Platelet-Derived Growth Factor C Is Upregulated in Human Uterine Fibroids and Regulates Uterine Smooth Muscle Cell Growth1

Suo, Guangli; Jiang, Yong; Cowan, Bryan D.; Wang, Jean Y. J.

doi:10.1095/biolreprod.109.076869

Cited by 26 publications

(30 citation statements)

References 29 publications

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“…EGF and PDGF seem to increase DNA synthesis and polyploidization in leiomyoma cells through transient activation of kinase pathways [95–97]. PDGF also modulates the rate of cell proliferation in myometrium and leiomyoma cells [98–100]. …”

Section: Pathogenesis Of Uterine Leiomyomamentioning

confidence: 99%

Uterine Fibroids: Pathogenesis and Interactions with Endometrium and Endomyometrial Junction

Ciavattini

Giuseppe

Stortoni

et al. 2013

Obstetrics and Gynecology International

171

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Uterine leiomyomas (fibroids or myomas) are benign tumors of uterus and clinically apparent in a large part of reproductive aged women. Clinically, they present with a variety of symptoms: excessive menstrual bleeding, dysmenorrhoea and intermenstrual bleeding, chronic pelvic pain, and pressure symptoms such as a sensation of bloatedness, increased urinary frequency, and bowel disturbance. In addition, they may compromise reproductive functions, possibly contributing to subfertility, early pregnancy loss, and later pregnancy complications. Despite the prevalence of this condition, myoma research is underfunded compared to other nonmalignant diseases. To date, several pathogenetic factors such as genetics, microRNA, steroids, growth factors, cytokines, chemokines, and extracellular matrix components have been implicated in the development and growth of leiomyoma. This paper summarizes the available literature regarding the ultimate relative knowledge on pathogenesis of uterine fibroids and their interactions with endometrium and subendometrial myometrium.

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Section: Pathogenesis Of Uterine Leiomyomamentioning

confidence: 99%

Uterine Fibroids: Pathogenesis and Interactions with Endometrium and Endomyometrial Junction

Ciavattini

Giuseppe

Stortoni

et al. 2013

Obstetrics and Gynecology International

171

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“…Studies have shown that growth factors can induce proliferation of leiomyoma cells. TGFB1 and PDGF increased leiomyoma cell proliferation in culture [106,107]. Leiomyoma cells grown subcutaneously and treated with PDGF grew larger tumors than untreated mice [107].…”

Section: Regulation Of Growth Factors and Their Receptors By Progestementioning

confidence: 99%

“…TGFB1 and PDGF increased leiomyoma cell proliferation in culture [106,107]. Leiomyoma cells grown subcutaneously and treated with PDGF grew larger tumors than untreated mice [107]. Furthermore, inhibiting PDGFR with lentiviral RNA reduced tumor size of subcutaneous leiomyoma lesions.…”

Section: Regulation Of Growth Factors and Their Receptors By Progestementioning

confidence: 99%

“…First, Suo et al [107] grew human leiomyoma xenografts, subcutaneously in Rag2−/−γc−/− double knock out female mice. Before grafting, a green fluorescence protein (GFP)-luciferase (LUC) fusion gene was introduced into leiomyoma cells using lentiviral-mediated gene transfer to allow for the monitoring of transplanted leiomyoma cells in mice using bioluminescence-based whole animal imaging.…”

Section: Animal Model Insights To Elucidate the Role Of Progesterone mentioning

confidence: 99%

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The role of progesterone signaling in the pathogenesis of uterine leiomyoma

Kim

Sefton

2012

Molecular and Cellular Endocrinology

162

120

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Uterine leiomyomas are benign tumors that originate from the myometrium. Evidence points to ovarian steroid hormones, in particular, progesterone as major promoters of leiomyoma development and growth. While progesterone action in leiomyomas involves the classical nuclear receptor effects on gene regulation, there is growing evidence that signaling pathways are directly activated by the progesterone receptor (PR) and that PR can interact with growth factor signaling systems to promote proliferation and survival of leiomyomas. Studies investigating the genomic and non-genomic actions of PR and its role in leiomyoma growth are summarized here. Studies testing various selective progesterone receptor modulators for the treatment of leiomyomas are also highlighted. An increased understanding of the mechanisms associated with progesterone-driven growth of leiomyomas is critical in order to develop more efficient and targeted therapies for this prevalent disease.

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“…As control for transduction efficiency, pLKO-TurboGFP was used. The plasmids were prepared to produce lentiviral particles as previously described [19]. Lentivirus titer determination was performed according to the manufacturer’s instructions (Open Biosystems, Huntsville, AL).…”

Section: Methodsmentioning

confidence: 99%

Induction of TAp73 by platinum-based compounds to overcome drug resistance in p53 dysfunctional chronic lymphocytic leukemia

Tonino

Mulkens

Laar

et al. 2015

Leukemia & Lymphoma

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In chronic lymphocytic leukemia (CLL), strategies to overcome drug resistance due to p53 dysfunction are highly needed. Platinum-based compounds such as cisplatinum (CDDP) are active in fludarabine-refractory CLL through a largely unknown mechanism. We analyzed the mechanism of action of CDDP in the context of p53 dysfunctionality. In vitro treatment with CDDP did not induce death in quiescent CLL cells, but did induce apoptosis in CD40-ligand (and CpG) stimulated and proliferating cells, irrespective of p53 function. In the p53 dysfunctional prolymphocytic cell-line MEC1, CDDP treatment resulted in apoptosis, cell cycle arrest and ABL1-dependent expression of TAp73, CDKN1A, PUMA and BID. TAp73 RNA-interference decreased sensitivity to CDDP. Finally, both in vitro stimulated CLL cells and lymph node (LN) derived CLL cells showed increased TAp73 expression in comparison with quiescent peripheral blood derived cells. Activity of CDDP may therefore be mediated by TAp73, especially in the context of activation such as occurs in the LN microenvironment.

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Platelet-Derived Growth Factor C Is Upregulated in Human Uterine Fibroids and Regulates Uterine Smooth Muscle Cell Growth1

Cited by 26 publications

References 29 publications

Uterine Fibroids: Pathogenesis and Interactions with Endometrium and Endomyometrial Junction

Uterine Fibroids: Pathogenesis and Interactions with Endometrium and Endomyometrial Junction

The role of progesterone signaling in the pathogenesis of uterine leiomyoma

Induction of TAp73 by platinum-based compounds to overcome drug resistance in p53 dysfunctional chronic lymphocytic leukemia

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