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PeerJ 2020Bryozoans are small benthic colonial animals; their colonies consist of zooids which are composed of a cystid and polypide. According to morphological and molecular...
Bryozoans are small benthic colonial animals; their colonies consist of zooids which are composed of a cystid and polypide. According to morphological and molecular data, three classes of bryozoans are recognized: Phylactolaemata, Gymnolaemata and Stenolaemata. Bryozoans are active suspension feeders and their feeding apparatus, the lophophore, is fringed with a single row of ciliated tentacles. In gymnolaemates, the lophophore is bell-shaped and its tentacles may be equal in length (equitentacled lophophores) or some tentacles may be longer than others (obliquely truncated lophophores). In encrusting colonies, polypides with obliquely truncated lophophores usually border specific sites of excurrent water outlets (colony periphery and chimneys) where depleted water has to be removed. It is known that during colony astogeny, colony-wide water currents rearrange: new chimneys are formed and/or location of the chimneys within a given colony changes with time. Such rearrangement requires remodeling of the lophophore shape and lengthening of some tentacles in polypides surrounding water outlets. However, proliferating activity has not been described for bryozoans. Here, we compared the distribution of S-phase and mitotic cells in young and adult polypides in three species of Gymnolaemata. We tested the hypothesis that tentacle growth/elongation is intercalary and cell proliferation takes place somewhere at the lophophore base because such pattern does not interfere with the feeding process. We also present a detailed description of ultrastructure of two parts of the lophophore base: the oral region and ciliated pits, and uncover the possible function of the latter. The presence of stem cells within the ciliated pits and the oral region of polypides provide evidence that both sites participate in tentacle elongation. This confirms the suggested hypothesis about intercalary tentacle growth which provides a potential to alter a lophophore shape in adult polypides according to rearrangement of colony wide water currents during colony astogeny. For the first time deuterosome-like structures were revealed during kinetosome biogenesis in the prospective multiciliated epithelial cells in invertebrates. Tentacle regeneration experiments in demonstrated that among all epidermal cell types, only non-ciliated cells at the abfrontal tentacle surface are responsible for wound healing. Ciliated cells on the frontal and lateral tentacle surfaces are specialized and unable to proliferate, not even under wound healing. Tentacle regeneration in is very slow and similar to the morphallaxis type. We suggest that damaged tentacles recover their length by a mechanism similar to normal growth, powered by proliferation of cells both within ciliated pits and the oral region.
PubMed: 32523809
DOI: 10.7717/peerj.9179 -
Animals : An Open Access Journal From... Jul 2022The E2F family of transcription factor is divided into activators and repressors that control cell proliferation. Bovine mammary epithelial cells (BMECs) can be...
The E2F family of transcription factor is divided into activators and repressors that control cell proliferation. Bovine mammary epithelial cells (BMECs) can be immortalized using human papillomavirus 16 E6E7 (HPV16 E6E7) and simian vacuolating virus 40 large T antigen (SV40T). In addition, SV40T does not require E2F1, E2F2, and E2F3 activators to induce proliferation in mouse embryo fibroblasts (MEFs). However, we report that E2F3 activator is required to induce the proliferation of BMECs. Our results showed that, at an early stage, primary BMECs lacking the E2F1 expression have the capacity to proliferate and show E2F2 and E2F3 slight protein levels. At a late stage, primary BMECs deficient for E2F3 completely abolish any proliferative ability and exhibit a severe cell senescence signal, although the E2F2 can be expressed at a late stage of primary BMECs. Compared with the late stage of primary BMECs, the BMECs immortalized by SV40T and E6E7 restored the protein level of E2F3 and enhanced the CDK4, CDK6, cyclin D3, and CDK2 protein level, leading to proliferating robustly. Surprisingly, it was found that p53, p21, and p27 were upregulated in SV40T and E6E7-immortalized BMECs, relatively to primary BMECs. Notably, Cdc2 was almost expressed in primary BMECs. However, Cdc2 was elevated in BMECs immortalized by SV40T and E6E7. In conclusion, this study revealed a molecular mechanism where E2F3 controls the BMECs' proliferation and senescence.
PubMed: 35883337
DOI: 10.3390/ani12141790 -
Experimental and Therapeutic Medicine Nov 2017A previous study by our group showed that a 44-amino-acid fragment of pigment epithelium-derived factor (PEDF) facilitated corneal epithelial wound healing. In the...
Pigment epithelium-derived factor short peptides facilitate full-thickness cutaneous wound healing by promoting epithelial basal cell and hair follicle stem cell proliferation.
A previous study by our group showed that a 44-amino-acid fragment of pigment epithelium-derived factor (PEDF) facilitated corneal epithelial wound healing. In the present study this fragment was shortened to obtain peptides of 18, 20 and 29 amino acids in length, and their promoting effects on the healing of full-thickness skin wounds were assessed. Peptides were delivered periodically by topical application to punch wounds of mice. The wound healing speed was evaluated by measuring the reduction of wound areas at 4 and 7 days after injury. Histological analysis with Masson's trichrome staining was used to confirm epithelialization and dermal collagen deposition. Proliferation of epithelial basal cells was documented by 5-bromo-2'-deoxyuridine incorporation. Hair follicle stem cells were identified by immunostaining for leucine-rich repeat-containing G protein-coupled receptor 6. The results indicated that the 20- and 29-amino-acid short peptides significantly reduced the time required for wound healing compared to the vehicle. Histological analysis confirmed faster epithelial cell coverage of open wounds. Treatment with the PEDF peptide fragments also contributed to granulation, tissue formation by increasing the fibroblast population and enhancing collagen deposition in the dermis. Wounds treated with PEDF peptide fragments contained more basal cells proliferated in the epithelium. Moreover, hair follicle stem cells were also stimulated to proliferate by peptide exposure. In conclusion, the present study reported the identification of two short peptides that can enhance the healing of full-thickness skin wounds following topical application. The underlying mechanisms may involve activation of basal cell proliferation and mobilization of hair follicle stem cells.
PubMed: 29201190
DOI: 10.3892/etm.2017.5134 -
Acta Medica Indonesiana 2007Atherosclerosis is the leading cause of death and disability. The lesions of atherosclerosis represent a series of highly specific cellular and molecular responses. The... (Review)
Review
Atherosclerosis is the leading cause of death and disability. The lesions of atherosclerosis represent a series of highly specific cellular and molecular responses. The earliest changes that precede the formation of lesions of atherosclerosis take place in the endothelium (EC), with resultant endothelial dysfunction. The EC-induced injury can result in increased lipid permeability, macrophage recruitment, formation of foam cells, and recruitment of T-lymphocytes and platelet. After intimal injury, different cell types,including ECs, platelets, and inflammatory cells release mediators, such as growth factors and cytokines that induce multiple effects including phenotype change of vascular smooth muscle cells (VSMC) from the quiescent "contractile" phenotype state to the active "synthetic" state, that can migrate and proliferate from media to the intima. The inflammatory response simulates migration and proliferation of VSMC that become intermixed with the area of inflammation to form an intermediate lesion. These responses continue uninhibited and is accompanied by accumulation of new extra cellular matrix (ECM). The migratory and proliferative activities of VSMC are regulated by growth promoters such as platelet derived growth factors (PGF), endothelin-1 (ET-1), thrombin, fibroblast growth factor (FGF), interleukin-1 (IL-1) and inhibitors such as, heparin sulfates , nitric oxide (NO), transforming growth factor (TGF)-beta. The matrix metallo proteinases (MMPs) could also participate in the process of VSMC migration. MMPs could catalyze and remove the basement membrane around VSMC and facilitate contacts with the interstitial matrix. This could promote a change from quiescent, contractile VSMC to cells capable of migrating and proliferating to mediate repair. The VSMC regulation is a very complex process, VSMC are stimulated to proliferate and migrate by some kind of cytokines, growth factors, angiotensin II (Ang-II). Together with apoptosis, proliferation and migration of VSMC are vital to the pathogenesis of atherosclerosis and plaque rupture. Rupture of the plaque is associated with increased fibrous cap macrophage, increased VSMC apoptosis, and reduced fibrous cap VSMC. VSMC are the only cells with plaques capable of synthesizing structurally important collagen isoforms, and the apoptosis of VSMC might promote plaque rupture.
Topics: Apoptosis; Arteriosclerosis; Cardiovascular Physiological Phenomena; Cardiovascular System; Endothelium; Humans; Inflammation; Muscle, Smooth, Vascular
PubMed: 17933075
DOI: No ID Found -
Archives of Medical Science : AMS 2023To explore the function of interleukin 1α (IL-1α) in bladder cancer (BCa).
INTRODUCTION
To explore the function of interleukin 1α (IL-1α) in bladder cancer (BCa).
MATERIAL AND METHODS
Immunohistochemistry (IHC) was used to test the protein expression of IL-1α in BCa tissues. The relationship between IL-1α and clinical characteristics was analyzed by the Kaplan-Meier curve method. The gene and protein expression was tested by reverse transcription (RT-q-PCR) and western blot, respectively. Colony formation and MTT assays were used to detect the potential of proliferation , and scratch and transwell chamber assays were used to detect the potential of invasion . Markers of proliferation such as Ki-67 and proliferating cell nuclear antigen (PCNA) and markers of invasion such as MMP-2 and MMP-9 were detected by western blot. Xenograft study was used for the experiment.
RESULTS
We found that IL-1α was highly expressed in BCa patients while highly expressed IL-1α was significantly related to short overall survival and progression-free survival in BCa as well. Moreover, knockdown of IL-1α might inhibit the ability of cancer cells to proliferate and invade or migrate both and .
CONCLUSIONS
Our findings suggested that IL-1α might be a therapy target for BCa malignant progression.
PubMed: 36817666
DOI: 10.5114/aoms.2020.100677 -
Endocrine Journal 2013It has been thought that adipocytes lack proliferative ability and do not revert to precursor cells. However, numerous findings that challenge this notion have also been... (Review)
Review
It has been thought that adipocytes lack proliferative ability and do not revert to precursor cells. However, numerous findings that challenge this notion have also been reported. The idea that adipocytes dedifferentiate to fibroblast-like cells with increasing cell number was reported in 1975. This possibility has been ignored despite knowledge gained in the 1990s regarding adipocyte differentiation. Several studies on proliferation and dedifferentiation of adipocytes have been published, most of which were conducted from the perspective of regenerative medicine. However, the concept of proliferation of adipocytes remains unclear. In this study, we postulate a new population of adipocytes, which consist of small sized cells (less than 20 μm in diameter) expressing adipocyte markers, such as adiponectin and peroxisome proliferator-activated receptor γ (PPARγ), but not possessing large lipid droplets. These cells show marked ability to incorporate 5-bromo-2'-deoxyuridine (BrdU), for which reason we termed them "small proliferative adipocytes (SPA)". In addition, SPA are observed in the stromal vascular fraction. Since SPA are morphologically different from mature adipocytes, we regarded them as committed progenitor cells. When proliferation of adipocytes in vivo is assessed by measuring BrdU incorporation and expression levels of proliferating cell nuclear antigen (PCNA) in isolated fractions of adipocytes from adipose tissues, subcutaneous SPA proliferate less actively than visceral SPA. Treatment with pioglitazone increases the number of proliferating SPA in subcutaneous, but not visceral, fat, suggesting that SPA may be important in regulating systemic insulin sensitivity and glucose metabolism.
Topics: Adipocytes; Adipokines; Animals; Bromodeoxyuridine; Cell Dedifferentiation; Cell Differentiation; Cell Proliferation; Cells, Cultured; Humans; Immunohistochemistry; PPAR gamma; Pioglitazone; Proliferating Cell Nuclear Antigen; Stem Cells; Thiazolidinediones
PubMed: 23749173
DOI: 10.1507/endocrj.ej13-0141 -
Journal of Visualized Experiments : JoVE Oct 2017Ischemic stroke is a complex brain injury caused by a thrombus or embolus obstructing blood flow to parts of the brain. This leads to deprivation of oxygen and glucose,...
Ischemic stroke is a complex brain injury caused by a thrombus or embolus obstructing blood flow to parts of the brain. This leads to deprivation of oxygen and glucose, which causes energy failure and neuronal death. After an ischemic stroke insult, astrocytes become reactive and proliferate around the injury site as it develops. Under this scenario, it is difficult to study the specific contribution of astrocytes to the brain region exposed to ischemia. Therefore, this article introduces a methodology to study primary astrocyte reactivity and proliferation under an in vitro model of an ischemia-like environment, called oxygen glucose deprivation (OGD). Astrocytes were isolated from 1-4 day-old neonatal rats and the number of non-specific astrocytic cells was assessed using astrocyte selective marker Glial Fibrillary Acidic Protein (GFAP) and nuclear staining. The period in which astrocytes are subjected to the OGD condition can be customized, as well as the percentage of oxygen they are exposed to. This flexibility allows scientists to characterize the duration of the ischemic-like condition in different groups of cells in vitro. This article discusses the timeframes of OGD that induce astrocyte reactivity, hypertrophic morphology, and proliferation as measured by immunofluorescence using Proliferating Cell Nuclear Antigen (PCNA). Besides proliferation, astrocytes undergo energy and oxidative stress, and respond to OGD by releasing soluble factors into the cell medium. This medium can be collected and used to analyze the effects of molecules released by astrocytes in primary neuronal cultures without cell-to-cell interaction. In summary, this primary cell culture model can be efficiently used to understand the role of isolated astrocytes upon injury.
Topics: Animals; Astrocytes; Brain Ischemia; Cell Proliferation; Cells, Cultured; Disease Models, Animal; Rats
PubMed: 29155711
DOI: 10.3791/55108 -
Disease Models & Mechanisms Mar 2021Aminoacyl transfer RNA (tRNA) synthetases (aaRSs) not only load the appropriate amino acid onto their cognate tRNAs, but many of them also perform additional functions...
Aminoacyl transfer RNA (tRNA) synthetases (aaRSs) not only load the appropriate amino acid onto their cognate tRNAs, but many of them also perform additional functions that are not necessarily related to their canonical activities. Phenylalanyl tRNA synthetase (PheRS/FARS) levels are elevated in multiple cancers compared to their normal cell counterparts. Our results show that downregulation of PheRS, or only its α-PheRS subunit, reduces organ size, whereas elevated expression of the α-PheRS subunit stimulates cell growth and proliferation. In the wing disc system, this can lead to a 67% increase in cells that stain for a mitotic marker. Clonal analysis of twin spots in the follicle cells of the ovary revealed that elevated expression of the α-PheRS subunit causes cells to grow and proliferate ∼25% faster than their normal twin cells. This faster growth and proliferation did not affect the size distribution of the proliferating cells. Importantly, this stimulation proliferation turned out to be independent of the β-PheRS subunit and the aminoacylation activity, and it did not visibly stimulate translation.This article has an associated First Person interview with the joint first authors of the paper.
Topics: Amino Acids; Aminoacylation; Animals; Cell Proliferation; Drosophila melanogaster; Gene Knockdown Techniques; Mitosis; Organ Size; Organogenesis; Phenylalanine-tRNA Ligase; Protein Biosynthesis
PubMed: 33547043
DOI: 10.1242/dmm.048132 -
Nature Communications Dec 2022When Trypanosoma brucei parasites, the causative agent of sleeping sickness, colonize the adipose tissue, they rewire gene expression. Whether this adaptation affects...
When Trypanosoma brucei parasites, the causative agent of sleeping sickness, colonize the adipose tissue, they rewire gene expression. Whether this adaptation affects population behavior and disease treatment remained unknown. By using a mathematical model, we estimate that the population of adipose tissue forms (ATFs) proliferates slower than blood parasites. Analysis of the ATFs proteome, measurement of protein synthesis and proliferation rates confirm that the ATFs divide on average every 12 h, instead of 6 h in the blood. Importantly, the population of ATFs is heterogeneous with parasites doubling times ranging between 5 h and 35 h. Slow-proliferating parasites remain capable of reverting to the fast proliferation profile in blood conditions. Intravital imaging shows that ATFs are refractory to drug treatment. We propose that in adipose tissue, a subpopulation of T. brucei parasites acquire a slow growing behavior, which contributes to disease chronicity and treatment failure.
Topics: Adipose Tissue
PubMed: 36481558
DOI: 10.1038/s41467-022-34622-w -
Frontiers in Neuroanatomy 2021Using immunostaining and confocal microscopy, we here provide the first detailed description of otic neurogenesis in . We show that the otic vesicle comprises a...
Using immunostaining and confocal microscopy, we here provide the first detailed description of otic neurogenesis in . We show that the otic vesicle comprises a pseudostratified epithelium with apicobasal polarity (apical enrichment of Par3, aPKC, phosphorylated Myosin light chain, N-cadherin) and interkinetic nuclear migration (apical localization of mitotic, pH3-positive cells). A Sox3-immunopositive neurosensory area in the ventromedial otic vesicle gives rise to neuroblasts, which delaminate through breaches in the basal lamina between stages 26/27 and 39. Delaminated cells congregate to form the vestibulocochlear ganglion, whose peripheral cells continue to proliferate (as judged by EdU incorporation), while central cells differentiate into Islet1/2-immunopositive neurons from stage 29 on and send out neurites at stage 31. The central part of the neurosensory area retains Sox3 but stops proliferating from stage 33, forming the first sensory areas (utricular/saccular maculae). The phosphatase and transcriptional coactivator Eya1 has previously been shown to play a central role for otic neurogenesis but the underlying mechanism is poorly understood. Using an antibody specifically raised against Eya1, we characterize the subcellular localization of Eya1 proteins, their levels of expression as well as their distribution in relation to progenitor and neuronal differentiation markers during otic neurogenesis. We show that Eya1 protein localizes to both nuclei and cytoplasm in the otic epithelium, with levels of nuclear Eya1 declining in differentiating (Islet1/2+) vestibulocochlear ganglion neurons and in the developing sensory areas. Morpholino-based knockdown of Eya1 leads to reduction of proliferating, Sox3- and Islet1/2-immunopositive cells, redistribution of cell polarity proteins and loss of N-cadherin suggesting that Eya1 is required for maintenance of epithelial cells with apicobasal polarity, progenitor proliferation and neuronal differentiation during otic neurogenesis.
PubMed: 34616280
DOI: 10.3389/fnana.2021.722374