In contrast to humans, zebrafish have an outstanding ability to regenerate injured heart through a highly orchestrated process involving all cardiac structures. To replace the lost myocardium, resident cardiomyocytes (CMs) dedifferentiate and proliferate, invading the injured area. The response of the myocardium is preceded by the activation of the epicardium and endocardium, which form active scaffolds to provide mechanical and paracrine support to guide regeneration. New CMs use protrusions to migrate and invade fibrotic injured tissue, replacing it with functional myocardium. Here, we investigated the expression profile of the stress-responsive ankrd1a gene in different cardiac structures, at key time points during regeneration, aiming to gain insight into its precise roles during zebrafish heart regeneration. In the TgBAC(ankrd1a:EGFP) reporter line, transgene upregulation was restricted to the myocardium, initiated as early as 15 h post-cryoinjury, and consistently marked CMs bordering the injury or scar area during regeneration. Transcriptome profiling and immunostaining revealed a potential role of ankrd1a in regulating CMs' dedifferentiation, as well as changes in the expression of genes associated with antigen presentation and extracellular matrix composition in the ankrd1a mutant. Our results indicate that ankrd1a is dispensable for ventricular regeneration after cryoinjury, while it may serve as a marker and fine-tuner in the healing process of injured cardiac muscle.
{"title":"ankrd1a is consistently upregulated in cardiomyocytes bordering the injury or scar area and affects their dedifferentiation during zebrafish heart regeneration.","authors":"Srdjan Boskovic, Mirjana Novkovic, Andjela Milicevic, Emilija Milosevic, Jovana Jasnic, Mina Milovanovic, Snezana Kojic","doi":"10.1016/j.cdev.2026.204082","DOIUrl":"https://doi.org/10.1016/j.cdev.2026.204082","url":null,"abstract":"<p><p>In contrast to humans, zebrafish have an outstanding ability to regenerate injured heart through a highly orchestrated process involving all cardiac structures. To replace the lost myocardium, resident cardiomyocytes (CMs) dedifferentiate and proliferate, invading the injured area. The response of the myocardium is preceded by the activation of the epicardium and endocardium, which form active scaffolds to provide mechanical and paracrine support to guide regeneration. New CMs use protrusions to migrate and invade fibrotic injured tissue, replacing it with functional myocardium. Here, we investigated the expression profile of the stress-responsive ankrd1a gene in different cardiac structures, at key time points during regeneration, aiming to gain insight into its precise roles during zebrafish heart regeneration. In the TgBAC(ankrd1a:EGFP) reporter line, transgene upregulation was restricted to the myocardium, initiated as early as 15 h post-cryoinjury, and consistently marked CMs bordering the injury or scar area during regeneration. Transcriptome profiling and immunostaining revealed a potential role of ankrd1a in regulating CMs' dedifferentiation, as well as changes in the expression of genes associated with antigen presentation and extracellular matrix composition in the ankrd1a mutant. Our results indicate that ankrd1a is dispensable for ventricular regeneration after cryoinjury, while it may serve as a marker and fine-tuner in the healing process of injured cardiac muscle.</p>","PeriodicalId":29860,"journal":{"name":"Cells & Development","volume":" ","pages":"204082"},"PeriodicalIF":2.0,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147491933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The incidence of allergic asthma has been increasing worldwide in recent decades. Also, an increasing number of women are suffering from poor pregnancy outcome. However, the causal relationship between allergic asthma and embryonic growth in terms of cell morphogenesis has not been well elucidated. Here, we investigated the impact of allergic asthma on the morphogenesis of preimplantation embryos. Twenty-four female BALB/c were randomly divided into control (PBS), 50-μg (OVA1), 100-μg (OVA2) and 150-μg (OVA3). On Days-0 and -14, mice were induced intraperitoneally (i.p) with ovalbumin (OVA). On Days-21 until -23, mice were challenged with OVA via intranasal instillation (i.n). Control animals were sensitized and challenged with PBS. At the end of treatment (Day-25), 2-cell embryos were retrieved and cultured in vitro until the blastocysts hatched. Results showed reduced number of preimplantation embryos at all developing stages in all treated groups (p ≤ 0.0001). Uneven blastomere size, partial compaction- and cavitation-activity, low formation of trophectoderm (TE), as well as cell fragmentation were noted in all the treated groups. Maternal serum interleukin (IL)-4, immunoglobulin (Ig)-E and 8-hydroxydeoxyguanosine (8-OHdG) were notably high (p ≤ 0.0001, p ≤ 0.01) in contrast with low total antioxidant capacity (TAOC) (p ≤ 0.0001). Our findings indicated that OVA-induced allergic asthma had compromised cell morphogenesis through reduced blastomere cleavage division, partial compaction and cavitation-activity, impairment of TE production, and cell fragmentation leading to embryonic cell death via OS mechanism.
{"title":"Inflammation and oxidative stress impair preimplantation embryonic morphogenesis in allergic asthma model.","authors":"Che Ismail Wafriy, Y. S. Kamsani, M. Nor-Ashikin","doi":"10.2139/ssrn.4367239","DOIUrl":"https://doi.org/10.2139/ssrn.4367239","url":null,"abstract":"The incidence of allergic asthma has been increasing worldwide in recent decades. Also, an increasing number of women are suffering from poor pregnancy outcome. However, the causal relationship between allergic asthma and embryonic growth in terms of cell morphogenesis has not been well elucidated. Here, we investigated the impact of allergic asthma on the morphogenesis of preimplantation embryos. Twenty-four female BALB/c were randomly divided into control (PBS), 50-μg (OVA1), 100-μg (OVA2) and 150-μg (OVA3). On Days-0 and -14, mice were induced intraperitoneally (i.p) with ovalbumin (OVA). On Days-21 until -23, mice were challenged with OVA via intranasal instillation (i.n). Control animals were sensitized and challenged with PBS. At the end of treatment (Day-25), 2-cell embryos were retrieved and cultured in vitro until the blastocysts hatched. Results showed reduced number of preimplantation embryos at all developing stages in all treated groups (p ≤ 0.0001). Uneven blastomere size, partial compaction- and cavitation-activity, low formation of trophectoderm (TE), as well as cell fragmentation were noted in all the treated groups. Maternal serum interleukin (IL)-4, immunoglobulin (Ig)-E and 8-hydroxydeoxyguanosine (8-OHdG) were notably high (p ≤ 0.0001, p ≤ 0.01) in contrast with low total antioxidant capacity (TAOC) (p ≤ 0.0001). Our findings indicated that OVA-induced allergic asthma had compromised cell morphogenesis through reduced blastomere cleavage division, partial compaction and cavitation-activity, impairment of TE production, and cell fragmentation leading to embryonic cell death via OS mechanism.","PeriodicalId":29860,"journal":{"name":"Cells & Development","volume":"1943 1","pages":"203864"},"PeriodicalIF":3.9,"publicationDate":"2023-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91204783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mehedi Hasan, Shizuka Konishi, Miyuu Tanaka, T. Izawa, J. Yamate, M. Kuwamura
Coil-coiled domain containing 85c (Ccdc85c) is a causative gene for congenital hydrocephalus and subcortical heterotopia with frequent brain hemorrhage. We established Ccdc85c knockout (KO) rats and investigated the roles of CCDC85C and intermediate filament protein expression, including nestin, vimentin, GFAP, and cytokeratin AE1/AE3 during the lateral ventricle development in KO rats to evaluate the role of this gene. We found altered and ectopic expression of nestin and vimentin positive cells in the wall of the dorso-lateral ventricle in the KO rats during development from the age of postnatal day (P) 6, whereas both protein expression became faint in the wild-type rats. In the KO rats, there was a loss of cytokeratin expression on the surface of the dorso-lateral ventricle with ectopic expression and maldevelopment of ependymal cells. Our data also revealed disturbed GFAP expression at postnatal ages. These findings indicate that lack of CCDC85C disrupts the proper expression of intermediate filament proteins (nestin, vimentin, GFAP, and cytokeratin), and CCDC85C is necessary for normal neurogenesis, gliogenesis, and ependymogenesis.
{"title":"Disrupted neurogenesis, gliogenesis, and ependymogenesis in the Ccdc85c knockout rat for hydrocephalus model.","authors":"Mehedi Hasan, Shizuka Konishi, Miyuu Tanaka, T. Izawa, J. Yamate, M. Kuwamura","doi":"10.2139/ssrn.4367238","DOIUrl":"https://doi.org/10.2139/ssrn.4367238","url":null,"abstract":"Coil-coiled domain containing 85c (Ccdc85c) is a causative gene for congenital hydrocephalus and subcortical heterotopia with frequent brain hemorrhage. We established Ccdc85c knockout (KO) rats and investigated the roles of CCDC85C and intermediate filament protein expression, including nestin, vimentin, GFAP, and cytokeratin AE1/AE3 during the lateral ventricle development in KO rats to evaluate the role of this gene. We found altered and ectopic expression of nestin and vimentin positive cells in the wall of the dorso-lateral ventricle in the KO rats during development from the age of postnatal day (P) 6, whereas both protein expression became faint in the wild-type rats. In the KO rats, there was a loss of cytokeratin expression on the surface of the dorso-lateral ventricle with ectopic expression and maldevelopment of ependymal cells. Our data also revealed disturbed GFAP expression at postnatal ages. These findings indicate that lack of CCDC85C disrupts the proper expression of intermediate filament proteins (nestin, vimentin, GFAP, and cytokeratin), and CCDC85C is necessary for normal neurogenesis, gliogenesis, and ependymogenesis.","PeriodicalId":29860,"journal":{"name":"Cells & Development","volume":"79 1","pages":"203858"},"PeriodicalIF":3.9,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79305322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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