Several plasma membrane associated functions have been shown to differ in rats fed a high lard, carbohydrate free diet (L rats) from those observed in preparations from rats fed a high glucose, fat free diet (G rats). To explore the possibility that differences in the lipid components of the plasma membranes might contribute to these functional changes, groups of rats were fed each diet for 5 days and the lipids of their plasma membranes were separated and analyzed. The major differences found were a greater cholesterol content in the plasma membranes from L rats compared to those of G rats (12.2 +/- 2.20 versus 7.8 +/- 1.40 mg/100 mg membrane protein) and more than twice as much phosphatidyl serine and phosphadidyl inositol in the plasma membranes of the former group. Of several variations in fatty acid distribution found in the phospholipid and neutral lipid fractions, the most notable quantitatively were an increase in phospholipid oleic acid (18:1) and a decrease in phospholipid stearic acid (18:0) in L rat plasma membranes. Whether these changes are related to altered membrane function is not known.
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http://dx.doi.org/10.1093/jn/109.2.193 | DOI Listing |
Leukemia
January 2025
Department of Pathology, Duke University School of Medicine, Durham, NC, 27710, USA.
Multiple myeloma (MM) remains an incurable hematological malignancy that necessitates the identification of novel therapeutic strategies. Here, we report that intracellular levels of very long chain fatty acids (VLCFAs) control the cytotoxicity of MM chemotherapeutic agents. Inhibition of VLCFA biosynthesis reduced cell death in MM cells caused by the proteasome inhibitor, bortezomib.
View Article and Find Full Text PDFNat Commun
January 2025
College of Pharmaceutical Sciences, National Key Laboratory of Advanced Drug Delivery and Release Systems, Zhejiang University, Hangzhou, China.
Nicotinamide (NAM), a main precursor of NAD+, is essential for cellular fuel respiration, energy production, and other cellular processes. Transporters for other precursors of NAD+ such as nicotinic acid and nicotinamide mononucleotide (NMN) have been identified, but the cellular transporter of nicotinamide has not been elucidated. Here, we demonstrate that equilibrative nucleoside transporter 1 and 2 (ENT1 and 2, encoded by SLC29A1 and 2) drive cellular nicotinamide uptake and establish nicotinamide metabolism homeostasis.
View Article and Find Full Text PDFPlant Mol Biol
January 2025
Graduate School of Science and Technology, Kumamoto University, 2-39-1 Kurokami, Chuo-Ku, Kumamoto, 860-8555, Japan.
The applicability of a deep learning model for the virtual staining of plant cell structures using bright-field microscopy was investigated. The training dataset consisted of microscopy images of tobacco BY-2 cells with the plasma membrane stained with the fluorescent dye PlasMem Bright Green and the cell nucleus labeled with Histone-red fluorescent protein. The trained models successfully detected the expansion of cell nuclei upon aphidicolin treatment and a decrease in the cell aspect ratio upon propyzamide treatment, demonstrating its utility in cell morphometry.
View Article and Find Full Text PDFThe human () gene encodes a plasma membrane protein SLC39A8 (ZIP8) that mediates the specific uptake of the metals Cd, Mn, Zn, Fe, Co, and Se Pathogenic variants within are associated with congenital disorder of glycosylation type 2 (CDG type II) or Leigh-like syndrome. However, numerous mutations of uncertain significance are also linked to different conditions or benign traits. Our study characterized 21 variants and measured their impact on protein localization and intracellular levels of Cd, Zn, and Mn We identified four variants that disrupt protein expression, five variants with high retention in the endoplasmic reticulum, and 12 variants with localization to the plasma membrane.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Université de Tours, Inserm UMR1327 ISCHEMIA Membrane Signalling and Inflammation in reperfusion injuries, Tours, France.
Pathological left ventricular remodeling is a complex process following an acute myocardial infarction, leading to architectural disorganization of the cardiac tissue. This phenomenon is characterized by sterile inflammation and the exaggerated development of fibrotic tissue, which is non-contractile and poorly conductive, responsible for organ dysfunction and heart failure. At present, specific therapies are lacking for both prevention and treatment of this condition, and no biomarkers are currently validated to identify at-risk patients.
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