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1. Correction: Heparanase inhibition as a systemic approach to protect the endothelial glycocalyx and prevent microvascular complications in diabetes

Author

Gamez, Monica, E. Elhegni, Hesham, Fawaz, Sarah, Ho Ho, Kwan, W. Campbell, Neill, A. Copland, David, L. Onions, Karen, J. Butler, Matthew, J. Wasson, Elizabeth, Crompton, Michael, D. Ramnath, Raina, Qiu, Yan, Yamaguchi, Yu, P. Arkill, Kenton, O. Bates, David, E. Turnbull, Jeremy, V. Zubkova, Olga, I. Welsh, Gavin, Atan, Denize, C. Satchell, Simon, and R. Foster, Rebecca

Published
2024
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2. Heparanase inhibition as a systemic approach to protect the endothelial glycocalyx and prevent microvascular complications in diabetes

Author

Gamez, Monica, Elhegni, Hesham E., Fawaz, Sarah, Ho, Kwan Ho, Campbell, Neill W., Copland, David A., Onions, Karen L., Butler, Matthew J., Wasson, Elizabeth J., Crompton, Michael, Ramnath, Raina D., Qiu, Yan, Yamaguchi, Yu, Arkill, Kenton P., Bates, David O., Turnbull, Jeremy E., Zubkova, Olga V., Welsh, Gavin I., Atan, Denize, Satchell, Simon C., and Foster, Rebecca R.

Published
2024
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3. Blocking matrix metalloproteinase-mediated syndecan-4 shedding restores the endothelial glycocalyx and glomerular filtration barrier function in early diabetic kidney disease

Author

Ramnath, Raina D., Butler, Matthew J., Newman, Georgina, Desideri, Sara, Russell, Amy, Lay, Abigail C., Neal, Chris R., Qiu, Yan, Fawaz, Sarah, Onions, Karen L., Gamez, Monica, Crompton, Michael, Michie, Chris, Finch, Natalie, Coward, Richard J., Welsh, Gavin I., Foster, Rebecca R., and Satchell, Simon C.

Published
2020
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4. #457 Sparsentan has direct effects on the glomerular capillary wall to attenuate increased permeability after exposure to nephrotic syndrome plasma

Author

Crompton, Michael, primary, Watson, Judy J, additional, Colby, Elizabeth, additional, Clapper, Wilmelenne, additional, Jenkinson, Celia P, additional, Hendry, Bruce, additional, Komers, Radko, additional, Saleem, Moin, additional, Welsh, Gavin, additional, Foster, Rebecca R, additional, and Satchell, Simon C, additional

Published
2024
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5. Edison : a novel model of otitis media

Author

Crompton, Michael, Brown, Steve, and Burton, Martin

Subjects
617.8, Genetics (life sciences), Molecular genetics, Biology, genetics, deafness, otitis media, mouse
Abstract

Otitis media (OM) is characterised by inflammation of the middle ear and is a common cause of conductive hearing impairment that places a substantial social, medical and economic burden on healthcare systems globally. Despite the importance of the disease, the aetiology of chronic middle ear inflammatory disease remains poorly understood. The development and persistence of chronic OM is multi-factorial with a significant genetic component. A new mouse model of chronic OM, edison, was generated by N-ethyl-N-nitrosourea (ENU) mutagenesis and discovered in a recessive screen at MRC Harwell. Homozygous edison mice have craniofacial abnormalities, an emphysema-like lung phenotype and spontaneously develop a conductive hearing loss at 28 days as measured by ABR. Histological analysis shows the hearing loss is associated with the development of chronic OM in the middle ear, characterised by mucosal inflammation and highly cellular ear exudates. Similar to the Jeff and Junbo mutants, edison shows raised levels of Vegfa, Tnfα and Il-1β in middle ear fluids. A putative functional mutation was identified, resulting in a missense Leu972Pro change in a relatively unknown gene, Nischarin (Nisch). The identification of additional ENU-induced Nisch alleles, and subsequent characterisation, validated Nisch as the causative gene in edison. NISCH selectively binds ITGA5, which is thought to have a role in modulating VEGF signalling through SRC and FAK kinases. A significant genetic interaction between Nisch and Itga5 exists and impacts upon development of chronic OM. Mice heterozygous for Itga5-null and homozygous for edison alleles show a significantly increased penetrance and severity of chronic OM. Analysis of downstream pathways suggests that the edison allele is impacting upon both RAC1 and TGF-β/SMAD signalling. I also explored the potential use of the edison mouse as a model for bacterial challenge with the human otopathogen, NTHi. Similar to the Junbo infection model at MRC Harwell, the edison mouse was identified as a robust OM model for bacterial NTHi infection. The edison mouse highlights a new candidate gene for susceptibility to chronic OM and will provide further insight into the genetic pathways and pathogenic processes involved in chronic OM.

Published
2014

9. Mineralocorticoid receptor antagonism in diabetes reduces albuminuria by preserving the glomerular endothelial glycocalyx

Author

Crompton, Michael, primary, Ferguson, Joanne K., additional, Ramnath, Raina D., additional, Onions, Karen L., additional, Ogier, Anna S., additional, Gamez, Monica, additional, Down, Colin J., additional, Skinner, Laura, additional, Wong, Kitty H., additional, Dixon, Lauren K., additional, Sutak, Judit, additional, Harper, Steven J., additional, Pontrelli, Paola, additional, Gesualdo, Loreto, additional, Heerspink, Hiddo L., additional, Toto, Robert D., additional, Welsh, Gavin I., additional, Foster, Rebecca R., additional, Satchell, Simon C., additional, and Butler, Matthew J., additional

Published
2023
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10. Early mineralocorticoid receptor antagonism in diabetic nephropathy limits albuminuria by preserving the glomerular endothelial glycocalyx

Author

Crompton, Michael, primary, Ferguson, Joanne K., additional, Ramnath, Raina D., additional, Onions, Karen L., additional, Ogier, Anna S., additional, Down, Colin J., additional, Skinner, Laura, additional, Dixon, Lauren K., additional, Sutak, Judit, additional, Harper, Steven J., additional, Pontrelli, Paola, additional, Gesualdo, Loreto, additional, Welsh, Gavin I., additional, Foster, Rebecca R., additional, Satchell, Simon C., additional, and Butler, Matthew J., additional

Published
2021
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12. The Epidemiology of Otosclerosis in a British Cohort

Author

Crompton, Michael, primary, Cadge, Barbara A., additional, Ziff, Joanna L., additional, Mowat, Andrew J., additional, Nash, Robert, additional, Lavy, Jeremy A., additional, Powell, Harry R. F., additional, Aldren, Christopher P., additional, Saeed, Shakeel R., additional, and Dawson, Sally J., additional

Published
2019
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13. A mutation in Nischarin causes otitis media via LIMK1 and NF-κB pathways

Author

Crompton, Michael, primary, Purnell, Tom, additional, Tyrer, Hayley E., additional, Parker, Andrew, additional, Ball, Greg, additional, Hardisty-Hughes, Rachel E., additional, Gale, Richard, additional, Williams, Debbie, additional, Dean, Charlotte H., additional, Simon, Michelle M., additional, Mallon, Ann-Marie, additional, Wells, Sara, additional, Bhutta, Mahmood F., additional, Burton, Martin J., additional, Tateossian, Hilda, additional, and Brown, Steve D. M., additional

Published
2017
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Author

Justice, Monica J., Crompton, Michael, Purnell, Tom, Tyrer, Hayley, Parker, Andrew, Ball, Greg, Hardisty-Hughes, Rachel E., Gale, Richard, Williams, Debbie, Dean, Charlotte H., Simon, Michelle M., Mallon, Ann-Marie, Wells, Sara, Bhutta, Mahmood F., Burton, Martin J., Tateossian, Hilda, Brown, Steve D. M., Justice, Monica J., Crompton, Michael, Purnell, Tom, Tyrer, Hayley, Parker, Andrew, Ball, Greg, Hardisty-Hughes, Rachel E., Gale, Richard, Williams, Debbie, Dean, Charlotte H., Simon, Michelle M., Mallon, Ann-Marie, Wells, Sara, Bhutta, Mahmood F., Burton, Martin J., Tateossian, Hilda, and Brown, Steve D. M.

Published
2017

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Author

Justice, Monica J., Crompton, Michael, Purnell, Tom, Tyrer, Hayley, Parker, Andrew, Ball, Greg, Hardisty-Hughes, Rachel E., Gale, Richard, Williams, Debbie, Dean, Charlotte H., Simon, Michelle M., Mallon, Ann-Marie, Wells, Sara, Bhutta, Mahmood F., Burton, Martin J., Tateossian, Hilda, Brown, Steve D. M., Justice, Monica J., Crompton, Michael, Purnell, Tom, Tyrer, Hayley, Parker, Andrew, Ball, Greg, Hardisty-Hughes, Rachel E., Gale, Richard, Williams, Debbie, Dean, Charlotte H., Simon, Michelle M., Mallon, Ann-Marie, Wells, Sara, Bhutta, Mahmood F., Burton, Martin J., Tateossian, Hilda, and Brown, Steve D. M.

Published
2017

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Author

Justice, Monica J., Crompton, Michael, Purnell, Tom, Tyrer, Hayley, Parker, Andrew, Ball, Greg, Hardisty-Hughes, Rachel E., Gale, Richard, Williams, Debbie, Dean, Charlotte H., Simon, Michelle M., Mallon, Ann-Marie, Wells, Sara, Bhutta, Mahmood F., Burton, Martin J., Tateossian, Hilda, Brown, Steve D. M., Justice, Monica J., Crompton, Michael, Purnell, Tom, Tyrer, Hayley, Parker, Andrew, Ball, Greg, Hardisty-Hughes, Rachel E., Gale, Richard, Williams, Debbie, Dean, Charlotte H., Simon, Michelle M., Mallon, Ann-Marie, Wells, Sara, Bhutta, Mahmood F., Burton, Martin J., Tateossian, Hilda, and Brown, Steve D. M.

Published
2017

18. A new model for NTHi middle ear infection in the Junbo mutant mouse

Author

Hood, Derek, primary, Moxon, Richard, additional, Purnell, Tom, additional, Richter, Caroline, additional, Williams, Debbie, additional, Azar, Ali, additional, Crompton, Michael, additional, Wells, Sara, additional, Fray, Martin, additional, Brown, Steve D.M., additional, and Cheeseman, Michael T., additional

Published
2015
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19. What Have We Learned from Murine Models of Otitis Media?

Author

Tyrer, Hayley, Crompton, Michael, Bhutta, Mahmood F., Tyrer, Hayley, Crompton, Michael, and Bhutta, Mahmood F.

Abstract

Otitis media (OM) is a common cause of childhood hearing loss. The large medical costs involved in treating this condition have meant that research to understand the pathology of this disease and identify new therapeutic interventions is important. There is evidence that susceptibility to OM has a significant genetic component, although little is known about the key genetic pathways involved. Mouse models for disease have become an important resource to understand a variety of human pathologies, including OM, due to the ability to easily manipulate their genetic components. This has enabled researchers to create models of acute OM, and has aided in the identification of a number of new genes associated with chronic disease, through the use of mutagenesis programs. The use of mouse models has identified a number of key molecular signalling pathways involved in the development of this condition, with genes identified from models shown to be associated with human OM.

Published
2013

23. A new model for non-typeable Haemophilus influenzae middle ear infection in the Junbo mutant mouse

Author

Hood, Derek, Moxon, Richard, Purnell, Tom, Richter, Caroline, Williams, Debbie, Azar, Ali, Crompton, Michael, Wells, Sara, Fray, Martin, Brown, Steve D. M., and Cheeseman, Michael T.

Abstract

Acute otitis media, inflammation of the middle ear, is the most common bacterial infection in children and, as a consequence, is the most common reason for antimicrobial prescription to this age group. There is currently no effective vaccine for the principal pathogen involved, non-typeable Haemophilus influenzae (NTHi). The most frequently used and widely accepted experimental animal model of middle ear infection is in chinchillas, but mice and gerbils have also been used. We have established a robust model of middle ear infection by NTHi in the Junbo mouse, a mutant mouse line that spontaneously develops chronic middle ear inflammation in specific pathogen-free conditions. The heterozygote Junbo mouse (Jbo/+) bears a mutation in a gene (Evi1, also known as Mecom) that plays a role in host innate immune regulation; pre-existing middle ear inflammation promotes NTHi middle ear infection. A single intranasal inoculation with NTHi produces high rates (up to 90%) of middle ear infection and bacterial titres (104-105 colony-forming units/µl) in bulla fluids. Bacteria are cleared from the majority of middle ears between day 21 and 35 post-inoculation but remain in approximately 20% of middle ears at least up to day 56 post-infection. The expression of Toll-like receptor-dependent response cytokine genes is elevated in the middle ear of the Jbo/+ mouse following NTHi infection. The translational potential of the Junbo model for studying antimicrobial intervention regimens was shown using a 3 day course of azithromycin to clear NTHi infection, and its potential use in vaccine development studies was shown by demonstrating protection in mice immunized with killed homologous, but not heterologous, NTHi bacteria.

Published
2016
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