Phenylephrine, a small molecule, inhibits pectin methylesterases.

Biochem Biophys Res Commun

Department of Agricultural Chemistry (BK21 plus), Institute of Agriculture and Life Science (IALS), Gyeongsang National University, Jinju, 52828, Republic of Korea. Electronic address:

Published: January 2019

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.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2018.11.117DOI Listing

Publication Analysis

Top Keywords

phenylephrine small
8
small molecule
8
pectin methylesterases
8
pme
8
plant growth
8
root hair
8
molecule inhibits
4
pectin
4
inhibits pectin
4
methylesterases pectin
4

Similar Publications

Article Synopsis
  • Apigenin, a flavonoid thought to benefit cardiovascular health, was studied for its effects on vascular function in Spontaneously Hypertensive Rats (SHRs) to understand its mechanisms of action.
  • Vascular beds from SHRs were tested with varying doses of apigenin, showing that its ability to lower blood pressure depended on the presence of endothelial cells and was significantly reduced by inhibitors of nitric oxide and potassium channels.
  • The research concluded that apigenin causes vasodilation primarily through endothelial nitric oxide and calcium-activated potassium channels, suggesting its potential for therapeutic use in cardiovascular diseases and the need for more clinical studies.
View Article and Find Full Text PDF

Functional bias of contractile control in mouse resistance arteries.

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 PDF

PFKP inhibition protects against pathological cardiac hypertrophy by regulating protein synthesis.

Biochim 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 PDF

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 PDF

The functional role of m6A demethylase ALKBH5 in cardiomyocyte hypertrophy.

Cell 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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!