Water channel proteins, later called aquaporins, are transmembrane proteins that have as their main(specific) function the water transport across biological membranes. The first water channel protein (WCP), now called aquaporin 1, was identified or "seen" in situ (hence discovered) in the human red blood cell (RBC) membrane in 1985 by Benga's group (Cluj-Napoca, Romania). This was achieved by a very selective radiolabeling of RBC membrane proteins with the water transport inhibitor [203Hg]-p-chloromercuribenzene sulfonate (PCMBS), under conditions of specific inhibition. The presence and location of the WCP was discovered among the polypeptides migrating in the region of 35-60 kDa on the electrophoretogram of RBC membrane proteins. The work was first published in 1986 in Biochemistry and Eur. J. Cell Biol. and reviewed by Benga in several articles in 1988-2004. We have thus a world priority in the discovery of the first water channel in the RBC membrane, that was re-discovered by chance by the group of Agre (Baltimore, USA) in 1988, when they isolated a new protein from the RBC membrane, nick-named CHIP28 (channel-forming integral membrane protein of 28 kDa). However, in addition to the 28 kDa component, this protein had a 35-60 kDa glycosylated component, the one detected by Benga's group. Only in 1992 the Agre's group suggested that "it is likely that CHIP28 is a functional unit of membrane water channels". In 1993 CHIP28 was renamed aquaporin 1. Looking in retrospect, asking the crucial question, when was the first WCP, discovered, a fair and clear cut answer would be: the first WCP, now called aquaporin 1, was identified or "seen" (hence discovered) in situ in the human RBC membrane by Benga and coworkers in 1985. It was again "seen" when it was purified in 1988 and again identified when its water transport property was found byAgre's group in 1992. If we make a comparison with the discovery of New World of America, the first man who has "seen" a part, very small indeed, of The New Land was Columbus; later, others, including Amerigo Vespucci (from whom the name derived), have better "seen" and in the subsequent years many explorers discovered the complexity of the Americas. Consequently, the initial discovery of the first water channel by Benga's group must be properly credited; the omission of Gheorghe Benga from the 2003 Nobel Prize in Chemistry (half of which was awarded to Peter Agre "for the discovery of the water channels") was a new mistake in the award of Nobel Prizes. Benga's claim is presented on the web site of the Ad Astra Association (www.ad-astra.ro/benga). As can be seen on this site his recognition as a discoverer of the first water channel protein from the human RBC membrane is growing. Thousands of science-related professionals from hundreds of academic and research units, as well as participants in several international scientific events, have signed as supporters of Benga; his priority is also mentioned in several comments on the 2003 Nobel Prize as presented on the site.
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J Appl Physiol (1985)
January 2025
Medical Physics Graduate Program, Duke University, Durham, North Carolina, United States.
Hyperpolarized Xe MRI/MRS enables quantitative mapping of function in lung airspaces, membrane tissue, and red blood cells (RBCs) within the pulmonary capillaries. The RBC signal also exhibits cardiogenic oscillations that are reduced in pre-capillary pulmonary hypertension (PH). This effect is obscured in patients with concomitant defects in transfer from airspaces to RBCs, which increase RBC oscillation amplitudes.
View Article and Find Full Text PDFBioconjug Chem
January 2025
Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-5127, United States.
Red blood cells (RBCs) serve as natural transporters and can be modified to enhance the pharmacokinetics and pharmacodynamics of a protein cargo. Affinity targeting of Factor IX (FIX) to the RBC membrane is a promising approach to improve the (pro)enzyme's pharmacokinetics. For RBC targeting, purified human FIX was conjugated to the anti-mouse glycophorin A monoclonal antibody Ter119.
View Article and Find Full Text PDFBlood
January 2025
New York Blood Center, New York, New York, United States.
Babesiosis in sickle cell disease (SCD) is marked by severe anemia but the underlying red blood cell (RBC) rheological parameters remain largely undefined. Here, we describe altered RBC deformability from both primary (host RBC sickle hemoglobin mediated) and secondary changes (Babesia parasite infection mediated) to the RBC membrane using wild type AA, sickle trait AS and sickle SS RBCs. Our ektacytometry (LORRCA) analysis demonstrates that the changes in the host RBC bio-mechanical properties, pre- and post- Babesia infection, reside on a spectrum of severity, with wild type infected AA cells, despite showing a significant reduction of deformability under both shear and osmolarity gradients, exhibiting only a mild phenotype; compared to infected AS RBCs which show median changes in deformability and infected SS RBCs which exhibit the most dramatic impact of infection on cellular rheology, including an increase in Point of Sickling values.
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January 2025
Departamento de Biofísica e Radiobiologia, Universidade Federal de Pernambuco, Recife, Pernambuco 50670-901, Brazil. Electronic address:
Mannose-binding lectin (MBL) is an important glycoprotein of the human innate immune system. Furthermore, individuals with sickle cell anemia (SCA) and MBL deficiency seem more susceptible to vaso-occlusive crises, suggesting an MBL role on HbSS red blood cells (RBCs). This study investigated the interaction of MBL with HbA (healthy) and HbSS RBCs using optical tweezers (OT) and atomic force microscopy (AFM).
View Article and Find Full Text PDFFront Bioeng Biotechnol
January 2025
Department of Rheumatology and Immunology, The Third Affiliated Hospital of Southern Medical University, Institute of Clinical Immunology, Academy of Orthopedics, Guangzhou, Guangdong, China.
Introduction: Uricase replacement therapy is a promising approach for managing hyperuricemia and gout but is hindered by challenges such as short blood circulation time, reduced catalytic activity, and excessive hydrogen peroxide (HO) production. These limitations necessitate innovative strategies to enhance therapeutic efficacy and safety.
Methods: We designed and synthesized RBC@SeMSN@Uri, a red blood cell-coated biomimetic self-cascade bioreactor, which encapsulates uricase (Uri) and a selenium-based nano-scavenger (SeMSN) within RBC membranes.
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