Pseudomonas aeruginosa is an opportunistic human pathogen causing severe acute and chronic infections. Earlier we have shown that calcium (Ca(2+)) induces P. aeruginosa biofilm formation and production of virulence factors. To enable further studies of the regulatory role of Ca(2+), we characterized Ca(2+) homeostasis in P. aeruginosa PAO1 cells. By using Ca(2+)-binding photoprotein aequorin, we determined that the concentration of free intracellular Ca(2+) ([Ca(2+)]in) is 0.14±0.05μM. In response to external Ca(2+), the [Ca(2+)]in quickly increased at least 13-fold followed by a multi-phase decline by up to 73%. Growth at elevated Ca(2+) modulated this response. Treatment with inhibitors known to affect Ca(2+) channels, monovalent cations gradient, or P-type and F-type ATPases impaired [Ca(2+)]in response, suggesting the importance of the corresponding mechanisms in Ca(2+) homeostasis. To identify Ca(2+) transporters maintaining this homeostasis, bioinformatic and LC-MS/MS-based membrane proteomic analyses were used. [Ca(2+)]in homeostasis was monitored for seven Ca(2+)-affected and eleven bioinformatically predicted transporters by using transposon insertion mutants. Disruption of P-type ATPases PA2435, PA3920, and ion exchanger PA2092 significantly impaired Ca(2+) homeostasis. The lack of PA3920 and vanadate treatment abolished Ca(2+)-induced swarming, suggesting the role of the P-type ATPase in regulating P. aeruginosa response to Ca(2+).
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http://dx.doi.org/10.1016/j.ceca.2013.08.004 | DOI Listing |
Cell Biosci
January 2025
State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Fudan University, Shanghai, 200438, People's Republic of China.
Background: Neuropathic pain resulting from spinal cord injury (SCI) is associated with persistent hyperactivity of primary nociceptors. Anandamide (AEA) has been reported to modulate neuronal excitability and synaptic transmission through activation of cannabinoid type-1 receptors (CB1Rs) and transient receptor potential vanilloid 1 (TRPV1). However, the role of AEA and these receptors in the hyperactivity of nociceptors after SCI remains unclear.
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January 2025
School of Forestry, Northeast Forestry University, Harbin 150040, PR China; Key Laboratory of Sustainable Forest Ecosystem Management-Ministry of Education, Northeast Forestry University, Harbin 150040, PR China. Electronic address:
The diversity of host plants is an important reason for the global spread of Hyphantria cunea. However, no studies have explored the role of the antioxidant defense system with catalase (CAT) as the core at the molecular level in the adaptation of the H. cunea to host plant secondary metabolites.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Psychiatry, University of Cambridge, Cambridge, UK.
Background: Combinations of blood-based biomarkers have been used to detect Alzheimer's disease (AD). While these markers provide information about neuropathology, they fail to integrate the cellular dysfunction, such as disease-associated defects in lysosomal ion homeostasis. To understand cellular dysfunction in AD and its relation to the pathophysiology of the disease, we developed a multi-modal biomarker diagnostic platform that incorporates lysosomal ionic pH and Ca and plasma levels of Amyloid beta (Aβ), Amyloid beta (Aβ), phosphorylated Tau181 (pTau181), Neurofilament light (NfL) and Glial fibrillary acidic protein (GFAP).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky College of Medicine, Lexington, KY, USA.
Background: We have been investigating in vivo astrocytic Ca homeostasis in the primary somatosensory cortex (S1) of awake, head-restrained ambulating mice using two-photon technology. Prior results from our lab were obtained in neurons across aging, and in male and female C57Bl6/J mice (Case et al., 2023).
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January 2025
Univ. Lille, CNRS, UMR 8576 - UGSF - Unité de Glycobiologie Structurale Et Fonctionnelle, 59000, Lille, France.
Glycans are known to be fundamental for many cellular and physiological functions. Congenital disorders of glycosylation (CDG) currently encompassing over 160 subtypes, are characterized by glycan synthesis and/or processing defects. Despite the increasing number of CDG patients, therapeutic options remain very limited as our knowledge on glycan synthesis is fragmented.
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