2000 Fiscal Year Final Research Report Summary
The basic study on new treatment for cervical maturation and preterm labor using cytokine
| Project/Area Number |
10671529
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Hamamatsu University School Of Medicine |
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Principal Investigator |
KANAYAMA Naohiro Hamamatsu Univ. School of Medicine, Dept. Obstet & Gynecol, Professor, 医学部, 教授 (70204550)
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| Co-Investigator(Kenkyū-buntansha) |
TOKUNAGA Naoki Hamamatsu Univ. School of Medicine, Dept. Obstet & Gynecol, Assistant, 医学部・附属病院, 助手 (20283369)
SUMIMOTO Kazuhiro Hamamatsu Univ. School of Medicine, Dept. Obstet & Gynecol, Assistant, 医学部, 助手 (30126817)
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| Project Period (FY) |
1998 – 2000
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| Keywords | Cervical maturation / Interleukin-8 / DHEA-S / Hyalaronic acid / Urinary trypsin inhibitor / IL-8 receptor / P57kip2 |
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| Research Abstract |
The aim of this research was to develop a new treatment for regulation of cervical maturation. In rabbit experiments suppositories with interleukin-8 (IL-8) produced a marked cervical maturation in various cytokine supppositories. Inteleukin-1 (IL-1) suppositories induced a prominent uterine contractions. Suppositories with IL-8+IL-1 produced contractile response with increased frequency. Our data suggest that IL-8 does not only induce cervical maturation, but it also stimulates IL-1 induced uterine contraction. IL-8 plays a key role in an important process during labor and delivery.
We also studied the modification factors to express IL-8. Dehydroepiandrosterone sulfate (DHEA-S) is produced from fetal adrenal grand during pregnancy. We found that DHEA-S stimulated the IL-8 expression. Its mechanism was mainly due to promotion of IL-8 receptor. Heparan sulfate accelerated cervical maturation through upregulation of autocrine system of IL-8. Hyaluronic acid especially low molecular hyaluronic acid activated IL-8 expression. From the aspects of clinical base seminal plasma stimulated the production of IL-8 from the cervical tissue. It suggests that sexual intercourse is a risk factor for preterm labor.
Urinary trypsin inhibitor (UTI) inhibited cervical maturation. Its mechanism is mainly ascribed to inhibition of IL-8 expression of cervical cells. UTI also inhibited uterine muscle contraction due to suppression of calcium influx. UTI concentration is extremely high in amniotic fluid. Fetus expelled UTI to amniotic fluid profoundly. Thus, UTI is a specific substance of fetus. UTI may open anew aspect for the treatment of preterm labor.
P57kip2 regulates G1 cyclin. We found that P57kip2 knock out mice occurred pretem delivery. P57kip2 showed a marked proliferation of trophoblasts. This P57kip2 knock out mice may give a new way for the research of preterm delivery
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