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Copyright of Journal of Prevention & Treatment For Stomatological Diseases is the property of Journal of Prevention & Treatment For Stomatological Diseases Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Reversine is a purine derivative that has been investigated with regard to its biological effects, such as its anticancer properties and, mostly, its ability to induce the dedifferentiation of adult cells, increasing their plasticity. The obtained dedifferentiated cells have a high potential for use in regenerative procedures, such as regenerative dentistry (RD). Instead of replacing the lost or damaged oral tissues with synthetic materials, RD uses stem cells combined with matrices and an appropriate microenvironment to achieve tissue regeneration. However, the currently available stem cell sources present limitations, thus restricting the potential of RD. Based on this problem, new sources of stem cells are fundamental. This work aims to characterize mouse gingival fibroblasts (GFs) after dedifferentiation with reversine. Different administration protocols were tested, and the cells obtained were evaluated regarding their cell metabolism, protein and DNA contents, cell cycle changes, morphology, cell death, genotoxicity, and acquisition of stem cell characteristics. Additionally, their teratoma potential was evaluated after in vivo transplantation. Reversine caused toxicity at higher concentrations, with decreased cell metabolic activity and protein content. The cells obtained displayed polyploidy, a cycle arrest in the G2/M phase, and showed an enlarged size. Additionally, apoptosis and genotoxicity were found at higher reversine concentrations. A subpopulation of the GFs possessed stem properties, as supported by the increased expression of CD90, CD105, and TERT, the existence of a CD106+ population, and their trilineage differentiation capacity. The dedifferentiated cells did not induce teratoma formation. The extensive characterization performed shows that significant functional, morphological, and genetic changes occur during the dedifferentiation process. The dedifferentiated cells have some stem-like characteristics, which are of interest for RD. [ABSTRACT FROM AUTHOR]

Though it is well known that mammalian cardiomyocytes exit cell cycle soon after birth, the mechanisms that regulate proliferation remain to be fully elucidated. Recent studies reported that cardiomyocytes undergo dedifferentiation before proliferation, indicating the importance of dedifferentiation in cardiomyocyte proliferation. Since Runx1 is expressed in dedifferentiated cardiomyocytes, Runx1 is widely used as a dedifferentiation marker of cardiomyocytes; however, little is known about the role of Runx1 in the proliferation of cardiomyocytes. The purpose of this study was to clarify the functional significance of Runx1 in cardiomyocyte proliferation. qRT‐PCR analysis and immunoblot analysis demonstrated that Runx1 expression was upregulated in neonatal rat cardiomyocytes when cultured in the presence of FBS. Similarly, STAT3 was activated in the presence of FBS. Interestingly, knockdown of STAT3 significantly decreased Runx1 expression, indicating Runx1 is regulated by STAT3. We next investigated the effect of Runx1 on proliferation. Immunofluorescence microscopic analysis using an anti‐Ki‐67 antibody revealed that knockdown of Runx1 decreased the ratio of proliferating cardiomyocytes. Conversely, Runx1 overexpression using adenovirus vector induced cardiomyocyte proliferation in the absence of FBS. Finally, RNA‐sequencing analysis revealed that Runx1 overexpression induced upregulation of cardiac fetal genes and downregulation of genes associated with fatty acid oxidation. Collectively, Runx1 is regulated by STAT3 and induces cardiomyocyte proliferation by juvenilizing cardiomyocytes. [ABSTRACT FROM AUTHOR]

Glucagon-secreting pancreatic a-cells play pivotal roles in the development of diabetes. Glucagon promotes insulin secretion from b-cells. However, the long-term effect of glucagon on the function and phenotype of &#914-cells had remained elusive. In this study, we found that long-term glucagon intervention or glucagon intervention with the presence of palmitic acid downregulated &#914-cell-specific markers and inhibited insulin secretion in cultured &#914-cells. These results suggested that glucagon induced &#914-cell dedifferentiation under pathological conditions. Glucagon blockage by a glucagon receptor (GCGR) monoclonal antibody (mAb) attenuated glucagon-induced &#914-cell dedifferentiation. In primary islets, GCGR mAb treatment upregulated &#914-cell-specific markers and increased insulin content, suggesting that blockage of endogenous glucagon-GCGR signaling inhibited &#914-cell dedifferentiation. To investigate the possible mechanism, we found that glucagon decreased FoxO1 expression. FoxO1 inhibitor mimicked the effect of glucagon, whereas FoxO1 overexpression reversed the glucagon-induced &#914-cell dedifferentiation. In db/db mice and &#914-cell lineage-tracing diabetic mice, GCGR mAb lowered glucose level, upregulated plasma insulin level, increased &#914-cell area, and inhibited &#914-cell dedifferentiation. In aged &#914-cell-specific FoxO1 knockout mice (with the blood glucose level elevated as a diabetic model), the glucose-lowering effect of GCGR mAb was attenuated and the plasma insulin level, &#914-cell area, and &#914-cell dedifferentiation were not affected by GCGR mAb. Our results proved that glucagon induced &#914-cell dedifferentiation under pathological conditions, and the effect was partially mediated by FoxO1. Our study reveals a novel cross talk between a- and &#914-cells and is helpful to understand the pathophysiology of diabetes and discover new targets for diabetes treatment. [ABSTRACT FROM AUTHOR]

Plant cells in damaged tissue can be reprogrammed to acquire pluripotency and induce callus formation. However, in the aboveground organs of many species, somatic cells that are distal to the wound site become less sensitive to auxin-induced callus formation, suggesting the existence of repressive regulatory mechanisms that are largely unknown. Here we reveal that submergence-induced ethylene signals promote callus formation by releasing post-transcriptional silencing of auxin receptor transcripts in non-wounded regions. We determined that short-term submergence of intact seedlings induces auxin-mediated cell dedifferentiation across the entirety of Arabidopsis thaliana explants. The constitutive triple response 1-1 (ctr1-1) mutation induced callus formation in explants without submergence, suggesting that ethylene facilitates cell dedifferentiation. We show that ETHYLENE-INSENSITIVE 2 (EIN2) post-transcriptionally regulates the abundance of transcripts for auxin receptor genes by facilitating microRNA393 degradation. Submergence-induced calli in non-wounded regions were suitable for shoot regeneration, similar to those near the wound site. We also observed submergence-promoted callus formation in Chinese cabbage (Brassica rapa), indicating that this may be a conserved mechanism in other species. Our study identifies previously unknown regulatory mechanisms by which ethylene promotes cell dedifferentiation and provides a new approach for boosting callus induction efficiency in shoot explants. In this study, the authors find that submerging intact seedlings promotes auxin-induced callus formation in shoot explants. Short-term submergence activates EIN2-dependent ethylene signaling, which promotes miR393 degradation. This process induces accumulation of the transcripts encoding TIR1/AFB2 auxin receptors, resulting in enhanced auxin responses. These findings provide a potential method for breaking dormancy in cell dedifferentiation and for boosting callus induction efficiency during tissue culture. [ABSTRACT FROM AUTHOR]

Background: Stemness is defined as the potential of cells for self-renewal and differentiation. Many transcriptome-based methods for stemness evaluation have been proposed. However, all these methods showed low negative correlations with differentiation time and can't leverage the existing experimentally validated stem cells to recognize the stem-like cells. Methods: Here, we constructed a stemness index for single-cell samples (StemSC) based on relative expression orderings (REO) of gene pairs. Firstly, we identified the stemness-related genes by selecting the genes significantly related to differentiation time. Then, we used 13 RNA-seq datasets from both the bulk and single-cell embryonic stem cell (ESC) samples to construct the reference REOs. Finally, the StemSC value of a given sample was calculated as the percentage of gene pairs with the same REOs as the ESC samples. Results: We validated the StemSC by its higher negative correlations with differentiation time in eight normal datasets and its higher positive correlations with tumor dedifferentiation in three colorectal cancer datasets and four glioma datasets. Besides, the robust of StemSC to batch effect enabled us to leverage the existing experimentally validated cancer stem cells to recognize the stem-like cells in other independent tumor datasets. And the recognized stem-like tumor cells had fewer interactions with anti-tumor immune cells. Further survival analysis showed the immunotherapy-treated patients with high stemness had worse survival than those with low stemness. Conclusions: StemSC is a better stemness index to calculate the stemness across datasets, which can help researchers explore the effect of stemness on other biological processes. [ABSTRACT FROM AUTHOR]

Copyright of Jornal Brasileiro de Patologia e Medicina Laboratorial is the property of Sociedade Brasileira de Patologia Clinica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

As a novel class of noncoding RNAs, microRNAs (miRNAs) can effectively silence their target genes at the posttranscriptional level. Various biological processes, such as cell proliferation, differentiation, and motility, are regulated by miRNAs. In different diseases and different stages of disease, miRNAs have various expression patterns, which makes them candidate prognostic markers and therapeutic targets. Abnormal miRNA expression has been detected in numerous neoplastic diseases in humans, which indicates the potential role of miRNAs in tumorigenesis. Previous studies have indicated that miRNAs are involved in nearly the entire process of tumor development. MicroRNA‐302a, miR‐302b, miR‐302c, miR‐302d, and miR‐367 are members of the miR‐302/367 cluster that plays various biological roles in diverse neoplastic diseases by targeting different genes. These miRNAs have been implicated in several unique characteristics of cancer, including the evasion of growth suppressors, the sustained activation of proliferative signaling, the evasion of cell death and senescence, and the regulation of angiogenesis, invasion, and metastasis. This review provides a critical overview of miR‐302/367 cluster dysregulation and the subsequent effects in cancer and highlights the vast potential of members of this cluster as therapeutic targets and novel biomarkers. [ABSTRACT FROM AUTHOR]

Reduced expression of the key regulator of cardiac metabolism, transcription factor PPARα, in surgical samples of the auricles from patients with coronary heart disease and heart failure was detected by real-time quantitative PCR. These changes indicate reduced activity of this factor and a shift of energy metabolism from oxidative phosphorylation to glycolysis typical of dedifferentiated cells. Electron microscopy revealed dedifferentiated cardiomyocytes with disassembled contractile apparatus and disorganized sarcomeres. In the examined specimens from patients with heart failure, severe myocardial fibrosis was revealed. [ABSTRACT FROM AUTHOR]

Context: Ursolic acid (UA; 3β-hydroxy-urs-12-en-28-oic acid), one of the pentacyclic triterpenoids found in various plants and herbs, possesses some beneficial effects under pathological conditions, including combating hepatic fibrosis. Objective: This study investigates the effects of UA on renal tubulointerstitial fibrosis in vivo and in vitro. Materials and methods: In vivo, 24 male C57BL6 mice were divided into four groups. Eighteen mice were subjected to unilateral ureteral obstruction (UUO) and the remaining six sham-operated mice served as control. UUO mice received either vehicle or UA (50 or 100 mg/kg) by gastric gavage for 6 days. In vitro, HK-2 cells were treated with 10 or 50 μM UA and 10 ng/mL recombinant human transforming growth factor-β1 (TGF-β1). The molecular mechanisms of fibrosis were investigated. Results: UUO induced marked interstitial collagen I and fibronectin deposition and epithelial-mesenchymal transition (EMT), as evidenced by increased α-smooth muscle actin (α-SMA) and decreased E-cadherin. However, UA treatment significantly reduced collagen I and fibronectin accumulation in the fibrotic kidney. UA treatment also decreased α-SMA and preserved E-cadherin in vivo. In vitro, TGF-β1-treated HK-2 cells demonstrated elevated α-SMA, snail1, slug, TGF-β1, and p-smad3, as well as diminished E-cadherin. UA pretreatment prevented E-cadherin loss and diminished α-SMA expression in HK-2 cells. UA downregulated mRNA expression of snail1 and slug. UA also lowered TGF-β1 protein expression and p-Smad3 in HK-2 cells. Conclusions: UA attenuated renal tubulointerstitial fibrosis by inhibiting EMT, and such inhibition may be achieved by decreasing profibrotic factors. UA may be a novel therapeutic agent for renal fibrosis. [ABSTRACT FROM AUTHOR]

Plants reprogram somatic cells following injury and regenerate new tissues and organs. Upon perception of inductive cues, somatic cells often dedifferentiate, proliferate, and acquire new fates to repair damaged tissues or develop new organs from wound sites. Wound stress activates transcriptional cascades to promote cell fate reprogramming and initiate new developmental programs. Wounding also modulates endogenous hormonal responses by triggering their biosynthesis and/or directional transport. Auxin and cytokinin play pivotal roles in determining cell fates in regenerating tissues and organs. Exogenous application of these plant hormones enhances regenerative responses in vitro by facilitating the activation of specific developmental programs. Many reprogramming regulators are epigenetically silenced during normal development but are activated by wound stress and/or hormonal cues. [ABSTRACT FROM AUTHOR]

Copyright of Zeitschrift für Herz-, Thorax- und Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Although in recent years the study of gene expression variation in the absence of genetic or environmental cues or gene expression heterogeneity has intensified considerably, many basic and applied biological fields still remain unaware of how useful the study of gene expression heterogeneity patterns might be for the characterization of biological systems and/or processes. Largely based on the modulator effect chromatin compaction has for gene expression heterogeneity and the extensive changes in chromatin compaction known to occur for specialized cells that are naturally or artificially induced to revert to less specialized states or dedifferentiate, I recently hypothesized that processes that concur with cell dedifferentiation would show an extensive reduction in gene expression heterogeneity. The confirmation of the existence of such trend could be of wide interest because of the biomedical and biotechnological relevance of cell dedifferentiation-based processes, i.e., regenerative development, cancer, human induced pluripotent stem cells, or plant somatic embryogenesis. Here, I report the first empirical evidence consistent with the existence of an extensive reduction in gene expression heterogeneity for processes that concur with cell dedifferentiation by analyzing transcriptome dynamics along forearm regenerative development in Ambystoma mexicanum or axolotl. Also, I briefly discuss on the utility of the study of gene expression heterogeneity dynamics might have for the characterization of cell dedifferentiation-based processes, and the engineering of tools that afforded better monitoring and modulating such processes. Finally, I reflect on how a transitional reduction in gene expression heterogeneity for dedifferentiated cells can promote a long-term increase in phenotypic heterogeneity following cell dedifferentiation with potential adverse effects for biomedical and biotechnological applications. [ABSTRACT FROM AUTHOR]

A 46-year-old woman presented with headache and right hemiparesis. MRI demonstrated a mass in the left middle fossa. Total resection was performed. A histological examination of the tumor specimen showed several characteristic morphological features. A chordoid meningioma showing an epithelial-like palisade arrangement was observed. An anaplastic short spindle cell tumor exhibiting a fascicular pattern was considered to be a rhabdomyosarcoma. After conventional radiotherapy, the tumor was well controlled without any neurological deficit for 20 months. When subsequent recurrences were observed, the patient was treated by surgery, stereotactic radiosurgery and chemotherapy. Thirty-two months after the initial treatment, the patient died due to intracranial dissemination and an autopsy was performed. The histological examination of the recurrent and autopsy specimens showed a prominent sarcoma component. This case appears to be the first reported intracranial tumor diagnosed as a dedifferentiated chordoid meningioma with rhabdomyosarcomatous differentiation. [ABSTRACT FROM AUTHOR]

The different forms of diabetes mellitus differ in their pathogenesis but, ultimately, they are all characterized by progressive islet β-cell loss. Restoring the β-cell mass is therefore a major goal for future therapeutic approaches. The number of β-cells found at birth is determined by proliferation and differentiation of pancreatic progenitor cells, and it has been considered to remain mostly unchanged throughout adult life. Recent studies in mice have revealed an unexpected plasticity in islet endocrine cells in response to stress; under certain conditions, islet non-β-cells have the potential to reprogram into insulin producers, thus contributing to restore the β-cell mass. Here, we discuss the latest findings on pancreas and islet cell plasticity upon physiological, pathological and experimental conditions of stress. Understanding the mechanisms involved in cell reprogramming in these models will allow the development of new strategies for the treatment of diabetes, by exploiting the intrinsic regeneration capacity of the pancreas. [ABSTRACT FROM AUTHOR]

Small nuclear RNA (snRNA) is a class of non-coding RNAs that processes pre-mRNA and rRNA. Transcription of abundant snRNA species is regulated by the snRNA activating protein complex (SNAPc), which is conserved among multicellular organisms including plants. SRD2, a putative subunit of SNAPc in Arabidopsis thaliana, is essential for development, and the point mutation srd2- 1 causes severe defects in hypocotyl dedifferentiation and de novo meristem formation. Based on phenotypic analysis of srd2- 1 mutant plants, we previously proposed that snRNA content is a limiting factor in dedifferentiation in plant cells. Here, we performed functional complementation analysis of srd2- 1 using transgenic srd2- 1 Arabidopsis plants harboring SRD2 homologs from Populus trichocarpa (poplar), Nicotiana tabacum (tobacco), Oryza sativa (rice), the moss Physcomitrella patens, and Homo sapiens (human) under the control of the Arabidopsis SRD2 promoter. Only rice SRD2 suppressed the faulty tissue culture responses of srd2- 1, and restore the snRNA levels; however, interestingly, all SRD2 homologs except poplar SRD2 rescued the srd2- 1 defects in seedling development. These findings demonstrated that cell dedifferentiation and organogenesis induced during tissue culture require higher snRNA levels than does seedling development. [ABSTRACT FROM AUTHOR]

Extraskeletal mesenchymal chondrosarcoma (EMCS) is a rare and aggressive pathological variant of chondrosarcoma arising from soft tissues of mainly the extremities, meninges/dura, trunk, and orbits. EMCS comprises only 2 % of all soft tissue sarcomas and only 6 % of them arise from soft tissue in the head and neck region. It usually affects in the second and third decade of life and is common in women. It runs a very rapid clinical course with distant metastases and has poor prognosis and survival rates. Histologically it has a dimorphic presentation of small round mesenchymal cells interspersed with foci of cartilaginous differentiation. Radiographically it appears as a soft tissue lobulated mass with various patterns of calcification. This is the first case of primary and recurrent EMCS originating in the buccal space with unusual features of dedifferentiation. The diagnostic challenges in this case were the inconclusive FNAC results, lack of radiographic evidence of characteristic calcifications and presence of areas of myxoid material and dedifferentiation on histopathology. The clinical, cytological, histological, immunohistochemical, radiographic, PET-CT findings and management with review of literature is presented. The diagnostic and management pitfalls of this extremely rare tumor are also discussed. [ABSTRACT FROM AUTHOR]

A genetic transformation method via secondary somatic embryogenesis was developed for alfalfa ( Medicago sativa L.). Mature somatic embryos of alfalfa were infected by Agrobacterium strain GV3101 containing the binary vector pCAMBIA2301. pCAMBIA2301 harbors the uidA Gus reporter gene and npt II acts as the selectable marker gene. Infected primary embryos were placed on SH2K medium containing plant growth regulators to induce cell dedifferentiation and embryogenesis under 75 mg/L kanamycin selection. The induced calli were transferred to plant medium free of plant growth regulators for embryo formation while maintaining selection. Somatic embryos germinated normally upon transfer to a germination medium. Plants were recovered and grown in a tissue culture room before transfer to a greenhouse. Histochemical analysis showed high levels of GUS activity in secondary somatic embryos and in different organs of plants recovered from secondary somatic embryos. The presence and stable integration of transgenes in recovered plants were confirmed by polymerase chain reaction using transgene-specific primers and Southern blot hybridization using the npt II gene probe. The average transformation efficiency achieved via secondary somatic embryogenesis was 15.2%. The selection for transformation throughout the cell dedifferentiation and embryogenic callus induction phases was very effective, and no regenerated plants escaped the selection procedure. Alfalfa transformation is usually achieved through somatic embryogenesis using different organs of developed plants. Use of somatic embryos as explants for transformation can avoid the plant development phase, providing a faster procedure for introduction of new traits and facilitates further engineering of previously transformed lines. [ABSTRACT FROM AUTHOR]

Several AP2/ERF transcription factors are wound-induced regulators, which play key roles in controlling cell dedifferentiation. In this study, a novel AP2/ERF transcription factor, the WIND1- like gene ( ThWIND1- L), was isolated and characterized from Thellungiella halophila. ThWIND1- L cDNA clone contained a full open reading frame (ORF) of 1,068 bp encoding 356 amino acids. The predicted amino acid sequence of ThWIND1- L cDNA shared remarkably high degree of identity with the Arabidopsis RAP2.4 (WIND1). The expression of ThWIND1- L rapidly responded to the wound signals, ectopic expression of ThWIND1- L in Arabidopsis plants promoted callus tissue formation without the presence of exogenous hormones. Furthermore, overexpression of ThWIND1- L influenced some primary transcription factors (TFs), which have been shown to be involved in cell dedifferentiation and shoot regeneration. These results indicated ThWIND1-L might be a wound-induced regulator, which played an important role in the control of cell dedifferentiation. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Medicine & Health is the property of Journal of Modern Medicine & Health and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Increasing the extracellular Ca concentration from 0.5 to 3.0 mM induced marked increments in cytoplasmic Ca concentration (Ca ) and inhibition of parathyroid hormone (PTH) release of freshly isolated bovine parathyroid cells. 1,25-dihydroxycholecalciferol (1,25(OH)D; 0.1-100 ng/ml) did not affect (Ca ) and was also without acute effect on the secretion. During 4 days of monolayer culture, the parathyroid cells underwent significant increases in both number and size, and presence of 10-100 ng/ml 1,25(OH)D almost completely inhibited the cell proliferation, whereas the hypertrophy was unaffected. One day of culture with 0.1-100 ng/ml 1,25(OH)D was without effect on PTH release but after 4 days there was a dose-related reduction of recretion. At this time point and irrespective of the culture condition, PTH release was no longer suppressed by high extracellular Ca. Furthermore, Ca increased little upon increments in the extracellular Ca concentration as compared with freshly isolated cells. It is concluded that after prolonged exposure to 1,25(OH)D, PTH release is inhibited and, at high concentrations, the parathyroid cells cease to proliferate. However, 1,25(OH)D does not affect the development of functional dedifferentiation of parathyroid cells during monolayer culture. [ABSTRACT FROM AUTHOR]

The formation of secondary plasmodesmata was analyzed in Solanum nigrum L. protoplast cultures. Half and continuous secondary plasmodesmata were present in dedifferentiated, regenerating cells. The observed precursor stages confirm a recent, novel explanation for the establishment of secondary plasmodesmata. It is proposed that secondary plasmodesmata are formed after a process of membrane and vesicle fusion, with unexpected similarities to the common model for primary plasmodesmata formation during cell division. [ABSTRACT FROM AUTHOR]

Cell dedifferentiation was induced in Vicia faba root tissues by removing the whole root meristem (decapitation) and the behaviour of the nuclear DNA in the dedifferentiating cells was studied by means of cytophotometric and autoradiographic analyses. Cytophotometric determination after Feulgen-staining showed that: 1. the vast majority of nuclei in differentiated cells were in the DNA postsynthetic phase, but their Feulgen absorption was lower than that of DNA postsynthetic nuclei (G, 4 C) in the meristem; 2. such a Feulgen absorption was detected in certain nuclei after root decapitation; 3. all the mitoses in the dedifferentiating tissues were diploid, fully matching the Feulgen absorption of mitoses in the meristem. AfterH-thymidine (H-T) feeding of the decapitated roots and autoradiography, the following results were obtained: 1. two populations of labeled nuclei, characterized by two different levels of scattered labeling occurred in dedifferentiating tissues, slightly labeled nuclei being much more numerous than heavily labeled nuclei; 2. the percentage of labeled nuclei was much greater than that of DNA presynthetic nuclei in the root tissues; 3. almost all the mitoses were labeled after a 16-hourH-T feeding; 4. the percentage of slightly labeled nuclei paralleled that of dedifferentiating cells; 5. the duration of the DNA synthesis phase and that of the gap between completion of DNA synthesis and mitosis differed in heavily and slightly labeled nuclei; 6. all nuclei which entered DNA synthesis also entered mitosis. These results are interpreted to mean that: 1. after decapitation, two different DNA syntheses occur in the dedifferentiating root tissues of V. faba: DNA reduplication in cells which dedifferentiate starting from a DNA presynthetic nuclear condition (heavily labeled nuclei) and extra DNA synthesis in cells which dedifferentiate starting from a DNA postsynthetic nuclear condition (slightly labeled nuclei); 2. extra DNA synthesis is required in these dedifferentiating cells for entry into mitosis. [ABSTRACT FROM AUTHOR]

Using immunofluorescence microscopy, the cortical microtubular net which is regularly present in cells of young, growing tissue is shown to be absent, or largely reduced, in mature mesophyll cells of Nicotiana plumbaginifolia Viv., N. tabacum L., Petunia hybrida Hort. and Brassica napus L. The onset of division in protoplasts isolated from these fully differentiated tissues is preceded by a period of dedifferentiation. One of the early events during dedifferentiation, as shown for N. plumbaginifolia, is the re-establishment of a net of cortical microtubules, prior to spindle formation. These findings indicate that the presence of the cortical microtubular lattice is a prerequisite for protoplast division. Cell-wall regeneration, which also must precede division, occurs simultaneously with the formation of the lattice. However, the cortical microtubules seem to not exert any influence on the orientation of the microfibrils. [ABSTRACT FROM AUTHOR]

Cellular plasticity is a transformation of a terminally differentiated cell into another cell type, which has been long known to occur in disease and regeneration. However, white adipocytes (fat cells) have only recently been observed to undergo different types of cellular plasticity. Adipocyte transdifferentiation into myofibroblasts and cancer-associated fibroblasts occurs in fibrosis and cancer, respectively. On the other hand, reversible adipocyte dedifferentiation into adipocyte progenitor cells (preadipocytes) has been demonstrated in mammary gland and in dermal adipose tissue. Here we discuss the research on adipocyte plasticity, including the experimental approaches that allowed to detect and study it, the current state of the knowledge, major research questions which remain to be addressed, and the advances required to stimulate adipocyte plasticity research. In the future, the knowledge of the molecular mechanisms of adipocyte plasticity can be utilized both to prevent adipocyte plasticity in disease and to stimulate it for use in regenerative medicine. [ABSTRACT FROM AUTHOR]

Almost every organism has the ability of repairing damaged tissues or replacing lost and worn out body parts, nevertheless the degree of the response substantially differs between each species. Adult sea cucumbers from the Holothuria glaberrima species can eviscerate various organs and the intestinal system is the first one to regenerate. This process involves the formation of a blastema-like structure that derives from the torn mesentery edges by the intervention of specific cellular processes (e.g., cell dedifferentiation and division). Still, the genetic networks controlling the regenerative response in this model system are just starting to be unraveled. In this work we examined if and how the retinoic acid (RA) signaling pathway is involved in the regenerative response of this deuterostome. We first identified and characterized the holothurian orthologs for short chain dehydrogenase/reductase 7 (SDR7) and aldehyde dehydrogenase family 8A1 (ALDH8A1), two enzymes respectively associated with retinaldehyde and RA anabolism. We then showed that the SDR7 transcript was differentially expressed during specific stages of intestinal regeneration while ALDH8A1 did not show significant differences in regenerating tissues when compared to those of normal (non-eviscerated) organisms. Finally, we investigated the consequences of modulating RA signaling during intestinal regeneration using pharmacological tools. We showed that application of an inhibitor (citral) of the enzyme synthesizing RA or a retinoic acid receptor (RAR) antagonist (LE135) resulted in organisms with a significantly smaller intestinal rudiment when compared to those treated with DMSO (vehicle). The two inhibitors caused a reduction in cell division and cell dedifferentiation in the new regenerate when compared to organisms treated with DMSO. Results of treatment with tazarotene (an RAR agonist) were not significantly different from the control. Taken together, these results suggest that the RA signaling pathway is regulating the cellular processes that are crucial for intestinal regeneration to occur. Thus, RA might be playing a role in echinoderm regeneration that is similar to what has been described in other animal systems. [ABSTRACT FROM AUTHOR]