Search

Your search keyword '"Yu, G.Y."' showing total 208 results
Start Over Author "Yu, G.Y."
208 results on '"Yu, G.Y."'

4. The detector system of the Daya Bay reactor neutrino experiment

Author

An, F.P., Bai, J.Z., Balantekin, A.B., Band, H.R., Beavis, D., Beriguete, W., Bishai, M., Blyth, S., Brown, R.L., Butorov, I., Cao, D., Cao, G.F., Cao, J., Carr, R., Cen, W.R., Chan, W.T., Chan, Y.L., Chang, J.F., Chang, L.C., Chang, Y., Chasman, C., Chen, H.Y., Chen, H.S., Chen, M.J., Chen, Q.Y., Chen, S.J., Chen, S.M., Chen, X.C., Chen, X.H., Chen, X.S., Chen, Y.X., Chen, Y., Cheng, J.H., Cheng, J., Cheng, Y.P., Cherwinka, J.J., Chidzik, S., Chow, K., Chu, M.C., Cummings, J.P., de Arcos, J., Deng, Z.Y., Ding, X.F., Ding, Y.Y., Diwan, M.V., Dong, L., Dove, J., Draeger, E., Du, X.F., Dwyer, D.A., Edwards, W.R., Ely, S.R., Fang, S.D., Fu, J.Y., Fu, Z.W., Ge, L.Q., Ghazikhanian, V., Gill, R., Goett, J., Gonchar, M., Gong, G.H., Gong, H., Gornushkin, Y.A., Grassi, M., Greenler, L.S., Gu, W.Q., Guan, M.Y., Guo, R.P., Guo, X.H., Hackenburg, R.W., Hahn, R.L., Han, R., Hans, S., He, M., He, Q., He, W.S., Heeger, K.M., Heng, Y.K., Higuera, A., Hinrichs, P., Ho, T.H., Hoff, M., Hor, Y.K., Hsiung, Y.B., Hu, B.Z., Hu, L.M., Hu, L.J., Hu, T., Hu, W., Huang, E.C., Huang, H.Z., Huang, H.X., Huang, P.W., Huang, X., Huang, X.T., Huber, P., Hussain, G., Isvan, Z., Jaffe, D.E., Jaffke, P., Jen, K.L., Jetter, S., Ji, X.P., Ji, X.L., Jiang, H.J., Jiang, W.Q., Jiao, J.B., Johnson, R.A., Joseph, J., Kang, L., Kettell, S.H., Kohn, S., Kramer, M., Kwan, K.K., Kwok, M.W., Kwok, T., Lai, C.Y., Lai, W.C., Lai, W.H., Langford, T.J., Lau, K., Lebanowski, L., Lee, J., Lee, M.K.P., Lei, R.T., Leitner, R., Leung, J.K.C., Lewis, C.A., Li, B., Li, C., Li, D.J., Li, F., Li, G.S., Li, J., Li, N.Y., Li, Q.J., Li, S.F., Li, S.C., Li, W.D., Li, X.B., Li, X.N., Li, X.Q., Li, Y., Li, Y.F., Li, Z.B., Liang, H., Liang, J., Lin, C.J., Lin, G.L., Lin, P.Y., Lin, S.X., Lin, S.K., Lin, Y.C., Ling, J.J., Link, J.M., Littenberg, L., Littlejohn, B.R., Liu, B.J., Liu, C., Liu, D.W., Liu, H., Liu, J.L., Liu, J.C., Liu, S., Liu, S.S., Liu, X., Liu, Y.B., Lu, C., Lu, H.Q., Lu, J.S., Luk, A., Luk, K.B., Luo, T., Luo, X.L., Ma, L.H., Ma, Q.M., Ma, X.Y., Ma, X.B., Ma, Y.Q., Mayes, B., McDonald, K.T., McFarlane, M.C., McKeown, R.D., Meng, Y., Mitchell, I., Mohapatra, D., Monari Kebwaro, J., Morgan, J.E., Nakajima, Y., Napolitano, J., Naumov, D., Naumova, E., Newsom, C., Ngai, H.Y., Ngai, W.K., Nie, Y.B., Ning, Z., Ochoa-Ricoux, J.P., Olshevskiy, A., Pagac, A., Pan, H.-R., Patton, S., Pearson, C., Pec, V., Peng, J.C., Piilonen, L.E., Pinsky, L., Pun, C.S.J., Qi, F.Z., Qi, M., Qian, X., Raper, N., Ren, B., Ren, J., Rosero, R., Roskovec, B., Ruan, X.C., Sands, W.R., III, Seilhan, B., Shao, B.B., Shih, K., Song, W.Y., Steiner, H., Stoler, P., Stuart, M., Sun, G.X., Sun, J.L., Tagg, N., Tam, Y.H., Tanaka, H.K., Tang, W., Tang, X., Taychenachev, D., Themann, H., Torun, Y., Trentalange, S., Tsai, O., Tsang, K.V., Tsang, R.H.M., Tull, C.E., Tung, Y.C., Viaux, N., Viren, B., Virostek, S., Vorobel, V., Wang, C.H., Wang, L.S., Wang, L.Y., Wang, L.Z., Wang, M., Wang, N.Y., Wang, R.G., Wang, T., Wang, W., Wang, W.W., Wang, X.T., Wang, X., Wang, Y.F., Wang, Z., Wang, Z.M., Webber, D.M., Wei, H.Y., Wei, Y.D., Wen, L.J., Wenman, D.L., Whisnant, K., White, C.G., Whitehead, L., Whitten, C.A., Jr., Wilhelmi, J., Wise, T., Wong, H.C., Wong, H.L.H., Wong, J., Wong, S.C.F., Worcester, E., Wu, F.F., Wu, Q., Xia, D.M., Xia, J.K., Xiang, S.T., Xiao, Q., Xing, Z.Z., Xu, G., Xu, J.Y., Xu, J.L., Xu, J., Xu, W., Xu, Y., Xue, T., Yan, J., Yang, C.G., Yang, L., Yang, M.S., Yang, M.T., Ye, M., Yeh, M., Yeh, Y.S., Yip, K., Young, B.L., Yu, G.Y., Yu, Z.Y., Zeng, S., Zhan, L., Zhang, C., Zhang, F.H., Zhang, H.H., Zhang, J.W., Zhang, K., Zhang, Q.X., Zhang, Q.M., Zhang, S.H., Zhang, X.T., Zhang, Y.C., Zhang, Y.H., Zhang, Y.M., Zhang, Y.X., Zhang, Z.J., Zhang, Z.Y., Zhang, Z.P., Zhao, J., Zhao, Q.W., Zhao, Y.F., Zhao, Y.B., Zheng, L., Zhong, W.L., Zhou, L., Zhou, N., Zhou, Z.Y., Zhuang, H.L., Zimmerman, S., and Zou, J.H.

Published
2016
Full Text
View/download PDF

5. Claudin-10 Decrease in the Submandibular Gland Contributes to Xerostomia.

Author

He, L., Yuan, S.Z., Mao, X.D., Zhao, Y.W., He, Q.H., Zhang, Y., Su, J.Z., Wu, L.L., Yu, G.Y., and Cong, X.

Subjects
SUBMANDIBULAR gland, XEROSTOMIA, SJOGREN'S syndrome, TIGHT junctions, SALIVARY glands, MUSCARINIC acetylcholine receptors
Abstract

Tight junction proteins play a crucial role in paracellular transport in salivary gland epithelia. It is clear that severe xerostomia in patients with HELIX syndrome is caused by mutations in the claudin-10 gene. However, little is known about the expression pattern and role of claudin-10 in saliva secretion in physical and disease conditions. In the present study, we found that only claudin-10b transcript was expressed in human and mouse submandibular gland (SMG) tissues, and claudin-10 protein was dominantly distributed at the apicolateral membranes of acini in human, rat, and mouse SMGs. Overexpression of claudin-10 significantly reduced transepithelial electrical resistance and increased paracellular transport of dextran and Na+ in SMG-C6 cells. In C57BL/6 mice, pilocarpine stimulation promoted secretion and cation concentration in saliva in a dose-dependent increase. Assembly of claudin-10 to the most apicolateral portions in acini of SMGs was observed in the lower pilocarpine (1 mg/kg)–treated group, and this phenomenon was much obvious in the higher pilocarpine (10 mg/kg)–treated group. Furthermore, 7-, 14-, and 21-wk-old nonobese diabetic (NOD) and BALB/c mice were used to mimic the progression of hyposalivation in Sjögren syndrome. Intensity of claudin-10 protein was obviously lower in SMGs of 14- and 21-wk-old NOD mice compared with that of age-matched BALB/c mice. In the cultured mouse SMG tissues, interferon-γ (IFN-γ) downregulated claudin-10 expression. In claudin-10–overexpressed SMG-C6 cells, paracellular permeability was decreased. Furthermore, IFN-γ stimulation increased p-STAT1 level, whereas pretreatment with JAK/STAT1 antagonist significantly alleviated the IFN-γ–induced claudin-10 downregulation. These results indicate that claudin-10 functions as a pore-forming component in acinar epithelia of SMGs, assembly of claudin-10 is required for saliva secretion, and downregulation of claudin-10 induces hyposecretion. These findings may provide new clues to novel therapeutic targets on hyposalivation. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

9. The muon system of the Daya Bay Reactor antineutrino experiment

Author

An, F.P., Balantekin, A.B., Band, H.R., Beriguete, W., Bishai, M., Blyth, S., Brown, R.E., Butorov, I., Cao, G.F., Cao, J., Carr, R., Chan, Y.L., Chang, J.F., Chang, L., Chang, Y., Chasman, C., Chen, H.S., Chen, H.Y., Chen, Q.Y., Chen, S.J., Chen, S.M., Chen, X.C., Chen, X.H., Chen, Y., Chen, Y.X., Cheng, Y.P., Cherwinka, J.J., Chu, M.C., Cummings, J.P., Dale, E., de Arcos, J., Deng, Z.Y., Ding, Y.Y., Diwan, M.V., Draeger, E., Du, X.F., Dwyer, D.A., Edwards, W.R., Ely, S.R., Fu, J.Y., Ge, L.Q., Gill, R., Goett, J., Gonchar, M., Gong, G.H., Gong, H., Gu, W.Q., Guan, M.Y., Guo, X.H., Hackenburg, R.W., Han, G.H., Hans, S., He, M., He, Q., Heeger, K.M., Heng, Y.K., Hinrichs, P., Hor, Y.K., Hsiung, Y.B., Hu, B.Z., Hu, L.J., Hu, L.M., Hu, T., Hu, W., Huang, E.C., Huang, H.X., Huang, H.Z., Huang, X.T., Huber, P., Hussain, G., Isvan, Z., Jaffe, D.E., Jaffke, P., Jetter, S., Ji, X.L., Ji, X.P., Jiang, H.J., Jiao, J.B., Johnson, R.A., Kang, L., Kebwaro, J.M., Kettell, S.H., Kramer, M., Kwan, K.K., Kwok, M.W., Kwok, T., Lai, W.C., Lai, W.H., Lau, K., Lebanowski, L., Lee, J., Lei, R.T., Leitner, R., Leung, A., Leung, J.K.C., Lewis, C.A., Li, D.J., Li, F., Li, G.S., Li, Q.J., Li, W.D., Li, X.N., Li, X.Q., Li, Y.Z.B., Liang, H., Lin, C.J., Lin, G.L., Lin, P.Y., Lin, S.K., Link, J.M., Littenberg, L., Littlejohn, B.R., Liu, D.W., Liu, H., Liu, J.C., Liu, J.L., Liu, S.S., Liu, Y.B., Lu, C., Lu, H.Q., Luk, K.B., Ma, Q.M., Ma, X.B., Ma, X.Y., Ma, Y.Q., McDonald, K.T., McFarlane, M.C., McKeown, R.D., Meng, Y., Mitchell, I., Mohapatra, D., Morgan, J.E., Nakajima, Y., Napolitano, J., Naumov, D., Naumova, E., Nemchenok, I., Newsom, C., Ngai, H.Y., Ngai, W.K., Ning, Z., Ochoa-Ricoux, J.P., Olshevski, A., Patton, S., Pec, V., Pearson, C.E., Peng, J.C., Piilonen, L.E., Pinsky, L., Pun, C.S.J., Qi, F.Z., Qi, M., Qian, X., Raper, N., Ren, B., Ren, J., Rosero, R., Roskovec, B., Ruan, X.C., Shao, B.B., Steiner, H., Sun, G.X., Sun, J.L., Tam, Y.H., Tang, X., Themann, H., Tsang, K.V., Tsang, R.H.M., Tull, C.E., Tung, Y.C., Viren, B., Virostek, S., Vorobel, V., Wang, C.H., Wang, L.S., Wang, L.Y., Wang, L.Z., Wang, M., Wang, N.Y., Wang, R.G., Wang, W., Wang, W.W., Wang, X., Wang, Y.F., Wang, Z., Wang, Z.M., Webber, D.M., Wei, H.Y., Wei, Y.D., Wen, L.J., Whisnant, K., White, C.G., Whitehead, L., Wilhelmi, J., Wise, T., Wong, H.L.H., Wong, S.C.F., Worcester, E., Wu, Q., Xia, D.M., Xia, J.K., Xia, X., Xing, Z.Z., Xu, G.H., Xu, J., Xu, J.L., Xu, J.Y., Xu, Y., Xue, T., Yan, J., Yang, C.G., Yang, L., Yang, M.S., Yang, M.T., Ye, M., Yeh, M., Yeh, Y.S., Young, B.L., Yu, G.Y., Yu, J.Y., Yu, Z.Y., Zang, S.L., Zhan, L., Zhang, C., Zhang, F.H., Zhang, J.W., Zhang, K., Zhang, Q.M., Zhang, S.H., Zhang, Y.H., Zhang, Y.M., Zhang, Y.X., Zhang, Z.J., Zhang, Z.P., Zhang, Z.Y., Zhao, J., Zhao, Q.W., Zhao, Y., Zhao, Y.B., Zheng, L., Zhong, W.L., Zhou, L., Zhou, Z.Y., Zhuang, H.L., and Zou, J.H.

Published
2015
Full Text
View/download PDF

15. sj-docx-1-jdr-10.1177_00220345221118508 – Supplemental material for The Role of Endothelial Barrier Function in the Fibrosis of Salivary Gland

Author

Mao, X.D., Min, S.N., Zhu, M.Q., He, L., Zhang, Y., Li, J.W., Tian, Y.X., Yu, G.Y., Wu, L.L., and Cong, X.

Subjects
110599 Dentistry not elsewhere classified, FOS: Materials engineering, FOS: Clinical medicine, 91299 Materials Engineering not elsewhere classified
Abstract

Supplemental material, sj-docx-1-jdr-10.1177_00220345221118508 for The Role of Endothelial Barrier Function in the Fibrosis of Salivary Gland by X.D. Mao, S.N. Min, M.Q. Zhu, L. He, Y. Zhang, J.W. Li, Y.X. Tian, G.Y. Yu, L.L. Wu and X. Cong in Journal of Dental Research

Published
2022
Full Text
View/download PDF

18. The Role of Endothelial Barrier Function in the Fibrosis of Salivary Gland.

Author

Mao, X.D., Min, S.N., Zhu, M.Q., He, L., Zhang, Y., Li, J.W., Tian, Y.X., Yu, G.Y., Wu, L.L., and Cong, X.

Subjects
ENDOTHELIUM, SUBMANDIBULAR gland, MONOCYTES, SALIVARY glands, TIGHT junctions
Abstract

In the salivary glands, fibrosis occurs in many pathological conditions. Endothelial tight junction (TJ)–based barrier function plays a vital role in maintaining the homeostasis of the salivary glands. However, whether endothelial barrier function is changed and involved in the pathogenesis of glandular fibrosis is unknown. Here, by using a mouse model in which the main excretory duct of the submandibular gland (SMG) was ligated to induce inflammation and fibrosis, endothelial barrier function and TJ protein expression and distribution were examined. Both 4-kDa and 70-kDa fluorescence-labeled dextrans permeated more in the 1-, 3-, and 7-d ligated SMGs. Meanwhile, the mRNA level of claudin-5 was increased with an obvious redistribution from apicolateral membranes to lateral membranes and cytoplasm in the fibrotic glands. Notably, the TJ sealer AT1001 significantly attenuated the disrupted endothelial barrier function and thereby ameliorated the glandular fibrosis. Cytokine array detection showed that monocyte chemoattractant protein–1 (MCP-1) was highly enriched in the 3-d ligated SMGs, and MCP-1 directly impaired barrier function, increased claudin-5 expression, induced the relocalization of claudin-5, and activated p-ERK1/2 in cultured human endothelial cells. Furthermore, the upregulation and disorganization of claudin-5 as well as the elevation of MCP-1 and p-ERK1/2 signaling were also confirmed in fibrotic SMGs from patients with chronic sialadenitis and immunoglobulin G4–related sialadenitis. Altogether, our findings revealed that disrupted endothelial barrier function contributed to the progression of glandular fibrosis, and targeting endothelial TJs might be a promising approach to alleviate salivary gland fibrosis-related diseases. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

20. Activation of transient receptor potential vanilloid subtype 1 increases secretion of the hypofunctional, transplanted submandibular gland

Author

Zhang, Y., Cong, X., Shi, L., Xiang, B., Li, Y.M., Ding, Q.W., Ding, C., Wu, L.L., and Yu, G.Y.

Subjects
Salivary glands -- Genetic aspects, Capsaicin -- Properties, Aquaporins -- Properties, Gene expression -- Physiological aspects, Biological sciences
Abstract

Hyposecretion occurs in most patients early after submandibular gland auto-transplantation for severe keratoconjunctivitis sicca. Endogenous transient receptor potential vanilloid subtype 1 (TRPV 1) has been recently demonstrated in rabbit submandibular glands, and activation of TRPV1 by capsaicin increases secretion in isolated glands, but the TRPV1-mediated secretory mechanism remains to be elucidated. The purpose of this study was to verify whether activation of TRPV 1 by capsaicin could improve the secretion of transplanted gland and its underlying mechanism. The salivary flow of the transplanted glands was significantly decreased, and the mRNA and protein levels of TRPV1 and aquaporin 5 (AQP5) were downregulated in the transplanted glands. Topical capsaicin cream increased secretion and upregulated levels of TRPV1 and AQP5 in transplanted glands. Moreover, in cultured submandibular gland cells, capsaicin increased the mRNA expression of AQP5 and led to redistribution of AQP5 from the cytoplasm to the plasma membrane via TRPV1 activation. Capsaicin enhanced the phosphorylation of extracellular signal-regulated kinase (ERK). Preincubation of cells with PD98059, an inhibitor of ERK kinase, suppressed the capsaicin-induced mRNA expression of AQP5. In summary, the capsaicin-induced secretory mechanism involved activation of TRPV1 and upregulation of AQP5 in an ERK-dependent manner and promoted the redistribution of AQP5 in submandibular gland cells. Activation of TRPV 1 may provide a new therapeutic strategy to improve submandibular gland hypofunction. capsaicin; aquaporin 5; transient receptor potential vanilloid subtype 1; secretory mechanism doi: 10.1152/ajpgi.00528.2009.

Published
2010

21. Dynamic fluid-structure interaction analysis using boundary finite element method-finite element method

Author

Fan, S.C., Li, S.M., and Yu, G.Y.

Subjects
Fluid dynamics -- Research, Mechanics -- Research, Science and technology
Abstract

In this paper, the boundary finite element method (BFEM) is applied to dynamic fluid-structure interaction problems. The BFEM is employed to model the infinite fluid medium, while the structure is modeled by the finite element method (FEM). The relationship between the fluid pressure and the fluid velocity corresponding to the scattered wave is derived from the acoustic modeling. The BFEM is suitable for both finite and infinite domains, and it has advantages over other numerical methods. The resulting system of equations is symmetric and has no singularity problems. Two numerical examples are presented to validate the accuracy and efficiency of BFEM-FEM coupling for fluid-structure interaction problems. [DOI: 10.1115/1.1940664]

Published
2005

22. Relationship among coefficient matrices in symmetric Galerkin boundary element method for two-dimensional scalar problems

Author

Yu, G.Y.

Subjects
Mechanics -- Research, Science and technology
Abstract

Based on the assumption that solutions from different methods should be the same, the relationship among weakly singular, strongly singular and hypersingular matrices associated with symmetric Galerkin boundary element method (SGBEM) is derived in this paper. Hypersingularity is avoided through matrix manipulations so that only weakly and strongly singularities need to be solved. Compared with the advantages brought about by symmetry, the additional computation caused by matrix manipulations is not so important in many cases, especially for time-domain problems or when one wants to couple BEM with other symmetric schemes. Simplicity is the advantage of the current method over the traditional SGBEM. Both steady-state and time-domain potential problems have been studied, and two numerical examples are included to show the effectiveness and accuracy of the present formulation. [DOI: 10.1115/1.1598478]

Published
2003

23. A symmetric boundary element method/finite element method coupling procedure for two-dimensional elastodynamic problems

Author

Yu, G.Y.

Subjects
Physics -- Research, Mechanics -- Research, Science and technology
Abstract

In this paper, a symmetric collocation boundary element method (SCBEM)/finite element method (FEM) coupling procedure is given and applied to a two-dimensional elastodynamic problem. The use of symmetry for the boundary element method not only saves memory storage but also enables the employment of efficient symmetric equation solvers. This is especially important for BEM/ FEM coupling procedure. Compared with the symmetric Galerkin boundary element method (SGBEM) where double-space integration should be carried out, SCBEM is easier and faster. [DOI: 10.1115/1.1571856]

Published
2003

32. TNF-α Suppresses Autophagic Flux in Acinar Cells in IgG4-Related Sialadenitis

Author

Hong, Xia, Min, Sainan, Zhang, Yingying, Lin, Y.T., Wang, F., Huang, Yan, Yu, G.Y., Wu, Liling, Yang, Hongyu, Hong, Xia, Min, Sainan, Zhang, Yingying, Lin, Y.T., Wang, F., Huang, Yan, Yu, G.Y., Wu, Liling, and Yang, Hongyu

Abstract

IgG4-related sialadenitis (IgG4-RS) is a newly recognized immune-mediated systemic fibroinflammatory disease that affects salivary glands and leads to hyposalivation. Tumor necrosis factor–α (TNF-α) is a critical proinflammatory cytokine involved in several salivary gland disorders, but its role and mechanism regarding acinar cell injury in IgG4-RS are unknown. Here, we found that TNF-α level was significantly increased in serum and submandibular gland (SMG) of patients and that serum TNF-α level was negatively correlated with saliva flow rate. Ultrastructural observations of IgG4-RS SMGs revealed accumulation of large autophagic vacuoles, as well as dense fibrous bundles, decreased secretory granules, widened intercellular spaces, swollen mitochondria, and expanded endoplasmic reticulum. Expression levels of LC3 and p62 were both increased in patients’ SMGs. TNF-α treatment led to elevated levels of LC3II and p62 in both SMG-C6 cells and cultured human SMG tissues but did not further increase their levels when combined with bafilomycin A1 treatment. Moreover, transfection of Ad-mCherry-GFP-LC3B in SMG-C6 cells confirmed the suppression of autophagic flux after TNF-α treatment. Immunofluorescence imaging revealed that costaining of LC3 and the lysosomal marker LAMP2 was significantly decreased in patients, TNF-α–treated SMG-C6 cells, and cultured human SMGs, indicating a reduction in autophagosome-lysosome fusion. Furthermore, the ratio of pro/mature cathepsin D was elevated in vivo, ex vivo, and in vitro. TNF-α also appeared to induce abnormal acidification of lysosomes in acinar cells, as assessed by lysosomal pH and LysoTracker DND-26 fluorescence intensity. In addition, TNF-α treatment induced transcription factor EB (TFEB) redistribution in SMG-C6 cells, which was consistent with the changes observed in IgG4-RS patients. TNF-α increased the phosphorylation of extracellular signal–regulated kinase (ERK) 1/2, and inhibition of ERK1/2 by U0126 reversed TNF-α–induc

Published
2019

35. Tricellulin Modulates Transport of Macromolecules in the Salivary Gland.

Author

Min, S.N., Cong, X., Zhang, Y., Xiang, R.L., Zhou, Y., Yu, G.Y., and Wu, L.L.

Subjects
MACROMOLECULES, SALIVARY glands, SALIVA microbiology, ORAL hygiene, TIGHT junctions, EPITHELIAL cells, CLAUDINS, SUBMANDIBULAR gland, ANIMAL experimentation, CELL membranes, CELL receptors, COMPARATIVE studies, RESEARCH methodology, MEDICAL cooperation, MEMBRANE proteins, MICE, RATS, RESEARCH, EVALUATION research
Abstract

Volume and composition of saliva are crucial for oral and systemic health. How substances, particularly macromolecules, are transported across the salivary gland epithelium has not been established in detail. Tricellulin is a component of tricellular tight junctions that form a central tube to serve as an important route for macromolecule transport. Whether tricellulin is expressed in the submandibular gland (SMG) and involved in salivation has been unknown. Here, by using Western blotting and immunofluorescence, tricellulin was found to be characteristically localized at tricellular contacts of human, rat, and mouse SMGs. Knockdown of tricellulin significantly increased, whereas overexpression of tricellulin decreased, paracellular permeability for 40-kDa but not for 4-kDa fluorescein isothiocyanate-dextran, while transepithelial electrical resistance was unaffected. Conversely, claudin-4 knockdown and overexpression affected transepithelial electrical resistance but not 40-kDa fluorescein isothiocyanate-dextran transport, suggesting that tricellulin regulated transport of macromolecules but not ions, which were mainly regulated by bicellular tight junctions (bTJs). Moreover, tricellulin was dynamically redistributed from tri- to bicellular membranes in cholinergically stimulated SMG tissues and cells. Immunoglobulin-like domain-containing receptor 1 (ILDR1) recruits tricellulin to tricellular contacts. The proportion of macromolecules in the saliva was increased, whereas the amount of stimulated saliva was unchanged in Ildr1-/- mice, which displayed abnormal tricellulin distribution in SMGs. Furthermore, tricellulin interacted with bTJ proteins, such as occludin, claudin-1, claudin-3, claudin-4, and ZO-1, in rat SMG epithelial polarized cell line SMG-C6. Knockdown of tricellulin decreased occludin levels. Thus, we revealed a specific expression pattern of tricellulin in SMG epithelium. Tricellulin not only functioned as a barrier for macromolecules but also modulated the connection of bTJs to the tight junction complex. Alterations in tricellulin expression and distribution could thereby change salivary composition. Our study provided novel insights on salivary gland tight junction organization and function. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

46. A web-based software system for linkage analysis and information management

Author

Yu, G.Y., Liu, J.X., Xie, D.T., Thompson, R.M., Zayas, R., Raike, R.S., and Gomez, C.M.

Subjects
Human genetics -- Research, Laboratories -- Equipment and supplies, Genotype -- Methods, Software -- Product development, Internet -- Product information, Biological sciences
Published
2001

Catalog

Books, media, physical & digital resources
See catalog results