Pub Date : 2024-07-01DOI: 10.1016/j.mocell.2024.100077
Polash Kumar Biswas , Jinkyu Park
Vascular disease, including heart disease, stroke, and peripheral arterial disease, is one of the leading causes of death and disability and represents a significant global health issue. Since the development of human induced pluripotent stem cells (hiPSCs) in 2007, hiPSCs have provided unique and tremendous opportunities for studying human pathophysiology, disease modeling, and drug discovery in the field of regenerative medicine. In this review, we discuss vascular physiology and related diseases, the current methods for generating vascular cells (eg, endothelial cells, smooth muscle cells, and pericytes) from hiPSCs, and describe the opportunities and challenges to the clinical applications of vascular organoids, tissue-engineered blood vessels, and vessels-on-a-chip. We then explore how hiPSCs can be used to study and treat inherited vascular diseases and discuss the current challenges and future prospects. In the future, it will be essential to develop vascularized organoids or tissues that can simultaneously undergo shear stress and cyclic stretching. This development will not only increase their maturity and function but also enable effective and innovative disease modeling and drug discovery.
{"title":"Applications, challenges, and prospects of induced pluripotent stem cells for vascular disease","authors":"Polash Kumar Biswas , Jinkyu Park","doi":"10.1016/j.mocell.2024.100077","DOIUrl":"10.1016/j.mocell.2024.100077","url":null,"abstract":"<div><p>Vascular disease, including heart disease, stroke, and peripheral arterial disease, is one of the leading causes of death and disability and represents a significant global health issue. Since the development of human induced pluripotent stem cells (hiPSCs) in 2007, hiPSCs have provided unique and tremendous opportunities for studying human pathophysiology, disease modeling, and drug discovery in the field of regenerative medicine. In this review, we discuss vascular physiology and related diseases, the current methods for generating vascular cells (eg, endothelial cells, smooth muscle cells, and pericytes) from hiPSCs, and describe the opportunities and challenges to the clinical applications of vascular organoids, tissue-engineered blood vessels, and vessels-on-a-chip. We then explore how hiPSCs can be used to study and treat inherited vascular diseases and discuss the current challenges and future prospects. In the future, it will be essential to develop vascularized organoids or tissues that can simultaneously undergo shear stress and cyclic stretching. This development will not only increase their maturity and function but also enable effective and innovative disease modeling and drug discovery.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S101684782400102X/pdfft?md5=2bf771e13defe325e4bdc3720eb1e2b7&pid=1-s2.0-S101684782400102X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199358","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}
Pub Date : 2024-07-01DOI: 10.1016/j.mocell.2024.100074
Hyejin Mun , Sungyul Lee , Suyoung Choi , Ji-Hoon Jeong , Seungbeom Ko , Yoo Lim Chun , Benjamin Deaton , Clay T. Yeager , Audrey Boyette , Juliana Palmera , London Newman , Ping Zhou , Soona Shin , Dong-Chan Kim , Cari A. Sagum , Mark T. Bedford , Young-Kook Kim , Jaeyul Kwon , Junyang Jung , Jeong Ho Chang , Je-Hyun Yoon
Although binge alcohol-induced gut leakage has been studied extensively in the context of reactive oxygen species−mediated signaling, it was recently revealed that post-transcriptional regulation plays an essential role as well. Ethanol (EtOH)-inducible cytochrome P450-2E1 (CYP2E1), a key enzyme in EtOH metabolism, promotes alcohol-induced hepatic steatosis and inflammatory liver disease, at least in part by mediating changes in intestinal permeability. For instance, gut leakage and elevated intestinal permeability to endotoxins have been shown to be regulated by enhancing CYP2E1 mRNA and CYP2E1 protein levels. Although it is understood that EtOH promotes CYP2E1 induction and activation, the mechanisms that regulate CYP2E1 expression in the context of intestinal damage remain poorly defined. Specific miRNAs, including miR-132, miR-212, miR-378, and miR-552, have been shown to repress the expression of CYP2E1, suggesting that these miRNAs contribute to EtOH-induced intestinal injury. Here, we have shown that CYP2E1 expression is regulated post-transcriptionally through miRNA-mediated degradation, as follows: (1) the RNA-binding protein AU-binding factor 1 (AUF1) binds mature miRNAs, including CYP2E1-targeting miRNAs, and this binding modulates the degradation of corresponding target mRNAs upon EtOH treatment; (2) the serine/threonine kinase mammalian Ste20-like kinase 1 (MST1) mediates oxidative stress-induced phosphorylation of AUF1. Those findings suggest that reactive oxygen species−mediated signaling modulates AUF1/miRNA interaction through MST1-mediated phosphorylation. Thus, our study demonstrates the critical functions of AUF1 phosphorylation by MST1 in the decay of miRNAs targeting CYP2E1, the stabilization of CYP2E1 mRNA in the presence of EtOH, and the relationship of this pathway to subsequent intestinal injury.
{"title":"Targeting of CYP2E1 by miRNAs in alcohol-induced intestine injury","authors":"Hyejin Mun , Sungyul Lee , Suyoung Choi , Ji-Hoon Jeong , Seungbeom Ko , Yoo Lim Chun , Benjamin Deaton , Clay T. Yeager , Audrey Boyette , Juliana Palmera , London Newman , Ping Zhou , Soona Shin , Dong-Chan Kim , Cari A. Sagum , Mark T. Bedford , Young-Kook Kim , Jaeyul Kwon , Junyang Jung , Jeong Ho Chang , Je-Hyun Yoon","doi":"10.1016/j.mocell.2024.100074","DOIUrl":"10.1016/j.mocell.2024.100074","url":null,"abstract":"<div><p>Although binge alcohol-induced gut leakage has been studied extensively in the context of reactive oxygen species−mediated signaling, it was recently revealed that post-transcriptional regulation plays an essential role as well. Ethanol (EtOH)-inducible cytochrome P450-2E1 (CYP2E1), a key enzyme in EtOH metabolism, promotes alcohol-induced hepatic steatosis and inflammatory liver disease, at least in part by mediating changes in intestinal permeability. For instance, gut leakage and elevated intestinal permeability to endotoxins have been shown to be regulated by enhancing CYP2E1 mRNA and CYP2E1 protein levels. Although it is understood that EtOH promotes CYP2E1 induction and activation, the mechanisms that regulate CYP2E1 expression in the context of intestinal damage remain poorly defined. Specific miRNAs, including miR-132, miR-212, miR-378, and miR-552, have been shown to repress the expression of CYP2E1, suggesting that these miRNAs contribute to EtOH-induced intestinal injury. Here, we have shown that CYP2E1 expression is regulated post-transcriptionally through miRNA-mediated degradation, as follows: (1) the RNA-binding protein AU-binding factor 1 (AUF1) binds mature miRNAs, including CYP2E1-targeting miRNAs, and this binding modulates the degradation of corresponding target mRNAs upon EtOH treatment; (2) the serine/threonine kinase mammalian Ste20-like kinase 1 (MST1) mediates oxidative stress-induced phosphorylation of AUF1. Those findings suggest that reactive oxygen species−mediated signaling modulates AUF1/miRNA interaction through MST1-mediated phosphorylation. Thus, our study demonstrates the critical functions of AUF1 phosphorylation by MST1 in the decay of miRNAs targeting CYP2E1, the stabilization of CYP2E1 mRNA in the presence of EtOH, and the relationship of this pathway to subsequent intestinal injury.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824000992/pdfft?md5=dea4fa27555631752ec04bd247960d42&pid=1-s2.0-S1016847824000992-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141432333","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}
Pub Date : 2024-07-01DOI: 10.1016/S1016-8478(24)00123-7
{"title":"Cover and caption","authors":"","doi":"10.1016/S1016-8478(24)00123-7","DOIUrl":"10.1016/S1016-8478(24)00123-7","url":null,"abstract":"","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824001237/pdfft?md5=9bbf9a7846e8a9f21278537c79dcaed9&pid=1-s2.0-S1016847824001237-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141729637","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}
Pub Date : 2024-07-01DOI: 10.1016/j.mocell.2024.100078
Su Young Ki , Yong Taek Jeong
The sense of taste arises from the detection of chemicals in food by taste buds, the peripheral cellular detectors for taste. Although numerous studies have extensively investigated taste buds, research on neural circuits from primary taste neurons innervating taste buds to the central nervous system has only recently begun owing to recent advancements in neuroscience research tools. This minireview focuses primarily on recent reports utilizing advanced neurogenetic tools across relevant brain regions.
{"title":"Neural circuits for taste sensation","authors":"Su Young Ki , Yong Taek Jeong","doi":"10.1016/j.mocell.2024.100078","DOIUrl":"10.1016/j.mocell.2024.100078","url":null,"abstract":"<div><p>The sense of taste arises from the detection of chemicals in food by taste buds, the peripheral cellular detectors for taste. Although numerous studies have extensively investigated taste buds, research on neural circuits from primary taste neurons innervating taste buds to the central nervous system has only recently begun owing to recent advancements in neuroscience research tools. This minireview focuses primarily on recent reports utilizing advanced neurogenetic tools across relevant brain regions.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824001031/pdfft?md5=943f6fbac03ea00e32a61f10e91e1857&pid=1-s2.0-S1016847824001031-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199474","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}
Pub Date : 2024-06-11DOI: 10.1016/j.mocell.2024.100079
Ying Li , Li Wan , Hexin Li , Xiaokun Tang , Siyuan Xu , Gaoyuan Sun , Wei Huang , Min Tang
The nonsense-mediated mRNA decay (NMD) pathway and the p53 pathway, linked to tumorgenesis, are also promising targets for cancer treatment. NMD plays an important role in RNA quality control, while the p53 pathway is involved in cancer suppression. However, their individual and combined effects on cervical cancer are poorly understood. In this study, we evaluated the impacts of NMD inhibitor, Mouse double minute 2 homolog (MDM2) inhibitor, and their combination on cell apoptosis, cell cycle, and p53 target genes in human papillomavirus-18-positive HeLa cells. Our findings revealed that XR-2 failed to activate p53 or induce apoptosis in HeLa cells, whereas SMG1 (serine/threonine-protein kinase 1) inhibitor repressed cell proliferation at high concentrations. Notably, the combination of these 2 agents significantly inhibited cell proliferation, arrested the cell cycle, and triggered cell apoptosis. Mechanistically, MDM2 inhibitor and NMD inhibitor likely exert a synergistically through the truncated E6 protein. These results underscore the potential of employing a combination of MDM2 inhibitor and NMD inhibitor as a promising candidate for the clinical treatment of human papillomavirus-infected tumors.
{"title":"Small molecule NMD and MDM2 inhibitors synergistically trigger apoptosis in HeLa cells","authors":"Ying Li , Li Wan , Hexin Li , Xiaokun Tang , Siyuan Xu , Gaoyuan Sun , Wei Huang , Min Tang","doi":"10.1016/j.mocell.2024.100079","DOIUrl":"10.1016/j.mocell.2024.100079","url":null,"abstract":"<div><p>The nonsense-mediated mRNA decay (NMD) pathway and the p53 pathway, linked to tumorgenesis, are also promising targets for cancer treatment. NMD plays an important role in RNA quality control, while the p53 pathway is involved in cancer suppression. However, their individual and combined effects on cervical cancer are poorly understood. In this study, we evaluated the impacts of NMD inhibitor, Mouse double minute 2 homolog (MDM2) inhibitor, and their combination on cell apoptosis, cell cycle, and p53 target genes in human papillomavirus-18-positive HeLa cells. Our findings revealed that XR-2 failed to activate p53 or induce apoptosis in HeLa cells, whereas SMG1 (serine/threonine-protein kinase 1) inhibitor repressed cell proliferation at high concentrations. Notably, the combination of these 2 agents significantly inhibited cell proliferation, arrested the cell cycle, and triggered cell apoptosis. Mechanistically, MDM2 inhibitor and NMD inhibitor likely exert a synergistically through the truncated E6 protein. These results underscore the potential of employing a combination of MDM2 inhibitor and NMD inhibitor as a promising candidate for the clinical treatment of human papillomavirus-infected tumors.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824001043/pdfft?md5=ee94b83955f4b04d17c7a5c110530282&pid=1-s2.0-S1016847824001043-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317811","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}
Pub Date : 2024-06-01DOI: 10.1016/j.mocell.2024.100075
Ji Hye Han , Sun-Young Park , Seung-Hyun Myung , Junghee Park , Jeong Hwan Chang , Tae-Hyoung Kim
Excessive blood vessel wall thickening, known as intimal hyperplasia, can result from injury or inflammation and increase the risk of vascular diseases. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays key roles in tumor surveillance, autoimmune diseases, and apoptosis; however, its role in vascular stenosis remains controversial. Treatment with recombinant isoleucine zipper hexamerization domain soluble TRAIL (ILz(6):TRAIL) significantly inhibited the progression of neointimal hyperplasia (NH) induced by anastomosis of the carotid artery and jugular vein dose dependently, and adenovirus expressing secretable ILz(6):TRAIL also inhibited NH induced by balloon injury in the femoral artery of rats. This study demonstrated the preventive and partial regressive effects of ILz(6):TRAIL on anastomosis of the carotid artery and jugular vein- or balloon-induced NH.
{"title":"Suppression of neointimal hyperplasia induced by arteriovenous anastomosis and balloon injury in rats by multimeric tumor necrosis factor-related apoptosis-inducing ligand","authors":"Ji Hye Han , Sun-Young Park , Seung-Hyun Myung , Junghee Park , Jeong Hwan Chang , Tae-Hyoung Kim","doi":"10.1016/j.mocell.2024.100075","DOIUrl":"10.1016/j.mocell.2024.100075","url":null,"abstract":"<div><p>Excessive blood vessel wall thickening, known as intimal hyperplasia, can result from injury or inflammation and increase the risk of vascular diseases. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays key roles in tumor surveillance, autoimmune diseases, and apoptosis; however, its role in vascular stenosis remains controversial. Treatment with recombinant isoleucine zipper hexamerization domain soluble TRAIL (ILz(6):TRAIL) significantly inhibited the progression of neointimal hyperplasia (NH) induced by <em>a</em>nastomosis of the carotid <em>a</em>rtery and jugular <em>v</em>ein dose dependently, and adenovirus expressing secretable ILz(6):TRAIL also inhibited NH induced by balloon injury in the femoral artery of rats. This study demonstrated the preventive and partial regressive effects of ILz(6):TRAIL on <em>a</em>nastomosis of the carotid <em>a</em>rtery and jugular <em>v</em>ein- or balloon-induced NH.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824001006/pdfft?md5=6bc819e1ad1f76549c11b98a7f732c79&pid=1-s2.0-S1016847824001006-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186770","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}
Pub Date : 2024-06-01DOI: 10.1016/j.mocell.2024.100068
Jaeho Yoon , Santosh Kumar , Haeryung Lee , Zia Ur Rehman , Soochul Park , Unjoo Lee , Jaebong Kim
The coordinated movement of germ layer progenitor cells reaches its peak at the dorsal side, where the Bmp signaling gradient is low, and minimum at the ventral side, where the Bmp gradient is high. This dynamic cell movement is regulated by the interplay of various signaling pathways. The noncanonical Wnt signaling cascade serves as a pivotal regulator of convergence and extension cell movement, facilitated by the activation of small GTPases such as Rho, Rab, and Rac. However, the underlying cause of limited cell movement at the ventral side remains elusive. To explore the functional role of a key regulator in constraining gastrulation cell movement at the ventral side, we investigated the Bmp4-direct target gene, sizzled (szl), to assess its potential role in inhibiting noncanonical Wnt signaling. In our current study, we demonstrated that ectopic expression of szl led to gastrulation defects in a dose-dependent manner without altering cell fate specification. Overexpression of szl resulted in decreased elongation of Activin-treated animal cap and Keller explants. Furthermore, our immunoprecipitation assay unveiled the physical interaction of Szl with noncanonical Wnt ligand proteins (Wnt5 and Wnt11). Additionally, the activation of small GTPases involved in Wnt signaling mediation (RhoA and Rac1) was diminished upon szl overexpression. In summary, our findings suggest that Bmp4 signaling negatively modulates cell movement from the ventral side of the embryo by inducing szl expression during early Xenopus gastrulation.
{"title":"Sizzled (Frzb3) physically interacts with noncanonical Wnt ligands to inhibit gastrulation cell movement","authors":"Jaeho Yoon , Santosh Kumar , Haeryung Lee , Zia Ur Rehman , Soochul Park , Unjoo Lee , Jaebong Kim","doi":"10.1016/j.mocell.2024.100068","DOIUrl":"10.1016/j.mocell.2024.100068","url":null,"abstract":"<div><p>The coordinated movement of germ layer progenitor cells reaches its peak at the dorsal side, where the Bmp signaling gradient is low, and minimum at the ventral side, where the Bmp gradient is high. This dynamic cell movement is regulated by the interplay of various signaling pathways. The noncanonical Wnt signaling cascade serves as a pivotal regulator of convergence and extension cell movement, facilitated by the activation of small GTPases such as Rho, Rab, and Rac. However, the underlying cause of limited cell movement at the ventral side remains elusive. To explore the functional role of a key regulator in constraining gastrulation cell movement at the ventral side, we investigated the Bmp4-direct target gene, <em>sizzled (szl)</em>, to assess its potential role in inhibiting noncanonical Wnt signaling. In our current study, we demonstrated that ectopic expression of <em>szl</em> led to gastrulation defects in a dose-dependent manner without altering cell fate specification. Overexpression of <em>szl</em> resulted in decreased elongation of Activin-treated animal cap and Keller explants. Furthermore, our immunoprecipitation assay unveiled the physical interaction of Szl with noncanonical Wnt ligand proteins (Wnt5 and Wnt11). Additionally, the activation of small GTPases involved in Wnt signaling mediation (RhoA and Rac1) was diminished upon <em>szl</em> overexpression. In summary, our findings suggest that Bmp4 signaling negatively modulates cell movement from the ventral side of the embryo by inducing <em>szl</em> expression during early <em>Xenopus</em> gastrulation.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824000931/pdfft?md5=004b11b4790a71012924d9739a9b7366&pid=1-s2.0-S1016847824000931-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140958013","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}
Pub Date : 2024-06-01DOI: 10.1016/j.mocell.2024.100069
Jae Bum Kim
{"title":"In Memoriam: Dr Sang Dai Park, Renowned Pioneer in Molecular Biology and Genetic Engineering","authors":"Jae Bum Kim","doi":"10.1016/j.mocell.2024.100069","DOIUrl":"10.1016/j.mocell.2024.100069","url":null,"abstract":"","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824000943/pdfft?md5=96963d1e0f79c136a0dc9de1a0830d83&pid=1-s2.0-S1016847824000943-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141093800","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}
Pub Date : 2024-06-01DOI: 10.1016/j.mocell.2024.100076
Youni Kim , Hyun-Kyung Lee , Kyeong-Yeon Park , Tayaba Ismail , Hongchan Lee , Hong-Yeoul Ryu , Dong-Hyung Cho , Taeg Kyu Kwon , Tae Joo Park , Taejoon Kwon , Hyun-Shik Lee
The actin-based cytoskeleton is considered a fundamental driving force for cell differentiation and development. Destrin (Dstn), a member of the actin-depolymerizing factor family, regulates actin dynamics by treadmilling actin filaments and increasing globular actin pools. However, the specific developmental roles of dstn have yet to be fully elucidated. Here, we investigated the physiological functions of dstn during early embryonic development using Xenopus laevis as an experimental model organism. dstn is expressed in anterior neural tissue and neural plate during Xenopus embryogenesis. Depleting dstn promoted morphants with short body axes and small heads. Moreover, dstn inhibition extended the neural plate region, impairing cell migration and distribution during neurulation. In addition to the neural plate, dstn knockdown perturbed neural crest cell migration. Our data suggest new insights for understanding the roles of actin dynamics in embryonic neural development, simultaneously presenting a new challenge for studying the complex networks governing cell migration involving actin dynamics.
{"title":"Actin depolymerizing factor destrin governs cell migration in neural development during Xenopus embryogenesis","authors":"Youni Kim , Hyun-Kyung Lee , Kyeong-Yeon Park , Tayaba Ismail , Hongchan Lee , Hong-Yeoul Ryu , Dong-Hyung Cho , Taeg Kyu Kwon , Tae Joo Park , Taejoon Kwon , Hyun-Shik Lee","doi":"10.1016/j.mocell.2024.100076","DOIUrl":"10.1016/j.mocell.2024.100076","url":null,"abstract":"<div><p>The actin-based cytoskeleton is considered a fundamental driving force for cell differentiation and development. Destrin (Dstn), a member of the actin-depolymerizing factor family, regulates actin dynamics by treadmilling actin filaments and increasing globular actin pools. However, the specific developmental roles of <em>dstn</em> have yet to be fully elucidated. Here, we investigated the physiological functions of <em>dstn</em> during early embryonic development using <em>Xenopus laevis</em> as an experimental model organism. <em>dstn</em> is expressed in anterior neural tissue and neural plate during <em>Xenopus</em> embryogenesis. Depleting <em>dstn</em> promoted morphants with short body axes and small heads. Moreover, <em>dstn</em> inhibition extended the neural plate region, impairing cell migration and distribution during neurulation. In addition to the neural plate, <em>dstn</em> knockdown perturbed neural crest cell migration. Our data suggest new insights for understanding the roles of actin dynamics in embryonic neural development, simultaneously presenting a new challenge for studying the complex networks governing cell migration involving actin dynamics.</p></div>","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824001018/pdfft?md5=8f96d1e07e8e490be6c945bf1c40be5a&pid=1-s2.0-S1016847824001018-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199357","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}
Pub Date : 2024-06-01DOI: 10.1016/S1016-8478(24)00106-7
{"title":"Cover and caption","authors":"","doi":"10.1016/S1016-8478(24)00106-7","DOIUrl":"https://doi.org/10.1016/S1016-8478(24)00106-7","url":null,"abstract":"","PeriodicalId":18795,"journal":{"name":"Molecules and Cells","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1016847824001067/pdfft?md5=a254fd587efcbec8bcf558ab191e539d&pid=1-s2.0-S1016847824001067-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141423709","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}