Organogenesis最新文献_第7页

Persistent Wnt/β-catenin signaling in mouse epithelium induces the ectopic Dspp expression in cheek mesenchyme. 小鼠上皮中持续的Wnt/β-catenin信号传导可诱导颊间质中Dspp的异位表达。

IF 2.3 4区生物学

Organogenesis Pub Date : 2019-01-01 Epub Date: 2018-12-20 DOI: 10.1080/15476278.2018.1557026

Nan Zhou, Nan Li, Jing Liu, Yu Wang, Jun Gao, Yingzhang Wu, Xiaoyan Chen, Chao Liu, Jing Xiao

{"title":"Persistent Wnt/β-catenin signaling in mouse epithelium induces the ectopic Dspp expression in cheek mesenchyme.","authors":"Nan Zhou, Nan Li, Jing Liu, Yu Wang, Jun Gao, Yingzhang Wu, Xiaoyan Chen, Chao Liu, Jing Xiao","doi":"10.1080/15476278.2018.1557026","DOIUrl":"https://doi.org/10.1080/15476278.2018.1557026","url":null,"abstract":"Tooth development is accomplished by a series of epithelial-mesenchyme interactions. Epithelial Wnt/β-catenin signaling is sufficient to initiate tooth development by activating Shh, Bmps, Fgfs and Wnts in dental epithelium, which in turn, triggered the expression of odontogenic genes in the underlying mesenchyme. Although constitutive activation of Wnt/β-catenin signaling in oral ectoderm resulted in the continuous tooth formation throughout the life span, if the epithelial Wnt/β-catenin signaling could induce the mesenchyme other than oral mesenchyme still required to be elucidated. In this study, we found that in the K14-cre; Ctnnb1ex3f mice, the markers of dental epithelium, such as Pitx2, Shh, Bmp2, Fgf4, and Fgf8, were not only activated in the oral ectoderm, but also in the cheek epithelium. Surprisingly, the underlying cheek mesenchymal cells were elongated and expressed Dspp. Further investigations detected that the expression of Msx1 and Runx2 extended from oral to cheek mesenchyme. These findings suggested that epithelial Wnt/β-catenin signaling was capable of inducing Dspp expression in non-dental mesenchyme. Moreover, Dspp expression in the K14-cre; Ctnnb1ex3f oral mesenchyme was activated earlier than that in the wild type littermates. In contrast, although the elongated oral epithelial cells were detected in the K14-cre; Ctnnb1ex3f mice, the Amelogenin expression was suppressed. The differential effects of the persistent epithelial Wnt/β-catenin signaling on ameloblast and odontoblast differentiation might result from the altered BMP signaling. In summary, our findings suggested that the epithelial Wnt/β-catenin signaling could induce craniofacial mesenchyme into odontogenic program and promote odontoblast differentiation.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"15 1","pages":"1-12"},"PeriodicalIF":2.3,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2018.1557026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36844466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium. 牙上皮间充质Wnt/β-catenin信号传导诱导Wnt和BMP拮抗剂。

IF 2.3 4区生物学

Organogenesis Pub Date : 2019-01-01 Epub Date: 2019-06-26 DOI: 10.1080/15476278.2019.1633871

Xiaoyan Chen, Jing Liu, Nan Li, Yu Wang, Nan Zhou, Lei Zhu, Yiding Shi, Yingzhang Wu, Jing Xiao, Chao Liu

{"title":"Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium.","authors":"Xiaoyan Chen, Jing Liu, Nan Li, Yu Wang, Nan Zhou, Lei Zhu, Yiding Shi, Yingzhang Wu, Jing Xiao, Chao Liu","doi":"10.1080/15476278.2019.1633871","DOIUrl":"https://doi.org/10.1080/15476278.2019.1633871","url":null,"abstract":"Previous studies indicated that the elevated mesenchymal Wnt/β-catenin signaling deprived dental mesenchyme of odontogenic fate. By utilizing ex vivo or pharmacological approaches, Wnt/β-catenin signaling in the developing dental mesenchyme was suggested to suppress the odontogenic fate by disrupting the balance between Axin2 and Runx2. In our study, the Osr2-creKI; Ctnnb1ex3f mouse was used to explore how mesenchymal Wnt/β-catenin signaling suppressed the odontogenic fate in vivo. We found that all of the incisor and half of the molar germs of Osr2-creKI; Ctnnb1ex3fmice started to regress at E14.5 and almost disappeared at birth. The expression of Fgf3 and Msx1 was dramatically down-regulated in the E14.5 Osr2-creKI; Ctnnb1ex3f incisor and molar mesenchyme, while Runx2transcription was only diminished in incisor mesenchyme. Intriguingly, in the E14.5 Osr2-creKI; Ctnnb1ex3f incisor epithelium, the expression of Noggin was activated, while Shh was abrogated. Similarly, the Wnt and BMP antagonists, Ectodin and Noggin were also ectopically activated in the E14.5 Osr2-creKI; Ctnnb1ex3f molar epithelium. Recombination of E13.5 Osr2-creKI; Ctnnb1ex3f molar mesenchyme with E10.5 and E13.5 WT dental epithelia failed to develop tooth. Taken together, the mesenchymal Wnt/β-catenin signaling resulted in the loss of odontogenic fate in vivo not only by directly suppressing odontogenic genes expression but also by inducing Wnt and BMP antagonists in dental epithelium.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"15 2","pages":"55-67"},"PeriodicalIF":2.3,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2019.1633871","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37362980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

ATP6V1H facilitates osteogenic differentiation in MC3T3-E1 cells via Akt/GSK3β signaling pathway. ATP6V1H通过Akt/GSK3β信号通路促进MC3T3-E1细胞成骨分化。

IF 2.3 4区生物学

Organogenesis Pub Date : 2019-01-01 Epub Date: 2019-07-04 DOI: 10.1080/15476278.2019.1633869

Fusong Jiang, Haojie Shan, Chenhao Pan, Zubin Zhou, Keze Cui, Yuanliang Chen, Haibo Zhong, Zhibin Lin, Nan Wang, Liang Yan, Xiaowei Yu

{"title":"ATP6V1H facilitates osteogenic differentiation in MC3T3-E1 cells via Akt/GSK3β signaling pathway.","authors":"Fusong Jiang, Haojie Shan, Chenhao Pan, Zubin Zhou, Keze Cui, Yuanliang Chen, Haibo Zhong, Zhibin Lin, Nan Wang, Liang Yan, Xiaowei Yu","doi":"10.1080/15476278.2019.1633869","DOIUrl":"https://doi.org/10.1080/15476278.2019.1633869","url":null,"abstract":"Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of all diabetic patients, and osteoporosis is one of the complications during T2DM process. ATP6V1H (V-type proton ATPase subunit H) displays crucial roles in inhibiting bone loss, but its role in osteogenic differentiation remains unknown. Therefore in this study, we aimed to explore the biological role of ATP6V1H in osteogenic differentiation. OM (osteogenic medium) and HG (high glucose and free fatty acids) were used to induce the MC3T3-E1 cells into osteogenic differentiation in a T2DM simulating environment. CCK8 assay was used to detect cell viability. Alizarin Red staining was used to detect the influence of ATP6V1H on osteogenic differentiation. ATP6V1H expression increased in OM-MC3T3-E1 cells, while decreased in OM+HG-MC3T3-E1 cells. ATP6V1H promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. Overexpression of ATP6V1H inhibited Akt/GSK3β signaling pathway, while knockdown of ATP6V1H promoted Akt/GSK3β signaling pathway. ATP6V1H overexpression promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. The role of ATP6V1H in osteogenic differentiation in a T2DM simulating environment involved in Akt/GSK3β signaling pathway. These data demonstrated that ATP6V1H could serve as a potential target for osteogenic differentiation in a T2DM simulating environment.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"15 2","pages":"43-54"},"PeriodicalIF":2.3,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2019.1633869","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37130242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Corrigendum. 勘误表。

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 Epub Date: 2018-01-30 DOI: 10.1080/15476278.2017.1422894

引用次数: 0

Suppression of LRRC19 promotes cutaneous wound healing in pressure ulcers in mice. 抑制LRRC19促进小鼠压疮皮肤创面愈合。

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 Epub Date: 2018-02-20 DOI: 10.1080/15476278.2018.1436924

Jie Sun, Zhijing Wang, Xirui Wang

{"title":"Suppression of LRRC19 promotes cutaneous wound healing in pressure ulcers in mice.","authors":"Jie Sun, Zhijing Wang, Xirui Wang","doi":"10.1080/15476278.2018.1436924","DOIUrl":"https://doi.org/10.1080/15476278.2018.1436924","url":null,"abstract":"The ischemia-reperfusion (I/R) induced skin lesion has been identified as primary cause of pressure ulcer. Better understanding of the mechanism is required for new therapy development. Leucine rich repeat containing protein 19 (LRRC19) is a recently discovered transmembrane protein containing leucine-rich repeats and plays a role in immune response. To investigate the role of LRRC19 in pressure ulcers, mouse ulcer model was established with two cycles of I/R. The expression of LRRC19 was assessed during injury. siRNA mediated LRRC19 downregulation was applied to investigate the disease severity, immune cell infiltration and pro-inflammatory cytokines production. The primary skin fibroblasts were stimulated with IL-1β to dissect the molecular mechanism. LRRC19 was readily induced in I/R induced lesion site in a pattern mimicking the disease progress as measured by wound area. Knockdown of LRRC19 by siRNA significantly alleviated the disease severity and attenuated immune cell infiltration and pro-inflammatory cytokines production. In primary skin fibroblast model, siRNA knockdown of LRRC19 suppressed IL-1β mediated NFκB activation and its downstream cytokines production. LRRC19 was a novel factor for I/R-induced tissue damage by promoting NFκB dependent pro-inflammatory response. Our results supported that LRRC19 could be a potential therapeutic target for pressure ulcers.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"14 1","pages":"13-24"},"PeriodicalIF":2.3,"publicationDate":"2018-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2018.1436924","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35847320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

Embryonic skin development and repair. 胚胎皮肤发育和修复。

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 Epub Date: 2018-02-15 DOI: 10.1080/15476278.2017.1421882

Michael S Hu, Mimi R Borrelli, Wan Xing Hong, Samir Malhotra, Alexander T M Cheung, Ryan C Ransom, Robert C Rennert, Shane D Morrison, H Peter Lorenz, Michael T Longaker

引用次数: 0

Effect of TAK1 on osteogenic differentiation of mesenchymal stem cells by regulating BMP-2 via Wnt/β-catenin and MAPK pathway. TAK1通过Wnt/β-catenin和MAPK途径调控BMP-2对间充质干细胞成骨分化的影响。

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 DOI: 10.1080/15476278.2018.1455010

Hongpeng Yang, Yue Guo, Dawei Wang, Xiaofei Yang, Chengzhi Ha

{"title":"Effect of TAK1 on osteogenic differentiation of mesenchymal stem cells by regulating BMP-2 via Wnt/β-catenin and MAPK pathway.","authors":"Hongpeng Yang, Yue Guo, Dawei Wang, Xiaofei Yang, Chengzhi Ha","doi":"10.1080/15476278.2018.1455010","DOIUrl":"https://doi.org/10.1080/15476278.2018.1455010","url":null,"abstract":"Mesenchymal stem cells (MSCs) have the ability to differentiate into osteoblasts and chondrocytes. In vitro osteogenic differentiation is critical but the molecular mechanism has yet to be further clarified. The role of TGF-β activated kinase 1 (TAK1) in MSCs osteogenesis differentiation has not been reported. By adding si-TAK1 and rhTAK1, the osteogenic differentiation of MSCs was measured. Expression levels of the osteoblastic marker genes during osteogenic differentiation of MSCs were checked. As well as molecules involved in BMP and Wnt/β-catenin signaling pathways. The phosphorylation of p38 and JNK was also checked. TAK1 is essential for mineralization of MSCs at low concentration, but excessive rhTAK1 inhibits mineralization of MSCs. It up regulates the expression levels of bone sialoprotein (BSP), osteocalcin (OSC), Alkaline phosphatase (ALP), and RUNX2 during osteogenic differentiation of MSCs. It can also promote TGF-β/BMP-2 gene expression and β-catenin expression, and down regulate GSK-3β expression. Meanwhile, TAK1 promotes the phosphorylation of p38 and JNK. Additionally, TAK1 up regulates the expression of BMP-2 at all concentration under the inhibition of p38 and JNK. Our results suggested that TAK1 is essential in MSCs osteogenesis differentiation, and functions as a double-edged sword, probably through regulation of β-catenin and p38/JNK.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":" ","pages":"36-45"},"PeriodicalIF":2.3,"publicationDate":"2018-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2018.1455010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40441366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 22

Erratum. 勘误表。

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 Epub Date: 2017-12-06 DOI: 10.1080/15476278.2017.1407509

引用次数: 0

Effects of porcine acellular dermal matrix treatment on wound healing and scar formation: Role of Jag1 expression in epidermal stem cells. 猪脱细胞真皮基质处理对伤口愈合和瘢痕形成的影响:表皮干细胞中Jag1表达的作用

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 Epub Date: 2018-04-27 DOI: 10.1080/15476278.2018.1436023

Xiao-Dong Chen, Shu-Bin Ruan, Ze-Peng Lin, Ziheng Zhou, Feng-Gang Zhang, Rong-Hua Yang, Ju-Lin Xie

{"title":"Effects of porcine acellular dermal matrix treatment on wound healing and scar formation: Role of Jag1 expression in epidermal stem cells.","authors":"Xiao-Dong Chen, Shu-Bin Ruan, Ze-Peng Lin, Ziheng Zhou, Feng-Gang Zhang, Rong-Hua Yang, Ju-Lin Xie","doi":"10.1080/15476278.2018.1436023","DOIUrl":"https://doi.org/10.1080/15476278.2018.1436023","url":null,"abstract":"Skin wound healing involves Notch/Jagged1 signaling. However, little is known how Jag1 expression level in epidermal stem cells (ESCs) contributes to wound healing and scar formation. We applied multiple cellular and molecular techniques to examine how Jag1 expression in ESCs modulates ESCs differentiation to myofibroblasts (MFB) in vitro, interpret how Jag1 expression in ESCs is involved in wound healing and scar formation in mice, and evaluate the effects of porcine acellular dermal matrix (ADM) treatment on wound healing and scar formation. We found that Jag1, Notch1 and Hes1 expression was up-regulated in the wound tissue during the period of wound healing. Furthermore, Jag1 expression level in the ESCs was positively associated with the level of differentiation to MFB. ESC-specific knockout of Jag1 delayed wound healing and promoted scar formation in vivo. In addition, we reported that porcine ADM treatment after skin incision could accelerate wound closure and reduce scar formation in vivo. This effect was associated with decreased expression of MFB markers, including α-SMA Col-1 and Col-III in wound tissues. Finally, we confirmed that porcine ADM treatment could increase Jag1, Notch1 and Hesl expression in wound tissues. Taken together, our results suggested that ESC-specific Jag1 expression levels are critical for wound healing and scar formation, and porcine ADM treatment would be beneficial in promoting wound healing and preventing scar formation by enhancing Notch/Jagged1 signaling pathway in ESCs.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"14 1","pages":"25-35"},"PeriodicalIF":2.3,"publicationDate":"2018-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2018.1436023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35810874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Prolongation of liver-specific function for primary hepatocytes maintenance in 3D printed architectures. 3D打印结构中原发性肝细胞维持的肝脏特异性功能延长。

IF 2.3 4区生物学

Organogenesis Pub Date : 2018-01-02 Epub Date: 2018-02-01 DOI: 10.1080/15476278.2018.1423931

Yohan Kim, Kyojin Kang, Sangtae Yoon, Ji Sook Kim, Su A Park, Wan Doo Kim, Seung Bum Lee, Ki-Young Ryu, Jaemin Jeong, Dongho Choi

{"title":"Prolongation of liver-specific function for primary hepatocytes maintenance in 3D printed architectures.","authors":"Yohan Kim, Kyojin Kang, Sangtae Yoon, Ji Sook Kim, Su A Park, Wan Doo Kim, Seung Bum Lee, Ki-Young Ryu, Jaemin Jeong, Dongho Choi","doi":"10.1080/15476278.2018.1423931","DOIUrl":"https://doi.org/10.1080/15476278.2018.1423931","url":null,"abstract":"Isolated primary hepatocytes from the liver are very similar to in vivo native liver hepatocytes, but they have the disadvantage of a limited lifespan in 2D culture. Although a sandwich culture and 3D organoids with mesenchymal stem cells (MSCs) as an attractive assistant cell source to extend lifespan can be used, it cannot fully reproduce the in vivo architecture. Moreover, long-term 3D culture leads to cell death because of hypoxic stress. Therefore, to overcome the drawback of 2D and 3D organoids, we try to use a 3D printing technique using alginate hydrogels with primary hepatocytes and MSCs. The viability of isolated hepatocytes was more than 90%, and the cells remained alive for 7 days without morphological changes in the 3D hepatic architecture with MSCs. Compared to a 2D system, the expression level of functional hepatic genes and proteins was higher for up to 7 days in the 3D hepatic architecture. These results suggest that both the 3D bio-printing technique and paracrine molecules secreted by MSCs supported long-term culture of hepatocytes without morphological changes. Thus, this technique allows for widespread expansion of cells while forming multicellular aggregates, may be applied to drug screening and could be an efficient method for developing an artificial liver.","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"14 1","pages":"1-12"},"PeriodicalIF":2.3,"publicationDate":"2018-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2018.1423931","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35759824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 27