Silencing Cofilin‐1 blocks <scp>PDGF</scp>‐induced proliferation in eutopic endometrium of endometriosis patients

Wang, Danbo; Xu, Yan‐Jun; Chen, Peng; Chen, Ying-Han; Li, Yan

doi:10.1002/cbin.10093

Cited by 9 publications

(8 citation statements)

References 23 publications

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“…A number of studies have indicated that factors regulating actin cytoskeleton, can exert regulatory functions on cell proliferation. For example, Cofilin phosphorylation mediates proliferation in response to platelet-derived growth factor (PDGF) in rat aortic smooth muscle cells (Won et al, 2008), and inhibition of Cofilin-1 expression blocks PDGFinduced proliferation in endometrium (Wang et al, 2013). Conversely, ectopic-expression of of ADFs and Cofilin suppress the motility and proliferation of human lung cancer cells (Lee et al, 2005).…”

Section: Discussionmentioning

confidence: 98%

Inhibiting actin depolymerization enhances osteoblast differentiation and bone formation in human stromal stem cells

et al. 2015

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Remodeling of the actin cytoskeleton through actin dynamics is involved in a number of biological processes, but its role in human stromal (skeletal) stem cells (hMSCs) differentiation is poorly understood. In the present study, we demonstrated that stabilizing actin filaments by inhibiting gene expression of the two main actin depolymerizing factors (ADFs): Cofilin 1 (CFL1) and Destrin (DSTN) in hMSCs, enhanced cell viability and differentiation into osteoblastic cells (OB) in vitro, as well as heterotopic bone formation in vivo. Similarly, treating hMSC with Phalloidin, which is known to stabilize polymerized actin filaments, increased hMSCs viability and OB differentiation. Conversely, Cytocholasin D, an inhibitor of actin polymerization, reduced cell viability and inhibited OB differentiation of hMSC. At a molecular level, preventing Cofilin phosphorylation through inhibition of LIM domain kinase 1 (LIMK1) decreased cell viability and impaired OB differentiation of hMSCs. Moreover, depolymerizing actin reduced FAK, p38 and JNK activation during OB differentiation of hMSCs, while polymerizing actin enhanced these signaling pathways. Our results demonstrate that the actin dynamic reassembly and Cofilin phosphorylation loop is involved in the control of hMSC proliferation and osteoblasts differentiation.

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Section: Discussionmentioning

confidence: 98%

Inhibiting actin depolymerization enhances osteoblast differentiation and bone formation in human stromal stem cells

et al. 2015

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“…PDGF to dobrze znany czynnik odpowiedzialny za indukcję proliferacji wielu rodzajów komórek (32) . Syntetyzowany jest nie tylko przez płytki krwi, lecz także przez komórki endotelialne, fibroblasty czy komórki mięśni gładkich.…”

Section: Płytkopochodny Czynnik Wzrostu (Pdgf)unclassified

“…PDGF is a well-known factor responsible for inducing proliferation of many types of cells (32) . It is synthesized not only by blood platelets but also by endothelial cells, fibroblasts and smooth muscle cells.…”

Section: Platelet-derived Growth Factor (Pdgf)mentioning

confidence: 99%

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Is it possible to diagnose endometriosis at the level of endometrium?

Szubert¹,

Ziętara²,

Suzin³

2016

Curr. Gynecol. Oncol.

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Endometrium pacjentek z endometriozą charakteryzuje się inną ekspresją cytokin, czynników angiogennych i hormonalnych niż u kobiet zdrowych. Endometrioza występuje głównie u kobiet w wieku reprodukcyjnym, z częstością około 7-10%. Mimo wielu badań i hipotez dotyczących patogenezy nie wykryto dotychczas swoistego markera dla endometriozy. Złotym standardem diagnostycznym, zwłaszcza w przypadku postaci otrzewnowej, której nie udaje się uwidocznić w badaniu ultrasonograficznym, pozostaje laparoskopia. Inne formy endometriozy-jajnikową (torbiele czekoladowe) i głęboko naciekającą-można rozpoznać w badaniu ultrasonograficznym. Obecnie poszukuje się markerów, które w określonej kombinacji zapewniłyby maksymalną czułość i swoistość nieinwazyjnego wykrywania endometriozy, nawet we wczesnych stadiach. Czułość oznaczeń wykonywanych z krwi nie jest niestety satysfakcjonująca w odniesieniu do otrzewnowej postaci choroby. W artykule zaprezentowano potencjalne cele diagnostyczne-wybrane czynniki wykrywane w endometrium, czyli interleukinę 8, czynnik wzrostu śródbłonka naczyniowego, płytkopochodny czynnik wzrostu i czynnik wzrostu nerwów. Pobranie endometrium do badań jest łatwe i może być wykonywane ambulatoryjnie. Diagnozowanie z poziomu endometrium ułatwiłoby rozpoznawanie endometriozy i znacząco zmniejszyło koszty związane z koniecznością przeprowadzania laparoskopii.

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“…Additionally, Peng et al [10] suggested that the expression of GATA-3 in endometrial epithelial cells of women with endometriosis was higher than that of healthy women. Specially, it has been proposed that number of proliferating endothelial cells increase in the endometrium of endometriosis patients [11,12], which implies that the proliferation of endometrial cells is important in the patho-genesis of endometriosis. However, to our knowledge, the role of GATA-3 in the proliferation of endometrial cells has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

GATA-3 Stimulates Proliferation of Endometriotic Cells

2019

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Objectives: This study aimed to investigate whether there was a correlation between the expression of GATA binding protein 3 (GATA-3) and the proliferation of endometrium cells from women with endometriosis. Material and methods: Endometrial tissue was collected from 20 women with endometriosis (experimental group) and 10 women without endometriosis (control group). The primary endometrial cells were then cultured and identified. Each group of cells were further divided into four groups. The control group was divided into control-no treatment (C-N), control-negative control (C-NC, transfected with a scrambled siRNA negative control), control-lentiviral transfection control (C-LC) and control-GATA-3 lentiviral transfection (C-G3); the experimental group was divided into experiment-no treatment (E-N), experiment-negative control (E-NC), experiment-lentiviral transfection control (E-LC) and experiment-siGATA-3 lentiviral transfection (E-siG3). RT-PCR and western blot were used respectively to detect the endometrium cells' GATA-3 mRNA and protein expression. Further, Cell Counting Kit-8 was used to measure the endometrium cells' proliferation. Results: The relative expression of GATA-3 mRNA and protein in the E-N group was significantly higher than in the D-N group and E-siG3 group (P < 0.05). The relative cell proliferation rate in the C-G3 group at 48 h, 72 h and 96 h was significantly higher than in the C-N, C-NC and C-LC groups (P < 0.05), while in the experimental group, the proliferation rate of the E-siG3 group was significantly lower than in the E-N, E-NC and E-LC groups (P < 0.05). Conclusions: This study suggests the role of GATA-3 in promoting proliferation of endometrial cells; therefore, GATA-3 may play an essential role in the development of endometriosis.

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Silencing Cofilin‐1 blocks PDGF‐induced proliferation in eutopic endometrium of endometriosis patients

Cited by 9 publications

References 23 publications

Inhibiting actin depolymerization enhances osteoblast differentiation and bone formation in human stromal stem cells

Inhibiting actin depolymerization enhances osteoblast differentiation and bone formation in human stromal stem cells

Is it possible to diagnose endometriosis at the level of endometrium?

GATA-3 Stimulates Proliferation of Endometriotic Cells

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