Regulation of fibroblast growth factor 8 (<i>FGF8</i>) in chicken embryonic stem cells differentiation into spermatogonial stem cells

Wang, Man; Zhang, Chen; Huang, Chuanli; Cheng, Shaoze; He, Na; Wang, Yilin; Ahmed, Mahmoud F.; Zhao, Ruihua; Jin, Jing; Zuo, Qisheng; Zhang, Yani; Li, Bichun

doi:10.1002/jcb.26402

Cited by 7 publications

(8 citation statements)

References 28 publications

(67 reference statements)

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“…In this study, we noted that MAPK1 expression changes caused corresponding changes in the ERK and WNT signaling pathways, suggesting that LncPGCAT‐1 and gga‐mir‐1591 regulate MAPK signaling via MAPK1 (Figure 5e). Furthermore, in a previous study, we demonstrated that activated MAPK (upregulated ERK) promotes PGC formation (M. Wang et al, 2018). To further demonstrate the relationship between LncPGCAT‐1 , gga‐mir‐1591, MAPK1 , and MAPK signals, we performed a rescue experiment (Figure 5b–d).…”

Section: Resultsmentioning

confidence: 71%

P53 and H3K4me2 activate N6‐methylated LncPGCAT‐1 to regulate primordial germ cell formation via MAPK signaling

Zuo

Jin

Zhou

et al. 2020

Journal Cellular Physiology

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Long noncoding RNAs (lncRNAs) participate in the formation of primordial germ cells (PGCs); however, the identity of the key lncRNAs and the molecular mechanisms responsible for the formation of PGCs remain unknown. Here, we identify a key candidate lncRNA (lncRNA PGC transcript‐1, LncPGCAT‐1) via RNA sequencing of embryonic stem cells, PGCs, and Spermatogonial stem cells (SSCs). Functional experiments confirmed that LncPGCAT‐1 positively regulated the formation of PGCs by elevating the expression of Cvh and C‐kit while downregulating the pluripotency(Nanog) in vitro and in vivo; PAS staining of genital ridges in vivo also showed that interference with LncPGCAT‐1 can significantly reduce the number of PGCs in genital ridges, while overexpression of LncPGCAT‐1 had the opposite result. The result of luciferase reporter assay combined with CHIP‐qPCR showed that the expression of LncPGCAT‐1 was promoted by the transcription factor P53 and high levels of H3K4me2. Mechanistically, the luciferase reporter assay confirmed that mitogen‐activated protein kinase 1 (MAPK1) was the target gene of LncPGCAT‐1 and gga‐mir‐1591. In the ceRNA system, high levels of N6 methylation of LncPGCAT‐1 enhanced the adsorption capacity of LncPGCAT‐1 for gga‐mir‐1591. Adsorption of gga‐mir‐1591 activated the MAPK1/ERK signaling cascade by relieving the gga‐mir‐1591‐dependent inhibition of MAPK1 expression. Moreover, LncPGCAT‐1 interacted with interleukin enhancer binding factor 3 (ILF3) to regulate the ubiquitination of P53 and phosphorylation of JNK. Interaction with ILF3 resulted in positive self‐feedback regulation of LncPGCAT‐1 and activation of JNK signaling, ultimately promoting PGC formation. Altogether, the study expands our knowledge of the function and molecular mechanisms of lncRNAs in PGC development.

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Section: Resultsmentioning

confidence: 71%

P53 and H3K4me2 activate N6‐methylated LncPGCAT‐1 to regulate primordial germ cell formation via MAPK signaling

Zuo

Jin

Zhou

et al. 2020

Journal Cellular Physiology

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“…FGFs play an important role in various developmental processes of chicken embryos [16,17] and in embryonic stem cell differentiation and primordial germ cells through the activation of MAPK/ERK signaling pathways [3,14]. Several chicken FGFs have been identified and functionally characterized, including FGF1 [2], FGF2, FGF4 [12,13], FGF8 [14], FGF12-13 [15],…”

Section: Discussionmentioning

confidence: 99%

“…Several FGFs have been isolated and well-characterized in chickens, including FGF1 [2], FGF2, FGF4 [12,13], FGF8 [14], FGF12-13 [15], and FGF19 [16]. These genes play important roles in various developmental processes of chicken embryos [16,17] and in embryonic stem cell differentiation and primordial germ cells through the activation of MAPK/ERK signaling pathways [3,14]. However, the FGF gene family in chickens still lacks identification and information on genome structure, physicochemical properties, and phylogenetic relationships.…”

Section: Introductionmentioning

confidence: 99%

Genome‑wide identification, organization, and expression profiles of the chicken fibroblast growth factor genes in public databases and Vietnamese indigenous Ri chickens against highly pathogenic avian influenza H5N1 virus infection

et al. 2023

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Objectives: Fibroblast growth factors (FGFs) play critical roles in embryo development, and immune responses to infectious diseases. In this study, to investigate the roles of FGFs, we performed genome-wide identification, expression, and functional analyses of FGF family members in chickens.Methods: Chicken FGFs genes were identified and analyzed by using bioinformatics approach. Expression profiles and Hierarchical cluster analysis of the FGFs genes in different chicken tissues were obtained from the genome-wide RNA-seq.Results: A total of 20 FGF genes were identified in the chicken genome, which were classified into seven distinct groups (A-F) in the phylogenetic tree. Gene structure analysis revealed that members of the same clade had the same or similar exon-intron structure.Chromosome mapping suggested that FGF genes were widely dispersed across the chicken genome and were located on chromosomes 1, 4-6, 9-10, 13, 15, 28, and Z. In addition, the interactions among FGF proteins and between FGFs and MAPK proteins are limited, indicating that the remaining functions of FGF proteins should be further investigated in chickens. KEGG pathway analysis showed that FGF gene interacts with MAPK genes and are involved in stimulating signaling pathway and regulating immune responses. Furthermore, this study identified 15 differentially expressed genes (DEG) in 21 different growth stages during early chicken embryo development. RNA-sequencing data identified the DEG of FGFs on 1-and 3-days post infection in two indigenous Ri chicken lines infected with the highly pathogenic avian influenza virus H5N1 (HPAIV). Finally, all the genes examined through qRT-PCR and RNA-Seq analyses showed similar responses to HPAIV infection in indigenous Ri chicken lines (R 2 = 0.92-0.95, p < 0.01).

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“…To date, a series of paracrine molecules excreted by MSCs have been discovered, including cytokines, growth factors, exosomes, and non-coding RNAs. Many of them are involved in the regulation of MAPK/ERK signaling pathway (Table 3) [45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62]. Of these, ERBB4, Spred1, miR-125b, HOTAIRM1-1, and miR-133a are negative regulators, while HIF-2α, IGF-1, TGF-β3, bFGF, VEGF, BDNF, METTL1, FGF8, IGF-1, SCGF-beta, HGF, MCP-1, miR-126, SMSCs-126-Exos, ApoE, IL-8, and IL-6 are positive regulators.…”

Section: Discussionmentioning

confidence: 99%

Human umbilical cord-derived mesenchymal stem cells not only ameliorate blood glucose but also protect vascular endothelium from diabetic damage through a paracrine mechanism mediated by MAPK/ERK signaling

et al. 2022

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Background Endothelial damage is an initial step of macro- and micro-vasculature dysfunctions in diabetic patients, accounting for a high incidence of diabetic vascular complications, such as atherosclerosis, nephropathy, retinopathy, and neuropathy. However, clinic lacks effective therapeutics targeting diabetic vascular complications. In field of regenerative medicine, mesenchymal stem cells, such as human umbilical cord-derived MSCs (hucMSCs), have great potential in treating tissue damage. Methods To determine whether hucMSCs infusion could repair diabetic vascular endothelial damage and how it works, this study conducted in vivo experiment on streptozotocin-induced diabetic rat model to test body weight, fasting blood glucose (FBG), serum ICAM-1 and VCAM-1 levels, histopathology and immunohistochemical staining of aorta segments. In vitro experiment was further conducted to determine the effects of hucMSCs on diabetic vascular endothelial damage, applying assays of resazurin staining, MTT cell viability, wound healing, transwell migration, and matrigel tube formation on human umbilical vein endothelial cells (HUVECs). RNA sequencing (RNAseq) and molecular experiment were conducted to clarify the mechanism of hucMSCs. Results The in vivo data revealed that hucMSCs partially restore the alterations of body weight, FBG, serum ICAM-1 and VCAM-1 levels, histopathology of aorta and reversed the abnormal phosphorylation of ERK in diabetic rats. By using the conditioned medium of hucMSCs (MSC-CM), the in vitro data revealed that hucMSCs improved cell viability, wound healing, migration and angiogenesis of the high glucose-damaged HUVECs through a paracrine action mode, and the altered gene expressions of IL-6, TNF-α, ICAM-1, VCAM-1, BAX, P16, P53 and ET-1 were significantly restored by MSC-CM. RNAseq incorporated with real-time PCR and Western blot results clarified that high glucose activated MAPK/ERK signaling in HUVECs, while MSC-CM reversed the abnormal phosphorylation of ERK and overexpressions of MKNK2, ERBB3, MYC and DUSP5 in MAPK/ERK signaling pathway. Conclusions HucMSCs not only ameliorated blood glucose but also protected vascular endothelium from diabetic damage, in which MAPK/ERK signaling mediated its molecular mechanism of paracrine action. Our findings provided novel knowledge of hucMSCs in the treatment of diabetes and suggested a prospective strategy for the clinical treatment of diabetic vascular complications.

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Regulation of fibroblast growth factor 8 (FGF8) in chicken embryonic stem cells differentiation into spermatogonial stem cells

Cited by 7 publications

References 28 publications

P53 and H3K4me2 activate N6‐methylated LncPGCAT‐1 to regulate primordial germ cell formation via MAPK signaling

P53 and H3K4me2 activate N6‐methylated LncPGCAT‐1 to regulate primordial germ cell formation via MAPK signaling

Genome‑wide identification, organization, and expression profiles of the chicken fibroblast growth factor genes in public databases and Vietnamese indigenous Ri chickens against highly pathogenic avian influenza H5N1 virus infection

Human umbilical cord-derived mesenchymal stem cells not only ameliorate blood glucose but also protect vascular endothelium from diabetic damage through a paracrine mechanism mediated by MAPK/ERK signaling

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