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The intestinal epithelium undergoes fast turnover, and the villus length in the small intestine gradually decreases from the duodenum to the ileum. However, the underlying mechanisms remain poorly understood. In this study, we investigate the regulatory mechanism underlying the regional disparity of villus length. A progressive strengthening of BMP signaling from the duodenum to the jejunum and ileum establishes a signaling gradient, resulting in differences in the rates of cell proliferation and apoptosis. We show that BMP signaling regulates the survival of the small intestine epithelial cells by inhibiting integrin expression and thereby inducing cell apoptosis. Combined with mathematical modeling, our data reveal that BMP signaling provides positional cues and antagonizes Wnt signaling to control villus growth, while Wnt signaling promotes BMP signaling to counteract excessive proliferation, thus maintaining villus length. Our findings provide insights into the signaling dynamics governing epithelial turnover and villus length in the small intestine.
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http://dx.doi.org/10.1038/s41467-025-60643-2 | DOI Listing |
Pulm Circ
July 2025
Division of Pulmonary, Critical Care, and Sleep Medicine Tufts Medical Center Boston Massachusetts USA.
Pulmonary arterial hypertension (PAH) is characterized by vasoconstriction, proliferation, fibrosis, and microthrombosis of the pulmonary vasculature, which causes elevated pulmonary arterial pressure and vascular resistance leading to right ventricular failure and death. Previous treatments targeted three known pathways involved in the development of PAH: endothelin, nitric oxide, and prostacyclin. Dysfunctional signaling of the transforming growth factor-beta (TGF-β) family, via bone morphogenetic protein (BMP) receptor 2 and activin signaling, has also been implicated in PAH leading to the development of a new class of therapies.
View Article and Find Full Text PDFComp Biochem Physiol C Toxicol Pharmacol
September 2025
Department of Biological Sciences, Clemson University, Clemson, SC, USA; Clemson University Center for Human Genetics, Greenwood, SC, USA. Electronic address:
Tetrabromobisphenol A (TBBPA), a widely used flame retardant in textiles and electronics, poses toxicological risks through both environmental and indoor exposures. Biomonitoring studies have detected significant TBBPA levels in prenatal environments, including cord blood, raising concerns about developmental impacts. Using zebrafish as a model, this study addresses critical gaps in understanding how developmental TBBPA exposures perturb regulatory pathways that govern dorsoventral patterning.
View Article and Find Full Text PDFJ Proteome Res
September 2025
State Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China.
Shell matrix proteins (SMPs) are fundamental biological macromolecules for mollusk shell formation, yet fewer than 400 SMPs in mollusks have been previously identified, hindering our understanding of how mollusks construct and maintain their shells. Here, we identified 1689 SMPs in the Pacific oyster using three different mass spectrometry techniques, representing a significant methodological advancement in shell proteomics, enabling a 6.52-fold increase in SMP identification compared to previous studies.
View Article and Find Full Text PDFDev Biol
September 2025
Division of Endocrinology, Boston Children's Hospital, Boston, MA 02115 USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115 USA; Harvard Stem Cell Institute, 7 Divinity Ave, Cambridge, MA 02138 USA. Electronic address:
The mechanisms mediating endochondral bone formation remain incompletely understood. Here, we show that CXXC Finger Protein 1 (CFP1) is required for the onset of chondrogenesis during forelimb development. CFP1-deficient mesenchymal progenitor cells (LMPs) retain an immature molecular signature with elevated FGF and SHH signaling and repressed BMP signaling, in part, due to (1) reduced expression of type I BMP receptors, (2) reduced Smad1 protein levels and (3) an altered extracellular niche.
View Article and Find Full Text PDFAm J Hematol
September 2025
Nephrology Division and Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
The bone morphogenetic protein (BMP)-SMAD signaling pathway is central to regulating hepcidin, the master regulator of systemic iron homeostasis. We have previously demonstrated that BMP6, BMP2, and, to a lesser extent, BMP5 are the major ligands contributing to hepcidin and iron homeostasis regulation in vivo. Hemojuvelin (HJV) and homeostatic iron regulator (HFE) are hepcidin modulators that are mutated in hereditary hemochromatosis.
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