Pub Date : 2024-10-01Epub Date: 2024-03-05DOI: 10.1002/jcb.30543
Ganesh Suraj Bose, Garima Kalakoti, Abhijeet P Kulkarni, Smriti Mittal
Obesity is defined as an abnormal accumulation of adipose tissue in the body and is a major global health problem due to increased morbidity and mortality. Adipose tissue is made up of adipocytes, which are fat-storing cells, and the differentiation of these fat cells is known as adipogenesis. Several transcription factors (TFs) such as CEBPβ, CEBPα, PPARγ, GATA, and KLF have been reported to play a key role in adipogenesis. In this study, we report one more TF AP-1, which is found to be involved in adipogenesis. Human mesenchymal stem cells were differentiated into adipocytes, and the expression pattern of different subunits of AP-1 was examined during adipogenesis. It was observed that C-FOS was predominantly expressed at an early stage (Day 2), whereas FRA2 expression peaked at later stages (Days 6 and 8) of adipogenesis. Chromatin immunoprecipitation-sequencing analysis revealed that C-FOS binds mainly to the promoters of WNT1, miR-30a, and ANAPC7 and regulates their expression during mitotic clonal expansion. In contrast, FRA2 binds to the promoters of CIDEA, NOTCH1, ARAF, and MYLK, regulating their expression and lipid metabolism. Data obtained clearly indicate that the differential expression of C-FOS and FRA2 is crucial for different stages of adipogenesis. This also raises the possibility of considering AP-1 as a therapeutic target for treating obesity and related disorders.
{"title":"AP-1/C-FOS and AP-1/FRA2 differentially regulate early and late adipogenic differentiation of mesenchymal stem cells.","authors":"Ganesh Suraj Bose, Garima Kalakoti, Abhijeet P Kulkarni, Smriti Mittal","doi":"10.1002/jcb.30543","DOIUrl":"10.1002/jcb.30543","url":null,"abstract":"<p><p>Obesity is defined as an abnormal accumulation of adipose tissue in the body and is a major global health problem due to increased morbidity and mortality. Adipose tissue is made up of adipocytes, which are fat-storing cells, and the differentiation of these fat cells is known as adipogenesis. Several transcription factors (TFs) such as CEBPβ, CEBPα, PPARγ, GATA, and KLF have been reported to play a key role in adipogenesis. In this study, we report one more TF AP-1, which is found to be involved in adipogenesis. Human mesenchymal stem cells were differentiated into adipocytes, and the expression pattern of different subunits of AP-1 was examined during adipogenesis. It was observed that C-FOS was predominantly expressed at an early stage (Day 2), whereas FRA2 expression peaked at later stages (Days 6 and 8) of adipogenesis. Chromatin immunoprecipitation-sequencing analysis revealed that C-FOS binds mainly to the promoters of WNT1, miR-30a, and ANAPC7 and regulates their expression during mitotic clonal expansion. In contrast, FRA2 binds to the promoters of CIDEA, NOTCH1, ARAF, and MYLK, regulating their expression and lipid metabolism. Data obtained clearly indicate that the differential expression of C-FOS and FRA2 is crucial for different stages of adipogenesis. This also raises the possibility of considering AP-1 as a therapeutic target for treating obesity and related disorders.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140028124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this study, we investigate the effect of neuregulin 4 (NRG4) on podocyte damage in a mouse model of diabetic nephropathy (DN) and we elucidate the underlying molecular mechanisms. In vivo experiments were conducted using a C57BL/6 mouse model of DN to determine the effect of NRG4 on proteinuria and podocyte injury, and in vitro experiments were performed with conditionally immortalized mouse podocytes treated with high glucose and NRG4 to assess the protective effects of NRG4 on podocyte injury. Autophagy-related protein levels and related signaling pathways were evaluated both in vivo and in vitro. The involvement of the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway was detected using chloroquine or AMPK inhibitors. The results showed that the AMPK/mTOR pathway was involved in the protective roles of NRG4 against high glucose-mediated podocyte injury. Also, NRG4 significantly decreased albuminuria in DN mice. PAS staining indicated that NRG4 mitigated glomerular volume and mesangium expansion in DN mice. Consistently, western blot and RT-PCR analyses confirmed that NRG4 decreased the expression of pro-fibrotic molecules in the glomeruli of DN mice. The immunofluorescence results showed that NRG4 retained expression of podocin and nephrin, whereas transmission electron microscopy revealed that NRG4 alleviated podocyte injury. In DN mice, NRG4 decreased podocyte apoptosis and increased expression of nephrin and podocin, while decreasing the expression of desmin and HIF1α. Overall, NRG4 improved albuminuria, glomerulosclerosis, glomerulomegaly, and hypoxia in DN mice. The in vitro experiments showed that NRG4 inhibited HG-induced podocyte injury and apoptosis. Furthermore, autophagy of the glomeruli decreased in DN mice, but reactivated following NRG4 intervention. NRG4 intervention was found to partially activate autophagy via the AMPK/mTOR signaling pathway. Consequently, when the AMPK/mTOR pathway was suppressed or autophagy was inhibited, the beneficial effects of NRG4 intervention on podocyte injury were diminished. These results indicate that NRG4 intervention attenuates podocyte injury and apoptosis by promoting autophagy in the kidneys of DN mice, in part, by activating the AMPK/mTOR signaling pathway.
{"title":"Neuregulin 4 Attenuates Podocyte Injury and Proteinuria in Part by Activating AMPK/mTOR-Mediated Autophagy in Mice.","authors":"Juntian Deng, Qiansheng Yang, Wanyu Zhu, Yanhua Zhang, Meng Lin, Juyan She, Jing Li, Yuxin Xiao, Jun Xiao, Xinyue Xu, Hebei He, Biao Zhu, Yan Ding","doi":"10.1002/jcb.30634","DOIUrl":"10.1002/jcb.30634","url":null,"abstract":"<p><p>In this study, we investigate the effect of neuregulin 4 (NRG4) on podocyte damage in a mouse model of diabetic nephropathy (DN) and we elucidate the underlying molecular mechanisms. In vivo experiments were conducted using a C57BL/6 mouse model of DN to determine the effect of NRG4 on proteinuria and podocyte injury, and in vitro experiments were performed with conditionally immortalized mouse podocytes treated with high glucose and NRG4 to assess the protective effects of NRG4 on podocyte injury. Autophagy-related protein levels and related signaling pathways were evaluated both in vivo and in vitro. The involvement of the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway was detected using chloroquine or AMPK inhibitors. The results showed that the AMPK/mTOR pathway was involved in the protective roles of NRG4 against high glucose-mediated podocyte injury. Also, NRG4 significantly decreased albuminuria in DN mice. PAS staining indicated that NRG4 mitigated glomerular volume and mesangium expansion in DN mice. Consistently, western blot and RT-PCR analyses confirmed that NRG4 decreased the expression of pro-fibrotic molecules in the glomeruli of DN mice. The immunofluorescence results showed that NRG4 retained expression of podocin and nephrin, whereas transmission electron microscopy revealed that NRG4 alleviated podocyte injury. In DN mice, NRG4 decreased podocyte apoptosis and increased expression of nephrin and podocin, while decreasing the expression of desmin and HIF1α. Overall, NRG4 improved albuminuria, glomerulosclerosis, glomerulomegaly, and hypoxia in DN mice. The in vitro experiments showed that NRG4 inhibited HG-induced podocyte injury and apoptosis. Furthermore, autophagy of the glomeruli decreased in DN mice, but reactivated following NRG4 intervention. NRG4 intervention was found to partially activate autophagy via the AMPK/mTOR signaling pathway. Consequently, when the AMPK/mTOR pathway was suppressed or autophagy was inhibited, the beneficial effects of NRG4 intervention on podocyte injury were diminished. These results indicate that NRG4 intervention attenuates podocyte injury and apoptosis by promoting autophagy in the kidneys of DN mice, in part, by activating the AMPK/mTOR signaling pathway.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-08-27DOI: 10.1002/jcb.30635
{"title":"RETRACTION: Posttreatment of Melatonin With CCl4 Better Reduces Fibrogenic and Oxidative Changes in Liver Than Melatonin Co-treatment.","authors":"","doi":"10.1002/jcb.30635","DOIUrl":"10.1002/jcb.30635","url":null,"abstract":"","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-07-17DOI: 10.1002/jcb.30622
Retraction: Z. Zhao, J.-Z. Guan, M. Wu, G.-H. Lai, and Z.-L. Zhu. Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats. Journal of Cellular Biochemistry 120, no. 3 (2019): 4599-4612, https://doi.org/10.1002/jcb.27748. The above article, published online on 9 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, the same sample used to depict the immunofluorescence staining in Figure 5B was found to have been used in a different scientific context in a previous publication from a different author group. Thus, the editors consider the conclusions of this article to be invalid.
撤回:Z. Zhao, J.-Z. Guan, M. Wu, G.-H.Guan, M. Wu, G.-H. Lai, and Z.-L.Lai, and Z.-L. Zhu.通过上调MDM4,下调microRNA-23b通过p53信号通路保护大鼠免受缺血再灌注损伤。Journal of Cellular Biochemistry 120, no.3 (2019):4599-4612, https://doi.org/10.1002/jcb.27748.上述文章于2018年12月9日在线发表于Wiley Online Library (wileyonlinelibrary.com),经作者、期刊主编Christian Behl和Wiley Periodicals LLC三方协商,已被撤回。之所以同意撤稿,是因为第三方对文章中的数据提出了质疑。我们发现,文章中介绍的结果与实验方法之间存在若干缺陷和不一致之处。此外,图 5B 中用于描绘免疫荧光染色的同一样本被发现在不同作者组之前发表的一篇文章中被用于不同的科学背景。因此,编者认为这篇文章的结论无效。
{"title":"RETRACTION: Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats.","authors":"","doi":"10.1002/jcb.30622","DOIUrl":"10.1002/jcb.30622","url":null,"abstract":"<p><strong>Retraction: </strong>Z. Zhao, J.-Z. Guan, M. Wu, G.-H. Lai, and Z.-L. Zhu. Downregulation of microRNA-23b Protects Against Ischemia-Reperfusion Injury via p53 Signaling Pathway by Upregulating MDM4 in Rats. Journal of Cellular Biochemistry 120, no. 3 (2019): 4599-4612, https://doi.org/10.1002/jcb.27748. The above article, published online on 9 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, the same sample used to depict the immunofluorescence staining in Figure 5B was found to have been used in a different scientific context in a previous publication from a different author group. Thus, the editors consider the conclusions of this article to be invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-09-29DOI: 10.1002/jcb.30628
{"title":"RETRACTION: MiR-125a Suppresses Malignancy of Multiple Myeloma by Reducing the Deubiquitinase USP5.","authors":"","doi":"10.1002/jcb.30628","DOIUrl":"10.1002/jcb.30628","url":null,"abstract":"","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-07-17DOI: 10.1002/jcb.30623
Retraction: Y. Wei, X. Zhang, S. Wen, S. Huang, Q. Huang, S. Lu, F. Bai, J. Nie, J. Wei, Z. Lu, and X. Lin. Methyl Helicterate Inhibits Hepatic Stellate Cell Activation Through Downregulating the ERK1/2 Signaling Pathway. Journal of Cellular Biochemistry 120, no. 9 (2019): 14936-14945, https://doi.org/10.1002/jcb.28756. The above article, published online on 22 April 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Multiple image elements in Figures 2A, 3B, and 4 were found to have been previously published by the same author group in a different scientific context. Furthermore, splicing affecting Figures 5B and 5C has been detected. The authors state that, due to inadequate data management, they were unable to verify whether Figures 2A, 3B, and 4 pertain to this study or to other works, and that Figure 5B and 5C were inappropriately employed. The article is retracted as the editors have lost confidence in the accuracy of the data presented and consider the conclusions of the article to be invalid. The authors agree with the decision to retract the article and would like to extend their sincere apologies for any inconvenience caused.
撤回:Y. Wei, X. Zhang, S. Wen, S. Huang, Q. Huang, S. Lu, F. Bai, J. Nie, J. Wei, Z. Lu, and X. Lin.通过下调 ERK1/2 信号通路抑制肝星状细胞活化。细胞生物化学杂志》120期,第9号(2019年):14936-14945, https://doi.org/10.1002/jcb.28756.上述文章于 2019 年 4 月 22 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经作者、期刊主编 Christian Behl 和 Wiley Periodicals LLC 协议撤回。之所以同意撤稿,是因为第三方对文章中的数据提出了质疑。图 2A、图 3B 和图 4 中的多个图像元素被发现曾由同一作者小组在不同的科学背景下发表过。此外,还发现了影响图 5B 和 5C 的拼接。作者表示,由于数据管理不完善,他们无法核实图 2A、3B 和 4 是否与本研究或其他作品有关,而且图 5B 和 5C 被不恰当地使用。由于编辑对文中数据的准确性失去信心,并认为文章的结论无效,因此撤稿。作者同意撤稿的决定,并对由此造成的不便表示诚挚的歉意。
{"title":"RETRACTION: Methyl Helicterate Inhibits Hepatic Stellate Cell Activation through Downregulating the ERK1/2 Signaling Pathway.","authors":"","doi":"10.1002/jcb.30623","DOIUrl":"10.1002/jcb.30623","url":null,"abstract":"<p><strong>Retraction: </strong>Y. Wei, X. Zhang, S. Wen, S. Huang, Q. Huang, S. Lu, F. Bai, J. Nie, J. Wei, Z. Lu, and X. Lin. Methyl Helicterate Inhibits Hepatic Stellate Cell Activation Through Downregulating the ERK1/2 Signaling Pathway. Journal of Cellular Biochemistry 120, no. 9 (2019): 14936-14945, https://doi.org/10.1002/jcb.28756. The above article, published online on 22 April 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Multiple image elements in Figures 2A, 3B, and 4 were found to have been previously published by the same author group in a different scientific context. Furthermore, splicing affecting Figures 5B and 5C has been detected. The authors state that, due to inadequate data management, they were unable to verify whether Figures 2A, 3B, and 4 pertain to this study or to other works, and that Figure 5B and 5C were inappropriately employed. The article is retracted as the editors have lost confidence in the accuracy of the data presented and consider the conclusions of the article to be invalid. The authors agree with the decision to retract the article and would like to extend their sincere apologies for any inconvenience caused.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-08-27DOI: 10.1002/jcb.30640
{"title":"RETRACTION: FV-429 Induced Apoptosis Through ROS-Mediated ERK2 Nuclear Translocation and p53 Activation in Gastric Cancer Cells.","authors":"","doi":"10.1002/jcb.30640","DOIUrl":"10.1002/jcb.30640","url":null,"abstract":"","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}