040

Hong Chen, C. Bai, Xiang-dong Wang

引用次数: 4

Role of Airway Epithelium-Origin Chemokines and their Receptors in COPD 气道上皮源性趋化因子及其受体在COPD中的作用

Journal of epithelial biology & pharmacology Pub Date : 2010-04-16 DOI: 10.2174/1875044301003010026

Hong Chen, D. Wang, Xiangdong Wang

{"title":"Role of Airway Epithelium-Origin Chemokines and their Receptors in COPD","authors":"Hong Chen, D. Wang, Xiangdong Wang","doi":"10.2174/1875044301003010026","DOIUrl":"https://doi.org/10.2174/1875044301003010026","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is characterized with the chronic airway inflammation associ- ated with progressive obstruction of airflow. Airway epithelial cells play an essential role of development in COPD. Chemokines as extracellular signaling proteins have been suggested to be involved in the inflammatory process of COPD. The present review summarized the variation of chemokines in the airway epithelium of COPD patients and discussed the potential roles of chemokines in the pathogenesis of COPD. Increased level of IL-8 was considered as a key and unique chemokine in the initiation and progress of COPD. Others like CXCR3 chemokines and eosinophils-related chemokines should be also considered. Further research will be necessary to explore whether targeting on these chemokines, particu- larly IL-8 and CXCRs, can be benefit to patients with COPD. It is also important to identify and validate a critical and specific chemokine with differential diagnostic value. The correlation of chemokines with disease severity, diagnosis and therapy in COPD should be further clarified. High-throughout technologies, e.g. genomics, proteomics and bioinformat- ics, can be more attractive approaches to validate the importance of chemokines in the disease. Although the exact role of chemokines in the pathogenesis of COPD still needs to be explored, anti-chemokines or receptor antagonists may be an al- terative of new therapies for patients with COPD. Keywards: COPD, epithelial cells, chemokines, BALF, sputum.","PeriodicalId":88010,"journal":{"name":"Journal of epithelial biology & pharmacology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2010-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68109972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Disruptive Effect of Epigallocatechin-3-Gallate on the Proliferation/Apoptosis Balance in the Olfactory Epithelium~!2009-11-15~!2010-02-05~!2010-03-05~! 没食子儿茶素-没食子酸酯对嗅上皮细胞增殖/凋亡平衡的破坏作用2009-11-15 2010-02-05 2010-03-05

Journal of epithelial biology & pharmacology Pub Date : 2010-03-08 DOI: 10.2174/1875044301003010020

L. Jungblut, D. Paz, A. Pozzi

{"title":"Disruptive Effect of Epigallocatechin-3-Gallate on the Proliferation/Apoptosis Balance in the Olfactory Epithelium~!2009-11-15~!2010-02-05~!2010-03-05~!","authors":"L. Jungblut, D. Paz, A. Pozzi","doi":"10.2174/1875044301003010020","DOIUrl":"https://doi.org/10.2174/1875044301003010020","url":null,"abstract":"The polyphenol epigallocatechin-3-gallate (EGCG), is the main active catechin of the green tea. It exerts a wide range of biochemical and pharmacological effects on different animal cells. EGCG acts as a scavenger of growth factors and it was demonstrated its antiproliferative and proapoptotic role in different cancer cells. Nevertheless, little is known about the effect of EGCG on normal cells. In the present work, we have studied the EGCG effect on the prolifera- tion/apoptosis balance in the olfactory epithelium of amphibian tadpoles. Animals treated with EGCG showed an increase in the number of apoptotic cells and a decrease in the basal proliferation. In addition, EGCG showed differential effect on the two classical growth factors signalling pathways, MAPK and PI3K route. EGCG treatment triggered a drop in phos- pho-ERK1/2 level without affecting the phospho-AKT level. These findings demonstrate the antiproliferative and proapoptotic effect of EGCG on normal olfactory cells and postulate the olfactory epithelium as a good experimental model for the study of the factors involved in neurogenesis process.","PeriodicalId":88010,"journal":{"name":"Journal of epithelial biology & pharmacology","volume":"229 1","pages":"20-25"},"PeriodicalIF":0.0,"publicationDate":"2010-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68109919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

The N-terminal 81-aa fragment is critical for UT-A1 urea transporter bioactivity. n端81-aa片段对UT-A1尿素转运蛋白的生物活性至关重要。

Journal of epithelial biology & pharmacology Pub Date : 2010-01-01 DOI: 10.2174/1875044301003010034

Haidong Huang, Yuan Yang, Douglas C Eaton, Jeff M Sands, Guangping Chen

{"title":"The N-terminal 81-aa fragment is critical for UT-A1 urea transporter bioactivity.","authors":"Haidong Huang, Yuan Yang, Douglas C Eaton, Jeff M Sands, Guangping Chen","doi":"10.2174/1875044301003010034","DOIUrl":"10.2174/1875044301003010034","url":null,"abstract":"The serine protease, furin, is involved in the activation of a number of proteins most notably epithelial sodium channels (ENaC). The urea transporter UT-A1, located in the kidney inner medullary collecting duct (IMCD), is important for urine concentrating ability. UT-A1's amino acid sequence has a consensus furin cleavage site (RSKR) in the N-terminal region. Despite the putative cleavage site, we find that UT-A1, either from the cytosolic or cell surface pool, is not cleaved by furin in CHO cells. This result was further confirmed by an inability of furin to cleave in vitro an (35)S-labeled UT-A1 or the 126 N-terminal UT-A1 fragment. Functionally, mutation of the furin site (R78A, R81A) does not affect UT-A1 urea transport activity. However, deletion of the 81-aa N-terminal portion does not affect UT-A1 cell surface trafficking, but seriously impair UT-A1 urea transport activity. Our results indicate that UT-A1 maturation and activation does not require furin-dependent cleavage. The N-terminal 81-aa fragment is required for proper UT-A1 urea transport activity, but its effect is not through changing UT-A1 membrane trafficking.","PeriodicalId":88010,"journal":{"name":"Journal of epithelial biology & pharmacology","volume":"3 ","pages":"34-39"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886301/pdf/nihms205808.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29064767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0