Abnormal uterus with polycysts, accumulation of uterine prostaglandins, and reduced fertility in mice heterozygous for acyl-CoA synthetase 4 deficiency

Biochem Biophys Res Commun. 2001 Jun 22;284(4):993-7. doi: 10.1006/bbrc.2001.5065.


Arachidonate released by various stimuli is rapidly reesterified into membrane phospholipids initiated by acyl-CoA synthetase (ACS) and subsequent acyl-transfer reactions. ACS4 is an arachidonate-preferring enzyme abundant in steroidogenic tissues and postulated to modulate eicosanoid production. Female mice heterozygous for ACS4 deficiency become pregnant less frequently and produce small litters with extremely low transmission of the disrupted alleles. Striking morphological changes, including extremely enlarged uteri and lumina filled with numerous proliferative cysts of various sizes, were detected in ACS4+/- females. Furthermore, marked accumulation of prostaglandins was seen in the uterus of the heterozygous females. These results indicate that ACS4 modulates female fertility and uterine prostaglandin production.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / metabolism
  • Animals
  • Chimera
  • Coenzyme A Ligases / deficiency*
  • Coenzyme A Ligases / genetics
  • Crosses, Genetic
  • Cysts / enzymology
  • Cysts / genetics*
  • Cysts / physiopathology
  • Dinoprost / metabolism
  • Dinoprostone / metabolism
  • Female
  • Genotype
  • Heterozygote
  • Infertility, Female / enzymology
  • Infertility, Female / genetics*
  • Litter Size
  • Male
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Prostaglandins / metabolism*
  • Restriction Mapping
  • Sex Ratio
  • Uterine Diseases / enzymology
  • Uterine Diseases / genetics*
  • Uterine Diseases / physiopathology
  • Uterus / metabolism*


  • Prostaglandins
  • 6-Ketoprostaglandin F1 alpha
  • Dinoprost
  • Coenzyme A Ligases
  • Dinoprostone