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. 2014 Sep;8(3):179-94.
doi: 10.1007/s12079-014-0234-x. Epub 2014 Jul 11.

Matrix production and remodeling as therapeutic targets for uterine leiomyoma

Caitlin Fujisawa  1 , John J Castellot Jr
Affiliations

Matrix production and remodeling as therapeutic targets for uterine leiomyoma

Caitlin Fujisawa et al. J Cell Commun Signal. 2014 Sep.

Abstract

Uterine leiomyoma, commonly known as fibroids, is a benign neoplasm of smooth muscle in women. The incidence of clinically symptomatic fibroids in reproductive-age women is approximately 20 %, with nearly 80 % of black women suffering from this condition. Symptoms include severe pain and hemorrhage; fibroids are also a major cause of infertility or sub-fertility in women. Uterine leiomyoma consist of hyperplastic smooth muscle cells and an excess deposition of extracellular matrix, specifically collagen, fibronectin, and sulfated proteoglycans. Extracellular matrix components interact and signal through integrin-β1 on the surface of uterine leiomyoma smooth muscle cells, provide growth factor storage, and act as co-receptors for growth factor-receptor binding. ECM and growth factor signaling through integrin-β1 and growth factor receptors significantly increases cell proliferation and ECM deposition in uterine leiomyoma. Growth factors TGF-β, IGF, PDGF, FGF and EGF are all shown to promote uterine leiomyoma progression and signal through multiple pathways to increase the expression of genes encoding matrix or matrix-modifying proteins. Decreasing integrin expression, reducing growth factor action and inhibiting ECM action on uterine leiomyoma smooth muscle cells are important opportunities to treat uterine leiomyoma without use of the current surgical procedures. Both natural compounds and chemicals are shown to decrease fibrosis and uterine leiomyoma progression, but further analysis is needed to make inroads in treating this common women's health issue.

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Figures

Fig. 1
Fig. 1
Collagen type 1 extracellular induction of intracellular cell progression and proliferation signals through AKAP13, RhoA, and MAPK/Erk1/2
Fig. 2
Fig. 2
Growth factor association with the ECM plays an integral role in cell cycle progression, cell proliferation and ECM deposition in UL SMC. Here MMP-2 degrades several ECM components, releasing growth factors to bind to their receptors. Several ECM components modulate growth factor binding to the respective receptor, such as HSPG with FGF, fibronectin with PDGF, and IGF to several ECM components
See this image and copyright information in PMC

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