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Synergistic mucus secretion by histamine and IL-4 through TMEM16A in airway epithelium
Kang, Ju Wan,Lee, Yong Hyuk,Kang, Min Jeong,Lee, Hyun Jae,Oh, Ryung,Min, Hyun Jin,Namkung, Wan,Choi, Jae Young,Lee, Sang Nam,Kim, Chang-Hoon,Yoon, Joo-Heon,Cho, Hyung-Ju American Physiological Society 2017 American journal of physiology. Lung cellular and Vol.313 No.3
<P>Histamine is an important mediator of allergic reactions, and mucus hypersecretion is a major allergic symptom. However, the direct effect of histamine on mucus secretion from airway mucosal epithelia has not been clearly demonstrated. TMEM16A is a Ca2+ -activated chloride channel, and it is closely related to fluid secretion in airway mucosal epithelia. We investigated whether histamine directly induces fluid secretion from epithelial cells or submucosal glands (SMG) and mechanisms related, therewith, in allergic airway diseases. In pig airway tissues from the nose or trachea, histamine was a potent secretagogue that directly induced strong responses. However, gland secretion from human nasal tissue was not induced by histamine, even in allergic rhinitis patients. Histamine type 1 receptor (H1R) and histamine type 2 receptor (H2R) were not noted in SMG by in situ hybridization. Cultured primary human nasal epithelial (NHE) cells were used for the measurement of short-circuit current changes with the Ussing chamber. Histamine-induced slight responses of anion secretions under normal conditions. The response was enhanced by IL-4 stimulation through TMEM16A, which might be related to fluid hypersecretion in allergic rhinitis. Pretreatment with IL-4 augmented the histamine response that was suppressed by a TMEM16A inhibitor. TMEM16A expression was enhanced by 24-h treatment of IL-4 in human nasal epithelial cells. The expression of TMEM16A was significantly elevated in an allergic rhinitis group, compared with a control group. We elucidated histamine-induced fluid secretions in synergy with IL-4 through TMEM16A in the human airway epithelium. In addition, we observed species differences between pigs and humans in terms of gland secretion of histamine.</P>
Kim, Juno,Namkung, Wan,Yoon, Jae Seok,Jo, Min Jae,Lee, Sung Hee,Kim, Kyung Hwan,Kim, Joo Young,Lee, Min Goo United States and Canadian Academy of Pathology [e 2009 Laboratory investigation Vol.89 No.8
<P>The formation of a pH gradient, which is characterized by intracellular alkalinization and extracellular acidification, plays a key role in the growth and metastasis of tumor cells. However, the underlying mechanisms of alkalinization-induced cell growth are not known. In this study, we investigated the roles of eukaryotic translation elongation factor 1 alpha (eEF1A) in alkalinization-induced cell growth. In all cell lines tested (NIH3T3, HEK293, and HeLa), cell growth was affected by the modulation of intracellular pH. In general, weak intracellular alkalinization produced increased cell growth, whereas intracellular acidification resulted in decreased cell growth. It is interesting to note that portions of actin-bound eEF1A proteins were gradually reduced from acidic to alkaline conditions, suggesting an increase in levels of functionally active, free-form eEF1A. Over-expression of eEF1A caused increased cell growth in HeLa cells. It should be noted that dissociation of eEF1A from actin by transfection with the actin-binding domain deleted eEF1A construct further increased cell growth under acidic conditions, whereas most of the intact eEF1A was bound to actin. Conversely, knockdown of eEF1A by treatment with eEF1A1 and eEF1A2 siRNAs nullified the effects of alkalinization-induced cell growth. The above findings suggest that an increase in free-form eEF1A under alkaline conditions plays a critical role in alkalinization-induced cell growth.</P>
길이方向의 鉛直휜을 附着한 鉛直圓筒으로 부터의 自然對流 熱傳達
崔仁圭,南宮圭完 연세대학교 산업기술연구소 1974 논문집 Vol.5 No.1
This paper presents the results of an experimental investigation on the free convective heat transfer from a vertical cylinder with longitudinal rectangular fin arrays. With 16 combinations of spacing and heights of fins attached on cylinders of various diameters (0.025m. 0.035m, 0.05m) and lengths (0.06m, 0.12m, 0.23m), 88 cases were investigated. Their features were found pretty different from those of a simple vertical plate or the fin arrays on a vertical plate. The effect of fin spacing S/D is not so dominant as expected. The effect of H/D is a little larger than that of S/D. The experimental work was focused to find the coefficients and exponents of correlation equation. Utilizing the governing groupings, the experimental equation was derived as equations (10) and (11) within the error of ±7%.
Choi, Ye Rin,Lee, Bom,Park, Jinhong,Namkung, Wan,Jeong, Kyu-Sung American Chemical Society 2016 JOURNAL OF THE AMERICAN CHEMICAL SOCIETY - Vol.138 No.47
<P>Adopting the concept of procarrier for the first time, we demonstrated the controlled transport of chloride ions across lipid and cellular membranes. Procarriers containing highly hydrophilic appendages were initially inactive due to the lack of their partitioning into lipophilic membranes but were activated to transport chloride ions in the presence of specific enzymes that were able to hydrolyze off the appendages to generate an active carrier under specific conditions. Namely, the procarrier with an ester-bond-linked appendage was most activated by an esterase (PLE) at pH = 7.4, whereas the procarrier with a glycosyl-bond-linked appendage was activated only by a glycosylase (AOG) under slightly acidic conditions (pH = 5.5-6). In addition to controlling chloride transport, hydrophilic appendages greatly increase the water solubility of the procarrier, which may improve the deliverability of a hydrophobic active carrier into a plasma membrane.</P>
Lee, Hyun Jae,Yoo, Jee Eun,Namkung, Wan,Cho, Hyung-Ju,Kim, Kyubo,Kang, Joo Wan,Yoon, Joo-Heon,Choi, Jae Young John WileySons, Ltd 2015 Physiological reports Vol.3 No.8
<P>Pendrin is an anion exchanger whose mutations are known to cause hearing loss. However, recent data support the linkage between pendrin expression and airway diseases, such as asthma. To evaluate the role of pendrin in the regulation of the airway surface liquid (ASL) volume and mucin expression, we investigated the function and expression of pendrin and ion channels and anion exchangers. Human nasal epithelial cells were cultured from 16 deaf patients carrying pendrin mutations (DFNB4) and 17 controls. The cells were treated with IL-13 to induce mucus hypersecretion. Airway surface liquid thickness was measured and real-time polymerase chain reaction was performed targeting various transporters and <I>MUC5AC</I>. Anion exchanger activity was measured using a pH-sensitive fluorescent probe. Periodic acid-Schiff staining was performed on the cultured cells and inferior turbinate tissues. The ASL layer of the nasal epithelia from DFNB4 subjects was thicker than the controls, and the difference became more prominent following IL-13 stimulation. There was no difference in anion exchange activity after IL-13 treatment in the cells from DFNB4 patients, while it increased in the controls. Goblet cell metaplasia induced by IL-13 treatment seen in the controls was not observed in the DFNB4 cells. Furthermore, the periodic acid-Schiff staining-positive area was lesser in the inferior turbinate tissues from DFNB4 patients that those from controls. Pendrin plays a critical role in ASL volume regulation and mucin expression as pendrin-deficient airway epithelial cells are refractory to stimulation with IL-13. Specific blockers targeting pendrin in the airways may therefore have therapeutic potential in the treatment of allergic airway diseases.</P>
Novel pendrin inhibitor attenuates lipopolysaccharide-induced acute lung injury in mice
( Eun Hye Lee ),( Jae Young Choi ),( Mi Hwa Shin ),( Wan Namkung ),( Ji Soo Choi ),( Su Hwan Lee ),( Ah Young Leem ),( Sang Hoon Lee ),( Kyung Soo Chung ),( Song Yee Kim ),( Ji Ye Jung ),( Young Ae Ka 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.0
Background: Pendrin is encoded by SLC26A4 and its mutation leads to congenital hearing loss. Additionally, pendrin is up-regulated in inflammatory airway diseases such as chronic obstructive pulmonary disease, allergic rhinitis, and asthma. In this study, the effects of a novel pendrin inhibitor, YS-01, were investigated in an LPS-induced acute lung injury (ALI) mice model, and the mechanism underlying the effect of YS-01 was examined. Methods: LPS (10 mg/kg) was intranasally instilled in wild type (WT) and pendrin-null mice. Lung injury parameters were assessed in the lung tissue and bronchoalveolar lavage fluid (BALF). Pendrin levels in the BALF of 41 pneumonia/ARDS patients and 25 control (solitary pulmonary nodule) patients were also measured. Results: LPS instillation induced lung injury in WT mice but not in pendrin-null mice. YS-01 treatment dramatically attenuated lung injury and reduced BALF cell counts and protein concentration after LPS instillation in WT mice. Proinflammatory cytokines and NF-κB activation were suppressed by YS-01 treatment in LPS-induced ALI mice. However, the protective effects of pendrin inhibitor lost after SCN- instillation. Furthermore, pendrin expression was upregulated in pneumonia/ARDS patient compared to that in control patient BALF (mean, 24.86 vs. 6.83 ng/mL, p < 0.001). Conclusions: A novel Pendrin inhibitor, YS-01, suppressed lung injury in LPS-induced ALI mice and our data provide a new strategy for the treatment of inflammatory airway diseases including sepsis-induced ALI.