Pectin methylesterases (PMEs) catalyze pectin demethylation and facilitate the determination of the degree of methyl esterification of cell wall in higher plants. The regulation of PME activity through endogenous proteinaceous PME inhibitors (PMEIs) alters the status of pectin methylation and influences plant growth and development. In this study, we performed a PMEI screening assay using a chemical library and identified a strong inhibitor, phenylephrine (PE). PE, a small molecule, competitively inhibited plant PMEs, including orange PME and Arabidopsis PME. Physiologically, cultivation of Brassica campestris seedlings in the presence of PE showed root growth inhibition. Microscopic observation revealed that PE inhibits elongation and development of root hairs. Molecular studies demonstrated that Root Hair Specific 12 (RHS12) encoding a PME, which plays a role in root hair development, was inhibited by PE with a Ki value of 44.1 μM. The biochemical mechanism of PE-mediated PME inhibition as well as a molecular docking model between PE and RHS12 revealed that PE interacts within the catalytic cleft of RHS12 and interferes with PME catalytic activity. Taken together, these findings suggest that PE is a novel and non-proteinaceous PME inhibitor. Furthermore, PE could be a lead compound for developing a potent plant growth regulator in agriculture.
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http://dx.doi.org/10.1016/j.bbrc.2018.11.117 | DOI Listing |
Molecules
November 2024
Laboratory of Cardiometabolic Pharmacology, Postgraduate Program in Pharmacology (UFPR), Federal University of Paraná, Curitiba 81531-980, PR, Brazil.
Sci Rep
October 2024
Department of Physiology and Pharmacology, Robarts Research Institute, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Constrictor agonists set arterial tone through two coupling processes, one tied to (electromechanical), the other independent (pharmacomechanical) of, membrane potential (V). This dual arrangement raises an intriguing question: is the contribution of each mechanism (1) fixed and proportionate, or (2) variable and functionally biased. Examination began in mouse mesenteric arteries with a vasomotor assessment to a classic G (phenylephrine) or G/G (U46619) agonist, in the absence and presence of nifedipine, to separate among the two coupling mechanisms.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
January 2025
Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200000, China. Electronic address:
Metabolic reprogramming precedes most alterations during pathological cardiac hypertrophy and heart failure (HF). Recent studies have revealed that Phosphofructokinase, platelet (PFKP) has a wealth of metabolic and non-metabolic functions. In this study, we explored the role of PFKP in cardiac hypertrophic growth and HF.
View Article and Find Full Text PDFNeurogastroenterol Motil
January 2025
Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Background: Inhibitory neuromuscular transmission in the gastrointestinal tract is mediated by intrinsic nitrergic and purinergic neurons. Purines activate G protein-coupled receptor P2Y receptors, increasing intracellular Ca that activates small conductance calcium-activated potassium (SK) channels. Little is known about the effect of adrenergic receptor activation on intestinal smooth muscle.
View Article and Find Full Text PDFCell Death Dis
September 2024
Human Phenome Institute, Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Centre, Zhangjiang Fudan International Innovation Center, Shanghai Key Laboratory of Bioactive Small Molecules, Fudan University, Shanghai, China.
Cardiomyocyte hypertrophy is a major outcome of pathological cardiac hypertrophy. The m6A demethylase ALKBH5 is reported to be associated with cardiovascular diseases, whereas the functional role of ALKBH5 in cardiomyocyte hypertrophy remains confused. We engineered Alkbh5 siRNA (siAlkbh5) and Alkbh5 overexpressing plasmid (Alkbh5 OE) to transfect cardiomyocytes.
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