This study demonstrates the existence of calcium channels in the apical membranes of the hepatopancreatic blister (B) cells of Marsupenaeus japonicus. Using brush-border membrane vesicles we demonstrated that the channel-mediated calcium passive flux was saturable and was stimulated by a transmembrane electrical potential difference and inhibited by barium. We raised a monoclonal antibody (Mab 24A4) against the calcium channel, which allowed us to inhibit the channel-mediated calcium uptake. By immunocytochemistry, using Mab 24A4, we demonstrated that these channels are located at the apical membrane of hepatopancreatic B cells. Finally, by measuring the calcium uptake in R- and B-enriched cell suspensions, we showed that only the plasma membrane of the B cells expresses a channel-mediated calcium uptake inhibited by barium, verapamil and the monoclonal antibody 24A4. The plasma membrane of R cells did not show calcium channels.
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http://dx.doi.org/10.1007/s00360-003-0375-3 | DOI Listing |
Front Pharmacol
January 2025
Department of Cardiovascular Center, First Affiliated Hospital of Huzhou University, Huzhou, China.
The emergence of targeted anti-tumor drugs has significantly prolonged the lifespan and improved the prognosis of cancer patients. Among these drugs, vascular endothelial growth factor (VEGF) inhibitors, particularly novel small molecule tyrosine kinase inhibitors (TKIs), are extensively employed as VEGF inhibitors; however, they are also associated with a higher incidence of complications, with hypertension being the most prevalent cardiovascular toxic side effect. Currently, it is widely accepted that TKIs-induced hypertension involves multiple mechanisms including dysregulation of the endothelin (ET) axis, reduced bioavailability of nitric oxide (NO), imbalance in NO-ROS equilibrium system, vascular rarefaction, and activation of epithelial sodium calcium channels; nevertheless, excessive activation of ET system appears to be predominantly responsible for this condition.
View Article and Find Full Text PDFNeurotherapeutics
January 2025
Departamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Chile. Electronic address:
Acute brain injuries (ABIs) encompass a broad spectrum of primary injuries such as ischemia, hypoxia, trauma, and hemorrhage that converge into secondary injury where some mechanisms show common determinants. In this regard, astroglial connexin and pannexin channels have been shown to play an important role. These channels are transmembrane proteins sharing similar topology and form gateways between adjacent cells named gap junctions (GJs) and pores into unopposed membranes named hemichannels (HCs).
View Article and Find Full Text PDFRedox Biol
January 2025
Laboratory for Research in Functional Nutrition, Instituto de Nutrición y Tecnología de los Alimentos, Universidad de Chile, Av. El Líbano 5524, Macul, Santiago, 7830490, Chile. Electronic address:
Caffeic acid phenethyl ester (CAPE) is a hydrophobic phytochemical typically found in propolis that acts as an antioxidant, anti-inflammatory and cardiovascular protector, among several other properties. However, the molecular entity responsible for recognising CAPE is unknown, and whether that molecular interaction is involved in developing an antioxidant response in the target cells remains an unanswered question. Herein, we hypothesized that a subfamily of TRP ion channels works as the molecular entity that recognizes CAPE at the plasma membrane and allows a fast shift in the antioxidant capacity of intact endothelial cells (EC).
View Article and Find Full Text PDFJ Venom Anim Toxins Incl Trop Dis
January 2025
School of Health Santa Casa BH, Belo Horizonte, MG, Brazil.
Background: This study examines the impact of Phα1β, a spider peptide derived from the venom of , on the Kv11.1 potassium channel in HEK293 cells transfected with the human ERG potassium channel. Phα1β inhibits high-voltage calcium channels and acts as an antagonist of the TRPA1 receptor, both of which play crucial roles in pain transduction pathways.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
Key Laboratory of Fermentation Engineering (Ministry of Education), Cooperative Innovation Center of Industrial Fermentation (Ministry of Education & Hubei Province), National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Glyn O. Phillips Hydrocolloid Research Centre at HBUT, School of Life and Health Sciences, Hubei University of Technology, Wuhan, 430068, China; Ministry-of-Education Key Laboratory for the Green Preparation and Application of Functional Materials, Hubei Key Laboratory of Polymer Materials, College of Health Science and Engineering, School of Materials Science and Engineering, Hubei University, Wuhan 430062, China. Electronic address:
Calcium-based nanomaterials-mediated Ca overload-induced pyroptosis and its application in tumor therapy have received considerable attention. However, the calcium buffering capacity of tumor cells can maintain mitochondrial calcium homeostasis, so it is important to effectively disrupt this homeostasis to activate pyroptosis. Here, a nano-modulator CUR@CaCO-PArg@HA (CCAH) was developed to regulate calcium overload in multiple channels and activate pyroptosis.
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