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Journal of Leukocyte Biology Nov 2023Monocytes (Mo) and macrophages (Mφ) play important roles in the function of tissues, organs, and systems of all animals during homeostasis, infection, injury, and... (Review)
Review
Monocytes (Mo) and macrophages (Mφ) play important roles in the function of tissues, organs, and systems of all animals during homeostasis, infection, injury, and disease. For decades, conventional wisdom has dictated that Mo and Mφ are end-stage cells that do not proliferate and that Mφ accumulation in tissues is the result of infiltration of Mo from the blood and subsequent differentiation to Mφ. However, reports from the early 1900s to the present describe evidence of Mo and Mφ proliferation in different tissues and contexts. The purpose of this review is to summarize both historical and current evidence for the contribution of Mφ proliferation to their accumulation in different tissues during homeostasis, infection, injury, and disease. Mφ proliferate in different organs and tissues, including skin, peritoneum, lung, heart, aorta, kidney, liver, pancreas, brain, spinal cord, eye, adipose tissue, and uterus, and in different species including mouse, rat, rabbit, and human. Mφ can proliferate at different stages of differentiation with infiltrating Mo-like cells proliferating in certain inflammatory contexts (e.g. skin wounding, kidney injury, bladder and liver infection) and mature resident Mφ proliferating in other inflammatory contexts (e.g. nematode infection, acetaminophen liver injury) and during homeostasis. The pathways involved in stimulating Mφ proliferation also may be context dependent, with different cytokines and transcription factors implicated in different studies. Although Mφ are known to proliferate in health, injury, and disease, much remains to be learned about the regulation of Mφ proliferation in different contexts and its impact on the homeostasis, injury, and repair of different organs and tissues.
Topics: Humans; Female; Mice; Rats; Animals; Rabbits; Monocytes; Macrophages; Cytokines; Homeostasis; Cell Proliferation
PubMed: 37555460
DOI: 10.1093/jleuko/qiad093 -
Biology Aug 2023Although microglia exist as a minor glial cell type in the normal state of the brain, they increase in number in response to various disorders and insults. However, it... (Review)
Review
Although microglia exist as a minor glial cell type in the normal state of the brain, they increase in number in response to various disorders and insults. However, it remains unclear whether microglia proliferate in the affected area, and the mechanism of the proliferation has long attracted the attention of researchers. We analyzed microglial mitosis using a facial nerve transection model in which the blood-brain barrier is left unimpaired when the nerves are axotomized. Our results showed that the levels of macrophage colony-stimulating factor (M-CSF), cFms (the receptor for M-CSF), cyclin A/D, and proliferating cell nuclear antigen (PCNA) were increased in microglia in the axotomized facial nucleus (axotFN). In vitro experiments revealed that M-CSF induced cFms, cyclin A/D, and PCNA in microglia, suggesting that microglia proliferate in response to M-CSF in vivo. In addition, M-CSF caused the activation of c-Jun N-terminal kinase (JNK) and p38, and the specific inhibitors of JNK and p38 arrested the microglial mitosis. JNK and p38 were shown to play roles in the induction of cyclins/PCNA and cFms, respectively. cFms was suggested to be induced through a signaling cascade of p38-mitogen- and stress-activated kinase-1 (MSK1)-cAMP-responsive element binding protein (CREB) and/or p38-activating transcription factor 2 (ATF2). Microglia proliferating in the axotFN are anticipated to serve as neuroprotective cells by supplying neurotrophic factors and/or scavenging excite toxins and reactive oxygen radicals.
PubMed: 37627005
DOI: 10.3390/biology12081121 -
The Tohoku Journal of Experimental... Aug 2021In insulin-resistant states such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. Failure of this β-cells proliferative response leads... (Review)
Review
In insulin-resistant states such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. Failure of this β-cells proliferative response leads to the development of diabetes. On the other hand, when organs are damaged, cells proliferate to repair the organs. Therefore, these proliferations are compensatory mechanisms aimed at maintaining whole-body homeostasis. We previously discovered vagal signal-mediated systems regulating adaptive proliferation of β-cells and hepatocytes. Neuron-mediated liver-β-cell inter-organ crosstalk is involved in promotion of β-cell proliferation during obesity, and in this system, vagal signals directly stimulate β-cell proliferation. Meanwhile, in the liver, the multi-step mechanisms whereby vagal nerve signals activate hepatic resident macrophages are involved in hepatocyte proliferation after severe injury. Diabetes mellitus develops on the pathological basis of insufficient insulin action. Insulin action insufficiency is attributable to insulin resistance, i.e., the failure of insulin to exert sufficient effects, and/or to impairment of insulin secretion. Impairment of insulin secretion is attributable not only to the β-cell dysfunction but also to functional β-cell mass reduction. In this regard, there are already therapeutic options to increase insulin secretion from residual β-cells, such as sulfonyl urea and incretin-related drugs. In contrast, there are as yet no applicable therapeutic strategies to increase functional β-cell mass in vivo. Therefore, we have conducted the basic investigations to tackle this issue based on the discovery of neuron-mediated liver-β-cell inter-organ crosstalk. This review introduces vagal signal-mediated regulatory systems of adaptive cell proliferation in vivo and efforts to develop cell-increasing therapies based on vagal nerve-mediated cell proliferation.
Topics: Cell Proliferation; Diabetes Mellitus, Type 2; Homeostasis; Humans; Insulin; Insulin Secretion; Insulin-Secreting Cells
PubMed: 34373421
DOI: 10.1620/tjem.254.245 -
Veterinary Immunology and... May 2020CellTrace Violet™ is a commonly used fluorescent dye used with flow cytometry to identify cell proliferation. Activated equine lymphocytes were examined using flow...
CellTrace Violet™ is a commonly used fluorescent dye used with flow cytometry to identify cell proliferation. Activated equine lymphocytes were examined using flow cytometry, microscopy and tritiated thymidine proliferation assays. CellTrace Violet™ was incorporated into the equine lymphocytes effectively. Equine lymphocytes proliferated when activated with pokeweed mitogen, but did not proliferate when previously stained with CellTrace Violet™. Serial dilutions of CellTrace Violet™ did not eliminate the inhibition of activated lymphocytes. Equine lymphocyte viability was greater than 90 % for both stained and unstained cells. Based on these data, CellTrace Violet™ is not recommended for the assessment of lymphocyte proliferation in equine cells. The mechanism of inhibition of equine lymphocyte proliferation by CellTrace Violet™ is unknown.
Topics: Animals; Cell Proliferation; Cell Survival; Concanavalin A; Flow Cytometry; Fluorescent Dyes; Horses; Lymphocyte Activation; Lymphocytes; Pokeweed Mitogens
PubMed: 32229340
DOI: 10.1016/j.vetimm.2020.110037 -
Frontiers in Neuroscience 2020Astrocytes exhibit a region-dependent molecular and functional heterogeneity in the CNS. Although cortical astrocytes proliferate robustly during the first postnatal...
Astrocytes exhibit a region-dependent molecular and functional heterogeneity in the CNS. Although cortical astrocytes proliferate robustly during the first postnatal week and become proliferation quiescent, the temporal proliferation dynamics of astrocytes in subcortical regions during postnatal development remain essentially unknown. Whether subcortical astrocytes mature similarly to cortical astrocytes is also unexplored. In this current study, we examined proliferation of subcortical, especially hypothalamic, astrocytes during postnatal development using genetic labeling of astrocytes and pulse-chase EdU labeling of proliferating cells. While a lower number of proliferating astrocytes was found in the hypothalamus compared to cortex during the first postnatal week, astrocyte proliferation is much more active in hypothalamus than in cortex from P15 to P30 in both proliferating astrocyte density and percentage, indicating a persistent and distinct proliferation pattern of astrocytes in hypothalamus. This observation is further confirmed by Ki67 immunostaining with genetically or immunolabeled astrocytes in hypothalamus and cortex during P15-30. In addition, astrocytes in representative subcortical regions have a modest growth of their domain size and exhibit a significantly smaller domain size compared to cortical astrocytes at P30 when astrocytes have generally completed postnatal maturation. However, the expression of astrocyte-derived Sparc, an important synaptogenic inhibitor, is consistently higher in hypothalamic astrocytes than in cortical astrocytes throughout postnatal development. In summary, our study unveiled a distinct proliferation and maturation pattern of subcortical, especially hypothalamic, astrocytes during postnatal development.
PubMed: 32457572
DOI: 10.3389/fnins.2020.00435 -
Medical Archives (Sarajevo, Bosnia and... Aug 2021Recent advances in stem cell technologies have rekindled an interest in the use of cell therapies to treat patients with Parkinson's disease. Although the...
BACKGROUND
Recent advances in stem cell technologies have rekindled an interest in the use of cell therapies to treat patients with Parkinson's disease. Although the transplantation of dopaminergic mesencephalic human fetal brain tissue has previously been reported in the treatment of patients with Parkinson's disease, this method is limited by the availability of tissue obtained from each human embryo.
OBJECTIVE
Our study aimed to isolate, culture, proliferate, and differentiate dopaminergic neurons from human neuroepithelial stem cells obtained from embryo reduction procedures performed in multifetal pregnancies following in vitro fertilization.
MATERIALS AND METHODS
A total of 201 human embryos were dissected for isolation and culture of neuroepithelial stem cells for proliferation and differentiation into dopaminergic neurons. All embryos were obtained from embryo reduction procedures performed in multifetal pregnancies after in vitro fertilization treatments.
RESULTS
Human neuroepithelial stem cells were isolated and cultured from embryos from 6.0 to 8.0 weeks. Neuroepithelial stem cells were successfully isolated, proliferated, and differentiated into dopaminergic neurons. The cells adhered to the surfaces of cell culture plates after 2 days and could be proliferated and differentiated into neurons within 4 days. Cultured cells expressed the dopaminergic marker tyrosine hydroxylase after 6 days, suggesting that these cells were successfully differentiated into dopaminergic neurons.
CONCLUSION
The successful isolation, culture, proliferation, and differentiation of human dopaminergic neurons from embryo reductions performed for multifetal pregnancies after in vitro fertilization suggests that this pathway may serve as a potential source of cell therapy materials for use in the treatment of Parkinson's disease.
Topics: Cell Differentiation; Cell Proliferation; Cells, Cultured; Dopaminergic Neurons; Female; Fertilization in Vitro; Humans; Pregnancy; Pregnancy Reduction, Multifetal; Stem Cells
PubMed: 34759448
DOI: 10.5455/medarh.2021.75.280-285 -
Journal of Endodontics Aug 2007There is continuing controversy regarding the potential for inflammatory apical cysts to heal after nonsurgical endodontic therapy. Molecular cell biology may provide... (Review)
Review
There is continuing controversy regarding the potential for inflammatory apical cysts to heal after nonsurgical endodontic therapy. Molecular cell biology may provide answers to a series of related questions. How are the epithelial cell rests of Malassez stimulated to proliferate? How are the apical cysts formed? How does the lining epithelium of apical cysts regress after endodontic therapy? Epithelial cell rests are induced to divide and proliferate by inflammatory mediators, proinflammatory cytokines, and growth factors released from host cells during periradicular inflammation. Quiescent epithelial cell rests can behave like restricted-potential stem cells if stimulated to proliferate. Formation of apical cysts is most likely caused by the merging of proliferating epithelial strands from all directions to form a three-dimensional ball mass. After endodontic therapy, epithelial cells in epithelial strands of periapical granulomas and the lining epithelium of apical cysts may stop proliferating because of a reduction in inflammatory mediators, proinflammatory cytokines, and growth factors. Epithelial cells will also regress because of activation of apoptosis or programmed cell death through deprivation of survival factors or by receiving death signals during periapical wound healing.
Topics: Apoptosis; Epithelial Cells; Humans; Periapical Periodontitis; Radicular Cyst; Remission, Spontaneous; Root Canal Therapy
PubMed: 17878074
DOI: 10.1016/j.joen.2007.02.006 -
Der Pathologe Jul 2020Proliferative changes seen in reactive mesothelial hyperplasia of a hydrocele sac may mimic malignant mesothelioma. There is no immunohistochemical staining that...
Proliferative changes seen in reactive mesothelial hyperplasia of a hydrocele sac may mimic malignant mesothelioma. There is no immunohistochemical staining that reliably separates benign from malignant mesothelial proliferations. However, the combined analysis of BAP1 by immunohistochemistry and CDKN2A by FISH has been reported to yield both a high specificity and sensitivity in this differential diagnosis. In addition, the evaluation of risk factors such as asbestos exposure or prior traumata may be helpful for the correct diagnosis. Exclusion of stromal invasion, which is diagnostic for malign mesothelioma, is of utmost importance. Therefore, extended histological workup is essential.
Topics: Cell Proliferation; Diagnosis, Differential; Humans; Immunohistochemistry; Lung Neoplasms; Male; Mesothelioma; Testicular Neoplasms; Testis; Tumor Suppressor Proteins; Ubiquitin Thiolesterase
PubMed: 32472158
DOI: 10.1007/s00292-020-00797-6 -
Archivos de Cardiologia de Mexico 2014Proliferation of adult mammalian ventricular cardiomyocytes has been ruled out by some researchers, who have argued that these cells are terminally differentiated;... (Review)
Review
Proliferation of adult mammalian ventricular cardiomyocytes has been ruled out by some researchers, who have argued that these cells are terminally differentiated; however, this dogma has been rejected because other researchers have reported that these cells can present the processes necessary to proliferate, that is, DNA synthesis, mitosis and cytokinesis when the heart is damaged experimentally through pharmacological and surgical strategies or due to pathological conditions concerning the cardiovascular system. This review integrates some of the available works in the literature evaluating the DNA synthesis, mitosis and cytokinesis in these myocytes, when the myocardium is damaged, with the purpose of knowing if their proliferation can be considered as a feasible phenomenon. The review is concluded with a reflection about the perspectives of the knowledge generated in this area.
Topics: Adult; Animals; Bromodeoxyuridine; Cell Differentiation; Cell Proliferation; Cytokinesis; DNA; Dogs; Heart Ventricles; Humans; Mice; Mitosis; Myocytes, Cardiac; Proliferating Cell Nuclear Antigen; RNA, Messenger; Rats
PubMed: 24792902
DOI: 10.1016/j.acmx.2014.01.002 -
In Vitro Cellular & Developmental... Jan 1990The adhesion and proliferation of mammalian fibroblasts (Flow 7000) on the surface of hydrophilic (copolymer of N-vinyl-2-pyrrolidone and methyl methacrylate) and...
The adhesion and proliferation of mammalian fibroblasts (Flow 7000) on the surface of hydrophilic (copolymer of N-vinyl-2-pyrrolidone and methyl methacrylate) and hydrophobic [polymethylmethacrylate (PMMA) stereocomplex] hydrogels with a wide range in water content were studied morphologically and quantitatively. It was demonstrated that cell proliferation on hydrogels by a static culture method decreased as the water content of the gels increased. However, it is remarkable that the cell proliferation on PMMA hydrogels with a high water content is equivalent to that on glass Petri dishes. The results obtained in the proliferation of cells on the surface of these hydrogels closely correspond to the state of cell adhesion. When fresh medium or air was perfused from the opposite side of the PMMA hydrogel membrane on which the cells were proliferating (perfusion method), the cells continued to grow into a higher density than with the conventional static culture method. In the case of fresh medium perfusion, the amount of proliferated cell was dependent on both the permeability of the membrane and the density of the membrane "scaffolding." Virus multiplication in the cultured cells increased in proportion to the cell density, whereas the cell function was similar in both culture methods.
Topics: Cell Adhesion; Cell Division; Cells, Cultured; Gels; Humans; Male; Membranes, Artificial; Microscopy, Electron, Scanning; Perfusion; Permeability; Water
PubMed: 2307638
DOI: 10.1007/BF02624154