Hyaluronic acid ameliorates the proliferative ability of human amniotic epithelial cells through activation of TGF-β/BMP signaling
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PROVIDER: PRJNA659755 | ENA |
REPOSITORIES: ENA
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Project description:Human amniotic epithelial cells (hAECs) are a useful and noncontroversial source of stem cells for cell therapy and regenerative medicine, but their limited proliferative ability hinders the acquisition of adequate quantities of cells for clinical use due to not expressing telomerase in hAECs. Our previous study showed that hyaluronic acid (HA), an important component of the extracellular matrix, promoted the proliferation of human amniotic mesenchymal stem cells. Herein, we hypothesize that HA might improve the proliferative capability of hAECs. In the present study, the role of HA on the proliferation of human amniotic epithelial cells (hAECs) in vitro was investigated for the first time. HA at molecular weight of 300 kDa showed an obvious pro-proliferation effect on hAECs. Furthermore, HA not only kept phenotypic characteristics and differentiation capabilities of hAECs, but significantly promoted the secretion of the anti-inflammatory factors such as IL-10 and TGF-β1, and the expression of stem cell pluripotent factors such as Oct4 and Nanog. Analysis of PCR microarray data and RT-qPCR validation showed that TGF-β/BMP signaling was activated in the presence of HA. Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling, significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B, SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs. These data suggest that HA is a safe and effective enhancer for in vitro expansion of hAECs, whose regulatory mechanism involves the TGF-β/BMP signaling.
| S-EPMC7532780 | biostudies-literature
Project description:This study investigated the mechanism by which 300 kDa HA (1 mg/mL) promotes the proliferation of hAECs. P1 hAECs in logarithmic growth phase were harvested, inoculated into 6-well plates at 3×105/well, and cultured with 5% CO2 at 37 °C. The medium was changed after 3 days, and then the cells were cultured for 18 or 36 h in the presence and absence of HA (300 kDa, 1 mg/mL). The total RNA was purified using the RNeasy MinElute kit (Qiagen, Valencia, CA, USA) according to the manufacturer’s instructions. cDNA was synthesized using a SuperScript III Reverse Transcriptase Kit (Invitrogen, Shanghai, China). Real-time PCR was conducted, and the 2–∆∆Ct method was used to quantify gene expression levels. The signal was collected by Agilent Feature Extraction software and analyzed by Agilent GeneSpring GX software.
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Project description:Hyaluronic acid was proposed to support soft tissue recession surgery and guided tissue regeneration. Nevertheless, the molecular mechanisms through which hyaluronic acid modulates the response of the connective tissue cells remain elusive. To elucidate the impact of hyaluronic acid on the connective tissue cells, we employed bulk RNA sequencing to unravel the changes in the genetic signature gingival fibroblasts exposed to 1.6% cross-linked hyaluronic acid and 0.2% natural hyaluronic acid hyaluronic acid. Transcriptome-wide changes were modest, even when implementing a minimum of 1.5 log2 fold-change and a significance threshold of 1.0 -log10; only a dozenth gene was differentially expressed and ranked according to the Manhattan distance. Upregulated were PLK3, SLC16A6, IL6, HBEGF, DGKE, DUSP4, PTGS2, FOXC2, ATAD2B, NFATC2, and downregulated were MMP24 and PLXNA2. RT-PCR analysis supported the impact of hyaluronic acid on increasing expression of the selected gene panel. The findings from bulk RNA sequencing suggest that gingival fibroblasts only show a weak response when exposed to hyaluronic acid.
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Project description:Intra-amniotic infection, the invasion of microbes into the amniotic cavity resulting in an inflammatory process, is a clinical condition that can lead to adverse pregnancy outcomes for the mother and fetus as well as severe long-term neonatal morbidities. Despite much research focused on the consequences of intra-amniotic infection, there is still little knowledge about the functional roles of innate immune cells that respond to invading microbes. In the current study, we performed RNA sequencing of sorted neutrophils and monocytes/macrophages from amniotic fluid from women with intra-amniotic infection to determine the transcriptomic differences between these innate immune cells. Further, we sought to identify specific transcriptomic pathways that were significantly altered by the maternal or fetal origin of amniotic fluid neutrophils and monocytes, the presence of a severe fetal inflammatory response, and pregnancy outcome (i.e. preterm or term delivery). We showed that significant transcriptomic differences exist between amniotic fluid neutrophils and monocytes/macrophages from women with intra-amniotic infection that are indicative of the distinct roles these cells play. We also found that amniotic fluid monocytes/macrophages of fetal origin display impaired ability to clear out microbes invading the amniotic cavity compared to those of maternal origin. Notably, we demonstrate that the transcriptomic changes in amniotic fluid monocytes/macrophages are heavily associated with the severity of the fetal inflammatory response, suggesting that the trafficking of fetal neutrophils throughout the umbilical cord is partially modulated by monocytes/macrophages in the amniotic cavity. Finally, we show that amniotic fluid neutrophils and monocytes/macrophages from preterm deliveries display enhanced transcriptomic activity compared to those from term deliveries, highlighting the protective role of these innate immune cells in this vulnerable period. Collectively, these findings demonstrate the underlying complexity of local innate immune responses in women with intra-amniotic infection, and provide new insights into the functions of amniotic fluid neutrophils and monocytes in the amniotic cavity.
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Project description:Differentiated chondrocytes from populations of human bone marrow stromal cells including skeletal stem cells (hBMSCs/SSCs) and induced pluripotent stem cells (hiPSCs) have the potential to restore damaged cartilage, yet chondrocyte hypertrophy is a barrier for translational therapy. However, hBMSCs/SSCs attached to a hyaluronic acid-coated fibrin microbead scaffold (HyA-FMBs) produce cartilage that resists hypertrophy. We show that HyA-FMBs initially suppress Bone Morphogenic Protein (BMP) signaling early in chondrogenic differentiation of hBMSCs/SSCs, then restore BMP signaling in a stable chondrogenic population enriched for Insulin-like Growth Factor Binding Protein 5 and Matrix Gla Protein. We subsequently developed a serumfree hiPSC differentiation strategy that inhibited, then activated BMP signaling in a purified subpopulation derived from ?chondrospheroids? that exhibited stable expression of Type II Collagen, Aggrecan (ACAN), and Lubricin (PRG4) and minimal e xpression of Type X Collagen. Overall, timed, and selective BMP signaling restrains chondrocyte hypertrophy, supporting the potential of chondrospheroid-derived cells for clinical utility in osteoarthritis.
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Project description:Fetal wounds repair by regeneration rather than wound healing and the environment is dominated by amniotic fluid. We are looking at early transcriptional regulation of keratinocytes cultured in amniotic fluid in vitro. Keratinocytes were isolated and expanded to passage three after which they were starved in DMEM for 12h then cultured for 24h in human amniotic fluid (50%), fcs (50%) or DMEM alone for another 24h. N=2, pooled replicates per CEL-file.
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