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Start Over Author "Peter Heppner" Journal communications biology
3 results on '"Peter Heppner"'

1. Characterisation of PDGF-BB:PDGFRβ signalling pathways in human brain pericytes: evidence of disruption in Alzheimer’s disease

Author

Leon C. D. Smyth, Blake Highet, Deidre Jansson, Jane Wu, Justin Rustenhoven, Miranda Aalderink, Adelie Tan, Susan Li, Rebecca Johnson, Natacha Coppieters, Renee Handley, Pritika Narayan, Malvindar K. Singh-Bains, Patrick Schweder, Clinton Turner, Edward W. Mee, Peter Heppner, Jason Correia, Thomas I.-H. Park, Maurice A. Curtis, Richard L. M. Faull, and Mike Dragunow

Subjects
Biology (General), QH301-705.5
Abstract

Smyth et al. use tissue microarrays from Alzheimer’s disease (AD) patient brains to show that PDGF-BB:PDGFRβ signalling components are reduced in AD. They then use primary human brain pericytes to elucidate a pathway by which PDGF-BB:PDGFRβ signalling in brain pericytes is disrupted in AD, thus impairing the blood brain barrier.

Published
2022
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2. Cardiac glycosides target barrier inflammation of the vasculature, meninges and choroid plexus

Author

Deidre Jansson, Victor Birger Dieriks, Justin Rustenhoven, Leon C. D. Smyth, Emma Scotter, Miranda Aalderink, Sheryl Feng, Rebecca Johnson, Patrick Schweder, Edward Mee, Peter Heppner, Clinton Turner, Maurice Curtis, Richard Faull, and Mike Dragunow

Subjects
Biology (General), QH301-705.5
Abstract

Jansson et al. design a high content screening system to target inflammation in human brain cells of the blood–brain barrier (pericytes and endothelial cells) to identify inflammatory modifiers. They identify cardiac glycosides as powerful regulators of neuroinflammatory pathways in brain barrier tissues such as vasculature, meninges and choroid plexus.

Published
2021
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3. Characterisation of PDGF-BB:PDGFRβ signalling pathways in human brain pericytes: evidence of disruption in Alzheimer's disease

Author

Leon C. D. Smyth, Blake Highet, Deidre Jansson, Jane Wu, Justin Rustenhoven, Miranda Aalderink, Adelie Tan, Susan Li, Rebecca Johnson, Natacha Coppieters, Renee Handley, Pritika Narayan, Malvindar K. Singh-Bains, Patrick Schweder, Clinton Turner, Edward W. Mee, Peter Heppner, Jason Correia, Thomas I.-H. Park, Maurice A. Curtis, Richard L. M. Faull, and Mike Dragunow

Subjects
Receptor, Platelet-Derived Growth Factor beta, Alzheimer Disease, Becaplermin, Medicine (miscellaneous), Brain, Humans, General Agricultural and Biological Sciences, Pericytes, General Biochemistry, Genetics and Molecular Biology
Abstract

Platelet-derived growth factor-BB (PDGF-BB):PDGF receptor-β (PDGFRβ) signalling in brain pericytes is critical to the development, maintenance and function of a healthy blood-brain barrier (BBB). Furthermore, BBB impairment and pericyte loss in Alzheimer’s disease (AD) is well documented. We found that PDGF-BB:PDGFRβ signalling components were altered in human AD brains, with a marked reduction in vascular PDGFB. We hypothesised that reduced PDGF-BB:PDGFRβ signalling in pericytes may impact on the BBB. We therefore tested the effects of PDGF-BB on primary human brain pericytes in vitro to define pathways related to BBB function. Using pharmacological inhibitors, we dissected distinct aspects of the PDGF-BB response that are controlled by extracellular signal-regulated kinase (ERK) and Akt pathways. PDGF-BB promotes the proliferation of pericytes and protection from apoptosis through ERK signalling. In contrast, PDGF-BB:PDGFRβ signalling through Akt augments pericyte-derived inflammatory secretions. It may therefore be possible to supplement PDGF-BB signalling to stabilise the cerebrovasculature in AD.

Published
2021

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