Abstract
Preterm premature rupture of membranes (pPROM) is a major cause of preterm birth. Recently, extracellular matrix-directed treatment is applied for wound healing. Here, we used a pregnant mouse model to test the efficacy of collagen type 1 gel for healing of the prematurely ruptured fetal membranes. Although injection of PBS into the ruptured fetal membranes resulted in 40% closure, injection of collagen type 1 improved closure rates to 90% within 72 h. Macrophages of the M2 wound healing phenotype were entrapped in the collagen layer. In primary human amnion mesenchymal cells, collagen type 1 gels activated collagen receptor discoidin domain receptor 2 (DDR2) to induce myosin light chain phosphorylation and migration of injured amnion mesenchymal cells. These findings define the mechanisms for matrix-directed therapeutics for pPROM.
Highlights
Preterm labor is the leading cause of perinatal morbidity and mortality[1]
This accelerated healing was accompanied by entrapment of arginase-1-positive macrophages and enhanced migration of amnion mesenchymal cells mediated by activation of motor protein, myosin, via collagen receptor, discoidin domain receptor 2 (DDR2)
Fetal membranes were ruptured with a 20 G needle (ø 0.91 mm, one puncture per gestational sac), and 20 μl of type 1 collagen gel (2 mg/ml) or phosphate buffered saline (PBS) was injected at the ruptured site between myometrium and fetal membranes
Summary
Preterm premature rupture of membrane (pPROM) is defined as the rupture of membrane occurring before 37 weeks of gestation, which is associated with 30–40% of preterm deliveries and occurs in approximately 1–3% of all pregnancies[2]. Using our mouse pPROM model, we found that injection of collagen gel into the ruptured site dramatically accelerated closure rates of amnion from 40 to 90%. This accelerated healing was accompanied by entrapment of arginase-1-positive macrophages and enhanced migration of amnion mesenchymal cells mediated by activation of motor protein, myosin, via collagen receptor, discoidin domain receptor 2 (DDR2)
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