ArticleProceedings of the National Academy of Sciences of the United States of America2012
Targeted disruption of Adamts16 gene in a rat genetic model of hypertension.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- TGFBI Maintains Fibrocartilage Homeostasis by Restraining O-GlcNAcylation to Inactivate and Destabilize ADAMTS16 in Temporomandibular Joint Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Current Advances in the Physiological Roles and Disease-Associated Mechanisms of ADAMTS16.International journal of molecular sciences · 2026Review
- A microfluidic platform integrating functional vascularized organoids-on-chip.Nature communications · 2024Article
- Six Decades of History of Hypertension Research at the University of Toledo: Highlighting Pioneering Contributions in Biochemistry, Genetics, and Host-Microbiota Interactions.Current hypertension reports · 2022Review
- A pan-cancer analysis of matrisome proteins reveals CTHRC1 and a related network as major ECM regulators across cancers.PloS one · 2022Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- ADAMTS Proteins and Vascular Remodeling in Aortic Aneurysms.Biomolecules · 2021Review
- RNO3 QTL regulates vascular structure and arterial stiffness in the spontaneously hypertensive rat.Physiological genomics · 2021Article
- DNA methylation differences associated with social anxiety disorder and early life adversity.Translational psychiatry · 2021Article
- Whole-genome screen identifies diverse pathways that negatively regulate ciliogenesis.Molecular biology of the cell · 2021Article
- ADAMTS proteases in cardiovascular physiology and disease.Open biology · 2020Review
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- Modularity/non-cumulativity of quantitative trait loci on blood pressure.Journal of human hypertension · 2020Review
- ADAMTS16 activates latent TGF-β, accentuating fibrosis and dysfunction of the pressure-overloaded heart.Cardiovascular research · 2020Article
- The secreted protease Adamts18 links hormone action to activation of the mammary stem cell niche.Nature communications · 2020Article
- Male mice lacking ADAMTS-16 are fertile but exhibit testes of reduced weight.Scientific reports · 2019Article
- Morphogenesis of the kidney and lung requires branch-tip directed activity of the Adamts18 metalloprotease.Developmental biology · 2019Article
- Secreted metalloproteases ADAMTS9 and ADAMTS20 have a non-canonical role in ciliary vesicle growth during ciliogenesis.Nature communications · 2019Article
- Blubber transcriptome responses to repeated ACTH administration in a marine mammal.Scientific reports · 2019Article
- Thick Ascending Limb Sodium Transport in the Pathogenesis of Hypertension.Physiological reviews · 2019Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
A disintegrin-like metalloproteinase with thrombospondin motifs-16 (Adamts16) is an important candidate gene for hypertension. The goal of the present study was to further assess the candidacy of Adamts16 by targeted disruption of this gene in a rat genetic model of hypertension. A rat model was generated by manipulating the genome of the Dahl Salt-sensitive (S) rat using zinc-finger nucleases, wherein the mutant rat had a 17 bp deletion in the first exon of Adamts16, introducing a stop codon in the transcript. Systolic blood pressure (BP) of the homozygous Adamts16(mutant) rats was lower by 36 mmHg compared with the BP of the S rats. The Adamts16(mutant) rats exhibited significantly lower aortic pulse wave velocity and vascular media thickness compared with S rats. Scanning electron and fluorescence microscopic studies indicated that the mechanosensory cilia of vascular endothelial cells from the Adamts16(mutant) rats were longer than that of the S rats. Furthermore, Adamts16(mutant) rats showed splitting and thickening of glomerular capillaries and had a longer survival rate, compared with the S rats. Taken together, these physiological observations functionally link Adamts16 to BP regulation and suggest the vasculature as the potential site of action of Adamts16 to lower BP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.