CXCR7 Inhibits Fibrosis via Wnt/<i>β</i>‐Catenin Pathways during the Process of Angiogenesis in Human Umbilical Vein Endothelial Cells

Shen, Meikun; Feng, Yifan; Wang, Jing; Yuan, Yuanzhi; Yuan, Fangyan

doi:10.1155/2020/1216926

Cited by 14 publications

(9 citation statements)

References 50 publications

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“…Notably, at 24 h, we observed a dose-dependent effect on wound healing, with the fastest migration occurring at 100 ng/mL, with a healing rate of 61.51% when compared to 37.50%, 53.81%, and 46.13% for the 0, 200, and 400 ng/mL groups, respectively. These finding are similar to those observed from Shen et al 66 Kuhlmann et al 67 identified that SDF-1 could promote endothelial cell migration by activating the Ca 2+ -activated K + channel with large conductance, therefore, it is likely a similar mechanism to enhance migration was activated in our study.…”

Section: Exploration Of the Optimum Loading Concentration Of Sdf-1supporting

confidence: 93%

“…Meanwhile, there was no statistical difference between the different SDF-1 concentrations tested (P > 0.05). Although Shen et al showed that 100 ng/mL SDF-1 could promote HUVECs proliferation within 24 h, 66 our result suggested that SDF-1 tended to stimulate HUVECs proliferation on the first day, and the effect was significant on the second and third day. These differential results may be due by different cell states, environments, and culture mediums used.…”

Section: Exploration Of the Optimum Loading Concentration Of Sdf-1contrasting

confidence: 92%

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SDF-1 Functionalized Hydrogel Microcarriers for Skin Flap Repair

Liu

Wang

et al. 2022

ACS Biomater. Sci. Eng.

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Critically sized skin flaps used to treat skin defects often suffer from necrosis due to insufficient blood supply. Hence there is an urgent need to improve the survival rate of skin flaps by promoting local angiogenesis. The delivery of growth factor loaded microcarriers have shown promise in enhancing defect repair, however, their rapid clearance from the defect site limits their regenerative potential. Thus, it is critical to develop microcarriers which can promote the sustained release of bioactive factors to effectively stimulate tissue repair. This study aimed to develop a stromal cell-derived factor 1 (SDF-1) loaded microcarrier coated with Matrigel (MC@SDF-1@Mat) to promote skin flap repair. SEM imaging showed that the surface of the microcarrier was coated by a porous Matrigel film. The drug release experiment showed that the Matrigel-coated microcarriers enhanced the sustained release of the model drug methylene blue when compared to uncoated group. MC@SDF-1@Mat significantly promoted the proliferation, migration, and angiogenesis of HUVECs via CCK-8, wound healing assay, and tube formation assay, respectively. Moreover, the murine random skin flap model was further established and treated. It was found that the flap necrosis area in the MC@SDF-1@Mat treated group was significantly reduced. H&E and Masson staining showed the histological structure and collagen organization exhibited a normal phenotype in the MC@SDF-1@Mat treated group. Additionally, CD31 immunohistochemical analysis showed that the MC@SDF-1@Mat treated group exhibited the greatest degree of neovascularization. In conclusion, our SDF-1 functionalized gelatin-based hydrogel microcarrier has potential clinical applications in promoting skin flap repair and drug delivery.

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Section: Exploration Of the Optimum Loading Concentration Of Sdf-1supporting

confidence: 93%

Section: Exploration Of the Optimum Loading Concentration Of Sdf-1contrasting

confidence: 92%

SDF-1 Functionalized Hydrogel Microcarriers for Skin Flap Repair

Liu

Wang

et al. 2022

ACS Biomater. Sci. Eng.

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“…Consistent with this, we found that CXCL12 activation of CXCR4 -but, interestingly, not CXCR7 -is required for CXCL12-induced upregulation of master transcription factor, Slug, which drives partial EndoMT during angiogenesis (Hultgren et al, 2020). By contrast, others have reported that CXCL12 activation of CXCR7 induces Wnt signaling to inhibit EndoMT-associated fibrosis (Shen et al, 2020).…”

Section: Regulatory Mechanisms That Govern the Endomt Program Signaling Pathways Regulating Endomtsupporting

confidence: 84%

Regulation of Partial and Reversible Endothelial-to-Mesenchymal Transition in Angiogenesis

Fang

Hultgren

Hughes

2021

Front. Cell Dev. Biol.

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During development and in several diseases, endothelial cells (EC) can undergo complete endothelial-to-mesenchymal transition (EndoMT or EndMT) to generate endothelial-derived mesenchymal cells. Emerging evidence suggests that ECs can also undergo a partial EndoMT to generate cells with intermediate endothelial- and mesenchymal-character. This partial EndoMT event is transient, reversible, and supports both developmental and pathological angiogenesis. Here, we discuss possible regulatory mechanisms that may control the EndoMT program to dictate whether cells undergo complete or partial mesenchymal transition, and we further consider how these pathways might be targeted therapeutically in cancer.

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“… 58 In a previous study, we reported that Wnt/β-catenin signaling suppression alleviates vascular fibrosis. 59 Together, the above findings suggest that Wnt/β-catenin signaling activation might play a critical role in CNV pathogenesis. Intriguingly, the Notum promoter was methylated and Wnt/β-catenin signaling was hyperactivated in laser-induced CNV tissues or VEGFA-stimulated ECs, as demonstrated above.…”

Section: Discussionmentioning

confidence: 82%

5-Aza-2′-Deoxycytidine Ameliorates Choroidal Neovascularization by Inhibiting the Wnt/β-Catenin Signaling Pathway

Wu,

Yang,

Dai

et al. 2024

Invest. Ophthalmol. Vis. Sci.

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Purpose Choroidal neovascularization (CNV) can constitute the final pathology of many ocular diseases and result in severe vision loss. Studies have demonstrated that DNA methylation is critical in retinal development, aging, and disorders. The current work investigated the effects and underlying mechanism of 5-Aza-2′-deoxycytidine (5-aza-dC), a suppressor of DNA methylation, in the pathological progression of CNV. Methods The DNA methylation profiles of retinal pigment epithelial (RPE)/choroidal complexes in normal and laser-induced CNV mice were assessed by Arraystar Mouse RefSeq Promoter Arrays. The CNV area and blood flow density and intensity were observed by optical coherence tomography angiography, and fluorescence leakage was examined by fundus fluorescein angiography in CNV mice with systemic administration of 5-aza-dC. The effects of 5-aza-dC on the biological functions of bEnd.3 cells were estimated by related assays. Notum gene promoter methylation was measured using bisulfite sequencing PCR. Methyltransferases and Wnt signaling-related genes were detected in animal and cell culture experiments by real-time PCR and immunoblot. Results Methyltransferases were upregulated, but Notum (a secretion inhibitor of Wnt signaling) was downregulated in the RPE/choroidal complexes of mice with experimental CNV. Intraperitoneal injection of 5-aza-dC inactivated the Wnt pathway and ameliorated the lesion area and the intensity and density of blood flow, as well as the degree of leakage in CNV. In vitro, vascular endothelial growth factor A (VEGFA) stimulation promoted methyltransferases expression and suppressed Notum expression, consequently activating Wnt signaling, whereas exogenous 5-aza-dC reversed VEGFA-induced hyperpermeability, proliferation, migration, and tube formation in bEnd.3 cells via demethylation of Notum promoter. Conclusions We observed that 5-aza-dC attenuates the growth of CNV by inhibiting the Wnt signaling pathway via promoter demethylation of the Wnt antagonist Notum. These findings provide a theoretical basis for methylation-based treatment with the Notum gene as a potential target for CNV treatment.

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CXCR7 Inhibits Fibrosis via Wnt/β‐Catenin Pathways during the Process of Angiogenesis in Human Umbilical Vein Endothelial Cells

Cited by 14 publications

References 50 publications

SDF-1 Functionalized Hydrogel Microcarriers for Skin Flap Repair

SDF-1 Functionalized Hydrogel Microcarriers for Skin Flap Repair

Regulation of Partial and Reversible Endothelial-to-Mesenchymal Transition in Angiogenesis

5-Aza-2′-Deoxycytidine Ameliorates Choroidal Neovascularization by Inhibiting the Wnt/β-Catenin Signaling Pathway

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