Acute lung injury (ALI) is a destructive respiratory disease characterized by alveolar structural destruction and excessive inflammation responses. Aerobic glycolysis of macrophages plays a crucial role in the pathophysiology of ALI. Previous studies have shown that the expression of the key rate-limiting enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in inflammatory cells is significantly increased, which promotes an increase in the rate of glycolysis in inflammatory cells. However, little is known about the biological functions of PFKFB3 in macrophage inflammation and ALI. In this study, we identified that PFKFB3 is markedly increased in lipopolysaccharide (LPS)-induced ALI mice and macrophages. Knockdown of pfkfb3 attenuated LPS-induced glycolytic flux, decreased the release of pro-inflammatory cytokines, and inactivated NF-κB signaling pathway in macrophages. Subsequently, we found that dehydrocostus lactone (DL), a natural sesquiterpene lactone, significantly decreased both the mRNA and protein levels of PFKFB3. Furthermore, it reduced the release of inflammatory cytokines and inactivated NF-κB pathways in vitro. Accordingly, DL alleviated LPS-induced pulmonary edema and reduced the infiltration of inflammatory cells in mouse lung tissue. In summary, our study reveals the vital role of PFKFB3 in LPS-induced inflammation and discovers a novel molecular mechanism underlying DL's protective effects on ALI.
急性肺损伤（ALI）是一种以肺泡结构破坏和过度炎症反应为特征的破坏性呼吸系统疾病。巨噬细胞的有氧糖酵解在 ALI 的病理生理学中起着至关重要的作用。以往的研究表明，炎症细胞中关键的限速酶 6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶 3（PFKFB3）的表达量显著增加，从而促进了炎症细胞中糖酵解速率的增加。然而，人们对 PFKFB3 在巨噬细胞炎症和 ALI 中的生物学功能知之甚少。在这项研究中，我们发现 PFKFB3 在脂多糖（LPS）诱导的 ALI 小鼠和巨噬细胞中明显增加。敲除 pfkfb3 可减轻 LPS 诱导的糖酵解通量，减少促炎细胞因子的释放，并使巨噬细胞中的 NF-κB 信号通路失活。随后，我们发现天然倍半萜内酯脱氢木内酯（DL）能显著降低 PFKFB3 的 mRNA 和蛋白水平。此外，它还减少了炎症细胞因子的释放，并使体外 NF-κB 通路失活。因此，DL 可减轻 LPS 诱导的肺水肿，并减少小鼠肺组织中炎性细胞的浸润。总之，我们的研究揭示了 PFKFB3 在 LPS 诱导的炎症中的重要作用，并发现了 DL 对 ALI 具有保护作用的新分子机制。
{"title":"Dehydrocostus Lactone Ameliorates LPS-Induced Acute Lung Injury by Inhibiting PFKFB3-Mediated Glycolysis","authors":"Yue Li, Xinrui Wang, Lirong Zhao, Boyu Pan, Xiao Xu, Dongrong Zhu","doi":"10.1002/jcb.30639","DOIUrl":"10.1002/jcb.30639","url":null,"abstract":"<div>\u0000 \u0000 <p>Acute lung injury (ALI) is a destructive respiratory disease characterized by alveolar structural destruction and excessive inflammation responses. Aerobic glycolysis of macrophages plays a crucial role in the pathophysiology of ALI. Previous studies have shown that the expression of the key rate-limiting enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in inflammatory cells is significantly increased, which promotes an increase in the rate of glycolysis in inflammatory cells. However, little is known about the biological functions of PFKFB3 in macrophage inflammation and ALI. In this study, we identified that PFKFB3 is markedly increased in lipopolysaccharide (LPS)-induced ALI mice and macrophages. Knockdown of <i>pfkfb3</i> attenuated LPS-induced glycolytic flux, decreased the release of pro-inflammatory cytokines, and inactivated NF-κB signaling pathway in macrophages. Subsequently, we found that dehydrocostus lactone (DL), a natural sesquiterpene lactone, significantly decreased both the mRNA and protein levels of PFKFB3. Furthermore, it reduced the release of inflammatory cytokines and inactivated NF-κB pathways in vitro. Accordingly, DL alleviated LPS-induced pulmonary edema and reduced the infiltration of inflammatory cells in mouse lung tissue. In summary, our study reveals the vital role of PFKFB3 in LPS-induced inflammation and discovers a novel molecular mechanism underlying DL's protective effects on ALI.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141988013","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}
Ernest Oduro-Kwateng, Musab Ali, Ibrahim Oluwatobi Kehinde, Zhichao Zhang, Mahmoud E. S. Soliman
<p>Protein–protein interactions, or PPIs, are a part of every biological activity and have been linked to a number of diseases, including cancer, infectious diseases, and neurological disorders. As such, targeting PPIs is considered a strategic and vital approach in the development of new medications. Nonetheless, the wide and flat contact interface makes it difficult to find small-molecule PP inhibitors. An alternative strategy would be to use the PPI interaction motifs as building blocks for the design of peptide-based inhibitors. Herein, we designed 12-mer peptide inhibitors to target p25-inducing-cyclin-dependent kinase (Cdk5) hyperregulation, a PPI that has been shown to perpetuate neuroinflammation, which is one of the major causal implications of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and frontotemporal dementia. We generated a library of 5 062 500 peptide combination sequences (PCS) derived from the interaction motif of Cdk5/p25 PP interface. The 20 amino acids were differentiated into six groups, namely, hydrophobic (aliphatic), aromatic, basic, acidic, unique, and polar uncharged, on the basis of their physiochemical properties. To preserve the interaction motif necessary for ideal binding, de novo modeling of all possible peptide sequence substitutions was considered. A set of filters, backed by the Support Vector Machine (SVM) algorithm, was then used to create a shortlisted custom peptide library that met specific bioavailability, toxicity, and therapeutic relevance, leading to a refined library of 15 PCS. A greedy algorithm and coarse-grained force field were used to predict peptide structure and folding before subsequent modeling studies. Molecular docking was performed to estimate the relative binding affinities, and out of the top hits, Pep15 was subjected to molecular dynamics simulations and binding free-energy calculations in comparison to a known peptide inhibitor with experimental data (template peptide). Interestingly, the identified peptide through our protocol, Pep15, was found to show a significantly higher binding affinity than the reference template peptide (−48.10 ± 0.23 kcal/mol and −17.53 ± 0.27 kcal/mol, respectively). In comparison to the template peptide, Pep15 was found to possess a more compact and buried surface area, tighter binding landscape, and reduced conformational variability, leading to enhanced structural and kinetic stability of the Cdk5/p25 complex. Notably, both peptide inhibitors were found to have a minimal impact on the architectural integrity of the Cdk5/p25 secondary structure.</p><p>Herein, we propose Pep15 as a novel and potentially disruptive peptide drug for Cdk5/p25-mediated neurodegenerative phenotypes that require further clinical investigation. The systematic protocol and findings of this report would serve as a valuable tool in the identification of critical PPI interface reactive residues, designing of analogs, and identification of more potent
{"title":"De Novo Rational Design of Peptide-Based Protein–Protein Inhibitors (Pep-PPIs) Approach by Mapping the Interaction Motifs of the PP Interface and Physicochemical Filtration: A Case on p25-Cdk5-Mediated Neurodegenerative Diseases","authors":"Ernest Oduro-Kwateng, Musab Ali, Ibrahim Oluwatobi Kehinde, Zhichao Zhang, Mahmoud E. S. Soliman","doi":"10.1002/jcb.30633","DOIUrl":"10.1002/jcb.30633","url":null,"abstract":"<p>Protein–protein interactions, or PPIs, are a part of every biological activity and have been linked to a number of diseases, including cancer, infectious diseases, and neurological disorders. As such, targeting PPIs is considered a strategic and vital approach in the development of new medications. Nonetheless, the wide and flat contact interface makes it difficult to find small-molecule PP inhibitors. An alternative strategy would be to use the PPI interaction motifs as building blocks for the design of peptide-based inhibitors. Herein, we designed 12-mer peptide inhibitors to target p25-inducing-cyclin-dependent kinase (Cdk5) hyperregulation, a PPI that has been shown to perpetuate neuroinflammation, which is one of the major causal implications of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and frontotemporal dementia. We generated a library of 5 062 500 peptide combination sequences (PCS) derived from the interaction motif of Cdk5/p25 PP interface. The 20 amino acids were differentiated into six groups, namely, hydrophobic (aliphatic), aromatic, basic, acidic, unique, and polar uncharged, on the basis of their physiochemical properties. To preserve the interaction motif necessary for ideal binding, de novo modeling of all possible peptide sequence substitutions was considered. A set of filters, backed by the Support Vector Machine (SVM) algorithm, was then used to create a shortlisted custom peptide library that met specific bioavailability, toxicity, and therapeutic relevance, leading to a refined library of 15 PCS. A greedy algorithm and coarse-grained force field were used to predict peptide structure and folding before subsequent modeling studies. Molecular docking was performed to estimate the relative binding affinities, and out of the top hits, Pep15 was subjected to molecular dynamics simulations and binding free-energy calculations in comparison to a known peptide inhibitor with experimental data (template peptide). Interestingly, the identified peptide through our protocol, Pep15, was found to show a significantly higher binding affinity than the reference template peptide (−48.10 ± 0.23 kcal/mol and −17.53 ± 0.27 kcal/mol, respectively). In comparison to the template peptide, Pep15 was found to possess a more compact and buried surface area, tighter binding landscape, and reduced conformational variability, leading to enhanced structural and kinetic stability of the Cdk5/p25 complex. Notably, both peptide inhibitors were found to have a minimal impact on the architectural integrity of the Cdk5/p25 secondary structure.</p><p>Herein, we propose Pep15 as a novel and potentially disruptive peptide drug for Cdk5/p25-mediated neurodegenerative phenotypes that require further clinical investigation. The systematic protocol and findings of this report would serve as a valuable tool in the identification of critical PPI interface reactive residues, designing of analogs, and identification of more potent ","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141988012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","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":"<div>\u0000 \u0000 <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></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-02","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}
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><b>RETRACTION:</b> 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. <i>Journal of Cellular Biochemistry</i> 120, no. 3 (2019): 4599-4612, https://doi.org/10.1002/jcb.27748.</p><p>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":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30622","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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><b>RETRACTION:</b> 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. <i>Journal of Cellular Biochemistry</i> 120, no. 9 (2019): 14936-14945, https://doi.org/10.1002/jcb.28756.</p><p>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":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30623","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
There are presently no acknowledged therapeutic targets or official drugs for the treatment of muscle fatigue. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is expressed in skeletal muscle, with an unknown role in muscle endurance. Here, we try to explore whether α7nAChR could act as a potential therapeutic target for the treatment of muscle fatigue. Results showed that nicotine and PNU-282987 (PNU), as nonspecific and specific agonists of α7nAChR, respectively, could both significantly increase C57BL6/J mice treadmill-running time in a time- and dose-dependent manner. The improvement effect of PNU on running time and ex vivo muscle fatigue index disappeared when α7nAChR deletion. RNA sequencing revealed that the differential mRNAs affected by PNU were enriched in glycolysis/gluconeogenesis signaling pathways. Further studies found that PNU treatment significantly elevates glycogen content and ATP level in the muscle tissues of α7nAChR+/+ mice but not α7nAChR-/- mice. α7nAChR activation specifically increased endogenous glycogen-targeting protein orosomucoid (ORM) expression both in vivo skeletal muscle tissues and in vitro C2C12 skeletal muscle cells. In ORM1 deficient mice, the positive effects of PNU on running time, glycogen and ATP content, as well as muscle fatigue index, were abolished. Therefore, the activation of α7nAChR could enhance muscle endurance via elevating endogenous anti-fatigue protein ORM and might act as a promising therapeutic strategy for the treatment of muscle fatigue.
目前还没有公认的治疗目标或治疗肌肉疲劳的正式药物。α7烟碱乙酰胆碱受体（α7nAChR）在骨骼肌中表达，在肌肉耐力中的作用尚不清楚。在此，我们试图探讨α7nAChR是否可以作为治疗肌肉疲劳的潜在治疗靶点。结果表明，尼古丁和PNU-282987（PNU）分别作为α7nAChR的非特异性和特异性激动剂，均能以时间和剂量依赖的方式显著增加C57BL6/J小鼠的跑步机跑步时间。当α7nAChR缺失时，PNU对跑步时间和体外肌肉疲劳指数的改善作用消失。RNA测序显示，受PNU影响的不同mRNA富集于糖酵解/糖元生成信号通路。进一步的研究发现，PNU能显著提高α7nAChR+/+小鼠肌肉组织中的糖原含量和ATP水平，但不能提高α7nAChR-/-小鼠的糖原含量和ATP水平。在 ORM1 缺乏的小鼠中，PNU 对跑步时间、糖原和 ATP 含量以及肌肉疲劳指数的积极影响被取消。因此，激活α7nAChR可通过提高内源性抗疲劳蛋白ORM来增强肌肉耐力，并可能成为治疗肌肉疲劳的一种有前景的治疗策略。
{"title":"Activation of α7 Nicotinic Acetylcholine Receptor Improves Muscle Endurance by Upregulating Orosomucoid Expression and Glycogen Content in Mice","authors":"Fei Chen, Zhen Zhang, Huimin Zhang, Pengyue Guo, Jiayi Feng, Hui Shen, Xia Liu","doi":"10.1002/jcb.30630","DOIUrl":"10.1002/jcb.30630","url":null,"abstract":"<div>\u0000 \u0000 <p>There are presently no acknowledged therapeutic targets or official drugs for the treatment of muscle fatigue. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is expressed in skeletal muscle, with an unknown role in muscle endurance. Here, we try to explore whether α7nAChR could act as a potential therapeutic target for the treatment of muscle fatigue. Results showed that nicotine and PNU-282987 (PNU), as nonspecific and specific agonists of α7nAChR, respectively, could both significantly increase C57BL6/J mice treadmill-running time in a time- and dose-dependent manner. The improvement effect of PNU on running time and ex vivo muscle fatigue index disappeared when α7nAChR deletion. RNA sequencing revealed that the differential mRNAs affected by PNU were enriched in glycolysis/gluconeogenesis signaling pathways. Further studies found that PNU treatment significantly elevates glycogen content and ATP level in the muscle tissues of α7nAChR<sup>+/+</sup> mice but not α7nAChR<sup>-/-</sup> mice. α7nAChR activation specifically increased endogenous glycogen-targeting protein orosomucoid (ORM) expression both in vivo skeletal muscle tissues and in vitro C2C12 skeletal muscle cells. In ORM1 deficient mice, the positive effects of PNU on running time, glycogen and ATP content, as well as muscle fatigue index, were abolished. Therefore, the activation of α7nAChR could enhance muscle endurance via elevating endogenous anti-fatigue protein ORM and might act as a promising therapeutic strategy for the treatment of muscle fatigue.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626835","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}
Bronchopulmonary dysplasia (BPD) is a serious disease that occurs in premature and low-birth-weight infants. In recent years, the incidence of BPD has not decreased, and there is no effective treatment for it. Oridonin (Ori) is a traditional Chinese medicine with a wide range of biological activities, especially pharmacological and anti-inflammatory. It is well known that inflammation plays a key role in BPD. However, the therapeutic effect of Ori on BPD has not been studied. Therefore, in the present study, we will observe the anti-inflammatory activity of Ori in an experimental animal model of BPD. Here, we showed that Ori could significantly decrease hyperoxia-induced alveolar injury, inhibit neutrophil recruitment, myeloperoxidase concentrations, and release inflammatory factors in BPD neonatal rats. Taken together, the experimental results suggested that Ori can significantly improve BPD in neonatal rats by inhibiting inflammatory response.
{"title":"Effect of Oridonin on Experimental Animal Model of Bronchopulmonary Dysplasia","authors":"Shanshan Zhang, Junfu Wang, Zhihong Xin, Chao Sun, Zhiye Ju, Xia Xue, Wen Jiang, Qian Xin, Jue Wang, Zhaohua Zhang, Yun Luan","doi":"10.1002/jcb.30632","DOIUrl":"10.1002/jcb.30632","url":null,"abstract":"<div>\u0000 \u0000 <p>Bronchopulmonary dysplasia (BPD) is a serious disease that occurs in premature and low-birth-weight infants. In recent years, the incidence of BPD has not decreased, and there is no effective treatment for it. Oridonin (Ori) is a traditional Chinese medicine with a wide range of biological activities, especially pharmacological and anti-inflammatory. It is well known that inflammation plays a key role in BPD. However, the therapeutic effect of Ori on BPD has not been studied. Therefore, in the present study, we will observe the anti-inflammatory activity of Ori in an experimental animal model of BPD. Here, we showed that Ori could significantly decrease hyperoxia-induced alveolar injury, inhibit neutrophil recruitment, myeloperoxidase concentrations, and release inflammatory factors in BPD neonatal rats. Taken together, the experimental results suggested that Ori can significantly improve BPD in neonatal rats by inhibiting inflammatory response.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141626836","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}
RETRACTION: A. Rajabian, H. R. Sadeghnia, A. Hosseini, S. H. Mousavi and M. T. Boroushaki, “3-Acetyl-11-Keto-β-Boswellic Acid Attenuated Oxidative Glutamate Toxicity in Neuron-like Cell Lines by Apoptosis Inhibition,” Journal of Cellular Biochemistry 121, no. 2 (2020): 1778-1789, https://doi.org/10.1002/jcb.29413.
The above article, published online on 23 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed due to concerns regarding the suspected splicing of western blot bands presented in the Bax panel of Figure 5c. Furthermore, concerns were raised regarding the unexpected similarity of flow cytometry data representing different experiments shown in Figure 5A (Co-treatment with AKBA 2.5 µM panel) and Figure 5B (Glutamate 8 mM panel). Although the authors provided some supporting data, it was not sufficient to alleviate the concerns. As a result, the editors consider the results and conclusion reported in this article unreliable.
撤回：A. Rajabian, H. R. Sadeghnia, A. Hosseini, S. H. Mousavi and M. T. Boroushaki, "3-Acetyl-11-Keto-β-Boswellic Acid Attenuated Oxidative Glutamate Toxicity in Neuron-like Cell Lines by Apoptosis Inhibition," Journal of Cellular Biochemistry 121, no. 2 (2020): 1778-1789, https://doi.org/10.1002/jcb.29413.The above article published online on 23 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC.同意撤稿的原因是对图 5c 的 Bax 面板中出现的 Western 印迹条带疑似拼接的担忧。此外，图5A（AKBA 2.5 µM联合处理面板）和图5B（谷氨酸8 mM面板）中代表不同实验的流式细胞仪数据意外相似也引起了关注。虽然作者提供了一些辅助数据，但不足以消除人们的疑虑。因此，编辑认为本文报告的结果和结论不可靠。
{"title":"RETRACTION: 3-Acetyl-11-Keto-β-Boswellic Acid Attenuated Oxidative Glutamate Toxicity in Neuron-like Cell Lines by Apoptosis Inhibition","authors":"","doi":"10.1002/jcb.30625","DOIUrl":"10.1002/jcb.30625","url":null,"abstract":"<p><b>RETRACTION:</b> A. Rajabian, H. R. Sadeghnia, A. Hosseini, S. H. Mousavi and M. T. Boroushaki, “3-Acetyl-11-Keto-β-Boswellic Acid Attenuated Oxidative Glutamate Toxicity in Neuron-like Cell Lines by Apoptosis Inhibition,” <i>Journal of Cellular Biochemistry</i> 121, no. 2 (2020): 1778-1789, https://doi.org/10.1002/jcb.29413.</p><p>The above article, published online on 23 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed due to concerns regarding the suspected splicing of western blot bands presented in the Bax panel of Figure 5c. Furthermore, concerns were raised regarding the unexpected similarity of flow cytometry data representing different experiments shown in Figure 5A (Co-treatment with AKBA 2.5 µM panel) and Figure 5B (Glutamate 8 mM panel). Although the authors provided some supporting data, it was not sufficient to alleviate the concerns. As a result, the editors consider the results and conclusion reported in this article unreliable.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30625","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141620078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
F. Gulluni, M. Martini, E. Hirsch, “Cytokinetic Abscission: Phosphoinositides and ESCRTs Direct the Final Cut,” Journal of Cellular Biochemistry 118, no. 11 (2017): 3561–3568, https://doi.org/10.1002/jcb.26066.
The authors hereby recognize that in writing the article above, they did not adequately acknowledge the significant contributions of sources [1] and [2], which profoundly influenced the shaping of the content of the article.
The compilation of this review benefited substantially from the insights and research provided by the aforementioned sources and the authors regret any oversight in properly attributing the influence of these sources within the text of their article.
F.Gulluni, M. Martini, E. Hirsch, "Cytokinetic Abscission：磷酸肌酸和 ESCRTs 指导最终切割》，《细胞生物化学杂志》第 118 期，第 11 号（2017 年）：3561-3568, https://doi.org/10.1002/jcb.26066.The 作者在此承认，在撰写上述文章时，他们没有充分肯定资料来源[1]和[2]的重要贡献，这些贡献对文章内容的形成产生了深远的影响。本综述的编撰在很大程度上得益于上述资料来源提供的见解和研究，作者对在文章正文中未能正确归因于这些资料来源的影响表示遗憾。
{"title":"Correction to “Cytokinetic Abscission: Phosphoinositides and ESCRTs Direct the Final Cut”","authors":"","doi":"10.1002/jcb.30626","DOIUrl":"10.1002/jcb.30626","url":null,"abstract":"<p>F. Gulluni, M. Martini, E. Hirsch, “Cytokinetic Abscission: Phosphoinositides and ESCRTs Direct the Final Cut,” <i>Journal of Cellular Biochemistry</i> 118, no. 11 (2017): 3561–3568, https://doi.org/10.1002/jcb.26066.</p><p>The authors hereby recognize that in writing the article above, they did not adequately acknowledge the significant contributions of sources [<span>1</span>] and [<span>2</span>], which profoundly influenced the shaping of the content of the article.</p><p>The compilation of this review benefited substantially from the insights and research provided by the aforementioned sources and the authors regret any oversight in properly attributing the influence of these sources within the text of their article.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30626","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Baiting Liu, Chenxi Li, Yunyao Bo, Guiping Tian, Lijun Yang, Jianjun Si, Lin Zhang, Yuan Yan
The current treatment of skin fibrosis is limited in its effectiveness due to a lack of understanding of the underlying mechanisms. Previous research has shown a connection between microRNAs (miRNAs) and the development of skin fibrosis. Therefore, investigating miRNA for the treatment of skin fibrotic diseases is highly important and merits further exploration. In this study, we have discovered that let-7f-5p could suppress the proliferation, migration, and expression of collagen type I alpha 1 (COL1A1) in human dermal fibroblasts (HDFs). It was further determined that let-7f-5p could target thrombospondin-1 (THBS1), thereby inhibiting the TGF-β2/Smad3 signaling pathway and exerting its biological effects. Additionally, let-7f-5p is regulated by Hsa_circ_0000437, which acts as a sponge molecule for let-7f-5p and consequently regulates the biological function of HDFs. Furthermore, our findings indicate that in vivo overexpression of let-7f-5p leads to a reduction in dermal thickness and COL1A1 expression, effectively inhibiting the progression of bleomycin (BLM)-induced skin fibrosis in mice. Hence, our research enhances the comprehension of the Hsa_circ_0000437/let-7f-5p/THBS1/TGF-β2/Smad3 regulatory network, highlighting the potential of let-7f-5p as a therapeutic approach for the treatment of skin fibrosis.
{"title":"Let‑7f‑5p Regulated by Hsa_circ_0000437 Ameliorates Bleomycin-Induced Skin Fibrosis","authors":"Baiting Liu, Chenxi Li, Yunyao Bo, Guiping Tian, Lijun Yang, Jianjun Si, Lin Zhang, Yuan Yan","doi":"10.1002/jcb.30629","DOIUrl":"10.1002/jcb.30629","url":null,"abstract":"<div>\u0000 \u0000 <p>The current treatment of skin fibrosis is limited in its effectiveness due to a lack of understanding of the underlying mechanisms. Previous research has shown a connection between microRNAs (miRNAs) and the development of skin fibrosis. Therefore, investigating miRNA for the treatment of skin fibrotic diseases is highly important and merits further exploration. In this study, we have discovered that let-7f-5p could suppress the proliferation, migration, and expression of collagen type I alpha 1 (COL1A1) in human dermal fibroblasts (HDFs). It was further determined that let-7f-5p could target thrombospondin-1 (THBS1), thereby inhibiting the TGF-β2/Smad3 signaling pathway and exerting its biological effects. Additionally, let-7f-5p is regulated by Hsa_circ_0000437, which acts as a sponge molecule for let-7f-5p and consequently regulates the biological function of HDFs. Furthermore, our findings indicate that in vivo overexpression of let-7f-5p leads to a reduction in dermal thickness and COL1A1 expression, effectively inhibiting the progression of bleomycin (BLM)-induced skin fibrosis in mice. Hence, our research enhances the comprehension of the Hsa_circ_0000437/let-7f-5p/THBS1/TGF-β2/Smad3 regulatory network, highlighting the potential of let-7f-5p as a therapeutic approach for the treatment of skin fibrosis.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616526","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号