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Role of selenium and 17β oestradiol in modulating lipid accumulation in in vitro models of obesity and NAFLD. (2024)
Journal Article
WALSH, S.K., PETTIGREW, K., MEZZANI, I., ALASWAD, I. and BERMANO, G. [2024]. Role of selenium and 17β oestradiol in modulating lipid accumulation in in vitro models of obesity and NAFLD. Food and medicine homology [online], Online First. Available from: https://doi.org/10.26599/FMH.2025.9420056

Abdominal obesity is prevalent in women and during menopause, making them more susceptible to weight gain, fat redistribution, and subsequent development of metabolic syndrome and associated diseases such as non-alcoholic fatty liver disease (NAFLD).... Read More about Role of selenium and 17β oestradiol in modulating lipid accumulation in in vitro models of obesity and NAFLD..

GPR55 regulates the responsiveness to, but does not dimerise with, α1A-adrenoceptors. (2021)
Journal Article
WALSH, S.K., LIPINA, C., ANG, S.Y., SATO, M., CHIA, L.Y., KOCAN, M., HUTCHINSON, D.S., SUMMERS, R.J. and WAINWRIGHT, C.L. 2021. GPR55 regulates the responsiveness to, but does not dimerise with, α1A-adrenoceptors. Biochemical pharmacology [online], 188, article ID 114560. Available from: https://doi.org/10.1016/j.bcp.2021.114560

Emerging evidence suggests that G protein coupled receptor 55 (GPR55) may influence adrenoceptor function/activity in the cardiovascular system. Whether this reflects direct interaction (dimerization) between receptors or signalling crosstalk has not... Read More about GPR55 regulates the responsiveness to, but does not dimerise with, α1A-adrenoceptors..

l-α-Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK-dependent pathway. (2019)
Journal Article
ROBERTSON-GRAY, O.J., WALSH, S.K., RYBERG, E., JÖNSSON-RYLANDER, A.-C., LIPINA, C. and WAINWRIGHT, C.L. 2019. l‐α‐Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK‐dependent pathway. Pharmacology research and perspectives [online], 7(3), article ID e00487. Available from: https://doi.org/10.1002/prp2.487

The phospholipid l-α-lysophosphatidylinositol (LPI), an endogenous ligand for GPR55, is elevated in patients with acute coronary syndrome, and a GPR55 antagonist cannabidiol (CBD) reduces experimental ischemia/reperfusion (I/R) injury. While LPI acti... Read More about l-α-Lysophosphatidylinositol (LPI) aggravates myocardial ischemia/reperfusion injury via a GPR55/ROCK-dependent pathway..

Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia-reperfusion injury through depletion of glutathione. (2019)
Journal Article
SKENE, K., WALSH, S.K., OKAFOR, O., GODSMAN, N., BARROWS, C., MEIER, P., GORDON, M.J., BEATTIE, J.H. and WAINWRIGHT, C.L. 2019. Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia-reperfusion injury through depletion of glutathione. British journal of nutrition [online], 121(9), pages 961-973. Available from: https://doi.org/10.1017/S0007114519000230

Zinc (Zn) plays an important role in maintaining the anti-oxidant status within the heart, and helps to counter the acute redox stress that occurs during myocardial ischaemia and reperfusion. Individuals with low zinc (Zn) levels are at greater risk... Read More about Acute dietary zinc deficiency in rats exacerbates myocardial ischaemia-reperfusion injury through depletion of glutathione..

GPR55 deficiency is associated with increased adiposity and impaired insulin signaling in peripheral metabolic tissues. (2018)
Journal Article
LIPINA, C., WALSH, S.K., MITCHELL, S.E., SPEAKMAN, J.R., WAINWRIGHT, C.L. and HUNDAL, H.S. 2019. GPR55 deficiency is associated with increased adiposity and impaired insulin signaling in peripheral metabolic tissues. FASEB journal [online], 33(1), pages 1299-1312. Available from: https://doi.org/10.1096/fj.201800171R

Emerging evidence indicates that G-protein coupled receptor 55 (GPR55), a nonclassic receptor of the endocannabinoid system that is activated by L-α-lysophosphatidylinositol and various cannabinoid ligands, may regulate endocrine function and energy... Read More about GPR55 deficiency is associated with increased adiposity and impaired insulin signaling in peripheral metabolic tissues..

Pharmacological profiling of the hemodynamic effects of cannabinoid ligands: a combined in vitro and in vivo approach. (2015)
Journal Article
WALSH, S.K., HEPBURN, C.Y., KEOWN, O., ÅSTRAND, A., LINDBLOM, A., RYBERG, E., HJORTH, S., LESLIE, S. J., GREASLEY, P.J. and WAINWRIGHT, C.L. 2015. Pharmacological profiling of the hemodynamic effects of cannabinoid ligands: a combined in vitro and in vivo approach. Pharmacology research and perspectives [online], 3(3), e00143. Available from: https://doi.org/10.1177/1715163515578124

The receptors mediating the hemodynamic responses to cannabinoids are not clearly defined due to the multifarious pharmacology of many commonly used cannabinoid ligands. While both CB1 and TRPV1 receptors are implicated, G protein-coupled receptor 55... Read More about Pharmacological profiling of the hemodynamic effects of cannabinoid ligands: a combined in vitro and in vivo approach..

GPR55 deletion in mice leads to age-related ventricular dysfunction and impaired adrenoceptor-mediated inotropic responses. (2014)
Journal Article
WALSH, S.K., HECTOR, E.E., ANDREASSON, A.-C., JONSSON-RYLANDER, A.-C. and WAINWRIGHT, C. L. 2014. GPR55 deletion in mice leads to age-related ventricular dysfunction and impaired adrenoceptor-mediated inotropic responses. PLoS ONE [online], 9(10), article number e108999. Available from: https://doi.org/10.1371/journal.pone.0108999

G protein coupled receptor 55 (GPR55) is expressed throughout the body and, although its exact physiological function is unknown, studies have suggested that it has a role in the cardiovascular system. In particular, GPR55 has been proposed as mediat... Read More about GPR55 deletion in mice leads to age-related ventricular dysfunction and impaired adrenoceptor-mediated inotropic responses..