ArticleCommunications biology2024
ADAMTS4 is a crucial proteolytic enzyme for versican cleavage in the amnion at parturition.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Supplementation with long-chain polyunsaturated fatty acids to extremely preterm infants associates with development of the intestinal microbiota.Pediatric research · 2026Article
- ADAMTS4 is expressed in different cells and tissues in leprosy skin lesions: A potential biomarker and therapeutic target for leprosy and its reactional phenomena.Histology and histopathology · 2026Article
- IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.Cell communication and signaling : CCS · 2025Article
- ADAMTS4 Reduction Contributes to Extracellular Matrix Deposition and Impaired Myogenesis in the Skeletal Muscle of Cigarette Smoke-Exposed Mice.Biomedicines · 2025Article
- Loss of the Endothelial Glycocalyx Component EMCN Leads to Glomerular Impairment.Circulation research · 2025Article
- Advancing necrotizing enterocolitis prediction through iterative monitoring.Translational pediatrics · 2024Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Hyalectan cleavage may play an important role in extracellular matrix remodeling. However, the proteolytic enzyme responsible for hyalectan degradation for fetal membrane rupture at parturition remains unknown. Here, we reveal that versican (VCAN) is the major hyalectan in the amnion, where its cleavage increases at parturition with spontaneous rupture of membrane. We further reveal that ADAMTS4 is a crucial proteolytic enzyme for VCAN cleavage in the amnion. Inflammatory factors may enhance VCAN cleavage by inducing ADAMTS4 expression and inhibiting ADAMTS4 endocytosis in amnion fibroblasts. In turn, versikine, the VCAN cleavage product, induces inflammatory factors in amnion fibroblasts, thereby forming a feedforward loop between inflammation and VCAN degradation. Mouse studies show that intra-amniotic injection of ADAMTS4 induces preterm birth along with increased VCAN degradation and proinflammatory factors abundance in the fetal membranes. Conclusively, there is enhanced VCAN cleavage by ADAMTS4 in the amnion at parturition, which can be reenforced by inflammation.
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Registered trials
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.