Journal of Developmental Medicine(Electronic Version)  2020, Vol. 8 Issue (4): 308-312 DOI: 10.3969/j.issn.2095-5340.2020.04.004 |
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ADAMTS L1 may increase the preterm birth by regulating apoptosis of amniotic membrane cell through interleukin-6
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| Li Wen, Li Shanshan, Shen Yongmei, et al
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Tianjin Key Laboratory of Human Development and Reproductive Regulation Prenatal Diagnosis Center, Tianjin Central Hospital of Obstetrics Gynecology, Tianjin 300100, China
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Abstract
【Abstract】 Objective To study whether a disintegrin-like and metalloproteinase with thrombospondin L1(ADAMTS L1) affects the apoptosis of amniotic membrane cells by participating in the process of interventional recombination, thereby becoming a potential factor of preterm birth. Methods First, we collected 20 placental tissues of full-term birth (FTB) and spontaneous premature birth (PTB)，and divided them into FTB group(10 cases) and PTB group(10 cases). QRT-PCR and Western blot were used to detect the mRNA and protein levels of ADAMTS L1 and interleukin-6 (IL-6) . Then we activated THP-1 cell line by PMA to simulate the metabolic environment in vivo. ADAMTS L1 was knocked down by lentivirus in WISH cell line (knocked down group), mRNA and protein levels of ADAMTSL1 and IL-6 were detected, and the data of knocked down group were compared with control group.
Results The expression of ADAMTS L1 in preterm tissues was significantly increased, according to the full term birth women, the mRNA level of ADAMTSL1 and IL-6 increased 11 and 15 times respectively, the expression of ADAMTSL1 and IL-6 protein increased 9 and 12 times respectively. Knockdown of ADAMTS L1 reduced WISH cell apoptosis.Compared with the control group, after knocking down ADAMTS L1, the mRNA level of apoptosis-related protein caspase3 dropped to 0.35 of the control group, and the protein level dropped to 0.3 of the control group. Conclusion This study used in vitro experiments to evaluate that ADAMTS L1 may promote apoptosis of human IL-6 secreted by macrophages during inflflammation can regulate ADAMTS L1, which in turn can cause spontaneous preterm labor. However, further research is needed to confirm our findings.
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Received: 15 June 2020
Published: 03 November 2020
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