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Regulation of Cyclic Guanosine Monophosphate-Dependent Protein Kinase in Human Uterine Tissues During the Menstrual Cycle¹

^a Department of Pathology, ^b Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019 Department of Physiology and Biophysics, ^c University of Illinois at Chicago, Chicago, Illinois 60612-7342 Department of Pathology, ^d Oregon Health Sciences University, Portland, Oregon 97201-3098 ProPath Laboratory, Inc., ^e Dallas, Texas 75207-4009 Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9032

ABSTRACT

Contractility of uterine smooth muscle is essential for the cyclic shedding of the endometrial lining and also for expulsion of the fetus during parturition. The nitric oxide (NO)-cGMP signaling pathway is involved in smooth muscle relaxation. The downstream target of this pathway essential for decreasing cytoplasmic calcium and muscle tone is the cGMP-dependent protein kinase (PKG). The present study was undertaken to localize expression of PKG in tissues of the female reproductive tract and to test the hypothesis that uterine smooth muscle PKG levels vary with the human menstrual cycle. Immunohistochemistry was used to localize PKG in myometrium, cervix, and endometrium obtained during proliferative and secretory phases. The PKG was localized to uterine and vascular smooth muscle cells in myometrium, stromal cells in endometrium, and a small percentage of cervical stromal cells. Using Western blot analysis and protein kinase activity assays, the expression of PKG was reduced significantly in progesterone-dominated uteri compared with myometrium from postmenopausal women or women in the proliferative phase. These findings support a role for PKG in the control of uterine and vascular smooth muscle contractility during the menstrual cycle.

FOOTNOTES

First decision: 22 May 2000.

¹ This study was supported by grants NIH HD32622 (T.L.C.), NIH P01-HD11149 (R.A.W.), and NIH HL59618 (P.deL.).

² Correspondence: Trudy L. Cornwell, Department of Pathology, VH Room G019, University of Alabama at Birmingham, 1670 University Blvd., Birmingham, AL 35294-0019. FAX: 205 934 1775; cornwell{at}path.uab.edu

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