Rat atrial natriuretic factor (ANF) is translated as a 152-amino acid precursor preproANF. PreproANF is converted to the 126-amino acid proANF, the storage form of ANF in the atria. ANF isolated from the blood is approximately 25 amino acids long. It is demonstrated here that rat cardiocytes in culture store and secrete proANF. Incubation of proANF with serum produced a smaller ANF peptide. PreproANF seems to be processed to proANF in the atria, and proANF appears to be released into the blood, where it is converted by a protease to a smaller peptide.
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http://dx.doi.org/10.1126/science.2933808 | DOI Listing |
Cells
January 2025
Institute of Anatomy & Cell Biology, Faculty of Medicine, Justus-Liebig-University, Aulweg 123, 35392 Giessen, Germany.
Vascular smooth muscle cell (SMC) relaxation by guanylyl cyclases (GCs) and cGMP is mediated by NO and its receptor soluble GC (sGC) or natriuretic peptides (NPs) ANP/BNP and CNP with the receptors GC-A and GC-B, respectively. It is commonly accepted that cultured SMCs differ from those in intact vessels. Nevertheless, cell culture often remains the first step for signaling investigations and drug testing.
View Article and Find Full Text PDFOrphanet J Rare Dis
January 2025
Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, 6-1 Kishibe-Shimmachi, Suita, Osaka, 564-8565, Japan.
Background: Transient receptor potential cation channel subfamily V member 2 (TRPV2) functions as a stretch-sensitive calcium channel, with overexpression in the sarcolemma of skeletal and cardiac myocytes leading to detrimental calcium influx and triggering muscle degeneration. In our previous pilot study, we showed that tranilast, a TRPV2 inhibitor, reduced brain natriuretic peptide levels in two patients with muscular dystrophy and advanced heart failure. Building on this, we performed a single-arm, open-label, multicenter study herein to evaluate the safety and efficacy of tranilast in the treatment of advanced heart failure in patients with muscular dystrophy.
View Article and Find Full Text PDFCommun Biol
January 2025
Obsidian Therapeutics, Cambridge, MA, USA.
Adoptive cell therapies (ACT) have shown reduced efficacy against solid tumor malignancies compared to hematologic malignancies, partly due to the immunosuppressive nature of the tumor microenvironment (TME). ACT efficacy may be enhanced with pleiotropic cytokines that remodel the TME; however, their expression needs to be tightly controlled to avoid systemic toxicities. Here we show T cells can be armored with membrane-bound cytokines with surface expression regulated using drug-responsive domains (DRDs) developed from the 260-amino acid protein human carbonic anhydrase 2 (CA2).
View Article and Find Full Text PDFBackground: N-terminal brain natriuretic peptide (NTproBNP) is a marker of cardiac health and a strong predictor of mortality, incident cardiovascular disease (CVD), and sudden cardiac death in community populations. A link between the menopause transition (MT), sex hormones, and NTproBNP has been suggested, though, no studies have formally examined how NTproBNP changes over the MT. In addition of being a marker of cardiac health, studies suggest NTproBNP to be related to cognitive performance, yet those studies have not considered the MT.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Background: Subclinical cardiovascular disease (CVD), assessed by high-sensitivity cardiac troponin T (hs-cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), is linked to cognitive decline, but the associations in hypertensive adults and the underlying brain pathologies remain unclear. It is also undetermined whether an intensive blood pressure treatment compared to a standard treatment may slow down cognitive decline associated with subclinical CVD.
Method: We conducted a post hoc analysis of the Systolic Blood Pressure Intervention Trial, where older adults with hypertension were randomized to an intensive treatment (systolic blood pressure (SBP) target of < 120 mm Hg) or standard treatment (< 140 mm Hg).
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