Collagen-binding basic fibroblast growth factor improves functional remodeling of scarred endometrium in uterine infertile women: a pilot study

Jiang, Pengju; Tang, Xiaohu; Wang, Huiyan; Dai, Chenyan; Su, Jing; Zhu, Hui; Song, Minmin; Liu, Jingyu; Nan, Ziqing; Ru, Tong; Li, Yaling; Wang, Jingmei; Yang, Jun; Chen, Bing; Dai, Jianwu; Hu, Yali

doi:10.1007/s11427-018-9520-2

Cited by 43 publications

(45 citation statements)

References 64 publications

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“…The data in our present study showed that the pathogenesis of IUA involves EEC-EMT. Previously, we found the proliferation of endometrium is suppressed in ΔNp63α overexpressed endometrium 8 , and bFGF promotes the proliferation of endometrium and functionally reconstructs endometrium in rats and patients 29,30 . Therefore, we tried to study the relationship between bFGF and ΔNp63α-induced EEC-EMT.…”

Section: Bfgf Reverses δNp63α Induced Eec-emt In Vitromentioning

confidence: 90%

“…Recently, in vitro study showed that bFGF inhibits the transition of fibroblast to myofibroblast 39 . In the human, we previously demonstrated that bFGF has the activity against fibrosis in fibrotic endometria 29 . In the present study, the administration of bFGF in IUA-like mice improved the endometrial fibrosis while ΔNp63α and SNAI1 levels in EECs were reduced, and E-cadherin was increased and Ncadherin and a-SMA were decreased.…”

Section: Discussionmentioning

confidence: 99%

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ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis

Zhao

Cao

et al. 2020

Cell Death Dis

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Epithelial homeostasis plays an essential role in maintaining endometrial function. But the epithelial role in endometrial fibrosis has been less studied. Previously, we showed that ectopic expression of ΔNp63α is associated with fibrosis process and epithelial dysfunction in endometria of patients with intrauterine adhesions (IUAs). Since ΔNp63α is profoundly involved in maintaining the epithelial homeostasis, we hereby focused on its roles in regulating the function and phenotype of endometrial epithelial cells (EECs) in context of endometrial fibrosis. We identified a typical type 2 epithelial-to-mesenchymal transition (EMT) in EECs from IUA patients and this process was induced by the forced expression of ΔNp63α in EECs. In transcriptomic analysis, we found that diverse signaling pathways regulated by ΔNp63α were involved in pro-EMT. We demonstrated that the DUSP4/GSK-3β/SNAI1 pathway was critical in transducing the pro-EMT signals initiated by ΔNp63α, while bFGF reversed ΔNp63α-induced EMT and endometrial fibrosis both in vitro and in vivo by blocking DUSP4/GSK3β/SNAI1 pathway. Taken together, our findings are important to understand the molecular mechanisms of endometrial fibrosis and to provide potential therapeutic targets.

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Section: Bfgf Reverses δNp63α Induced Eec-emt In Vitromentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis

Zhao

Cao

et al. 2020

Cell Death Dis

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“…The GO analysis of 1,093 DEGs identified many genes that were significantly enriched in the cell adhesion process (GO: 0007155, P = 1.92E-10), negative regulation of growth (GO: 0045926, P = 4.46E-05), angiogenesis (GO: 0001525, P = 4.63E-05), cell junction assembly (GO: 0034329, P = 2.99E-04), negative regulation of cell migration (GO: 0030336, P = 7.39E-04), the Wnt signaling pathway (GO: 0016055, P = 0.0017), and negative regulation of the BMP signaling pathway (GO: 0030514, P = 0.003) ( Table 2 and Figure 1). A blockade angiogenesis was considered as the main pathological change in the scarred thin endometrium (Jiang et al, 2019). Moreover, this study identified several DEGs-related signaling pathways by performing KEGG pathway enrichment analysis, including the vascular smooth muscle contraction pathway, extracellular matrix-receptor interaction, focal adhesion, tight junction, cell adhesion molecules, calcium signal transduction pathway, p53 signal transduction pathway, and adherens junction pathway (Table 3 and Figure 2).…”

Section: Genome-wide Patterns Of the Mrna Transcriptomic Landscapementioning

confidence: 99%

Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

et al. 2021

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Although the thin endometrium (TE) has been widely recognized as a critical factor in implantation failure, the contribution of miRNA–mRNA regulatory network to the development of disease etiology remains to be further elucidated. This study performed an integrative analysis of the miRNA–mRNA expression profiles in the thin and adjacent normal endometrium of eight patients with intrauterine adhesion to construct the transcriptomic regulatory networks. A total of 1,093 differentially expressed genes (DEGs) and 72 differentially expressed miRNAs (DEMs) were identified in the thin adhesive endometrium of the TE group compared with the control adjacent normal endometrial cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that the DEGs and the target genes of DEM were significantly enriched in angiogenesis, cell growth regulation, and Wnt signaling pathway. Multiple hub genes (CAV1, MET, MAL2, has-mir-138, ARHGAP6, CLIC4, RRAS, AGFG1, has-mir-200, and has-mir-429) were identified by constructing the miRNA–mRNA regulatory networks. Furthermore, a miRNA–mRNA pathway function analysis was conducted, and the hub genes were enriched in the FoxO signaling pathway, cell growth regulation, inflammatory response regulation, and regulation of autophagy pathways. Our study is the first to perform integrated mRNA-seq and miRNA-seq analyses in the thin adhesive endometrium and the control adjacent normal endometrial cells. This study provides new insights into the molecular mechanisms underlying the formation of thin endometrium.

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“…Collagen, as the predominant protein in the mammalian extracellular matrix (ECM), provides structural support for maintaining tissue integrity and contributes to the specificity of the ECM microenvironment (Gelse et al, 2003) for cell adherence and amplification (Shi et al, 2011;Wang et al, 2007). Several properties of collagen, including its biocompatibility, adhesiveness, and biodegradability, have made it an appropriate natural scaffold material for applications in regenerative medicine (Jiang et al, 2019;Chiu et al, 2012;Gautam et al, 2014;Kijeńska et al, 2012;Perea-Gil et al, 2015;Xu et al, 2014). Collagen scaffolds have been used in cardiac tissue engineering and been shown to promote cardiac commitment, vascularization, and electrical coupling in different MI models (Perea-Gil et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Injectable collagen scaffold promotes swine myocardial infarction recovery by long-term local retention of transplanted human umbilical cord mesenchymal stem cells

Wang

et al. 2020

Sci. China Life Sci.

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Stem cell therapy is an attractive approach for recovery from myocardial infarction (MI) but faces the challenges of rapid diffusion and poor survival after transplantation. Here we developed an injectable collagen scaffold to promote the long-term retention of transplanted cells in chronic MI. Forty-five minipigs underwent left anterior descending artery (LAD) ligation and were equally divided into three groups 2 months later (collagen scaffold loading with human umbilical mesenchymal stem cell (hUMSC) group, hUMSC group, and placebo group (only phosphate-buffered saline (PBS) injection)). Immunofluorescence staining indicated that the retention of transplanted cells was promoted by the collagen scaffold. Echocardiography and cardiac magnetic resonance imaging (CMR) showed much higher left ventricular ejection fraction (LVEF) and lower infarct size percentage in the collagen/hUMSC group than in the hUMSC and placebo groups at 12 months after treatment. There were also higher densities of vWf-, α-sma-, and cTnT-positive cells in the infarct border zone in the collagen/cell group, as revealed by immunohistochemical analysis, suggesting better angiogenesis and more cardiomyocyte survival after MI. Thus, the injectable collagen scaffold was safe and effective on a large animal myocardial model, which is beneficial for constructing a favorable microenvironment for applying stem cells in clinical MI. injectable collagen scaffold, mesenchymal stem cell, MI

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Collagen-binding basic fibroblast growth factor improves functional remodeling of scarred endometrium in uterine infertile women: a pilot study

Cited by 43 publications

References 64 publications

ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis

ΔNp63α-induced DUSP4/GSK3β/SNAI1 pathway in epithelial cells drives endometrial fibrosis

Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

Injectable collagen scaffold promotes swine myocardial infarction recovery by long-term local retention of transplanted human umbilical cord mesenchymal stem cells

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