Journal articles: '060602 Animal Physiology - Cell'

1

Razani, B. "Caveolae: From Cell Biology to Animal Physiology." Pharmacological Reviews 54, no. 3 (September 1, 2002): 431–67. http://dx.doi.org/10.1124/pr.54.3.431.

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RUNSTADLER, PETER W. "The Importance of Cell Physiology to the Performance of Animal Cell Bioreactors." Annals of the New York Academy of Sciences 665, no. 1 Biochemical E (October 1992): 380–90. http://dx.doi.org/10.1111/j.1749-6632.1992.tb42601.x.

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Akers, R. M. "Lactation physiology: A ruminant animal perspective." Protoplasma 159, no. 2-3 (June 1990): 96–111. http://dx.doi.org/10.1007/bf01322593.

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Koretsky, A. P. "Investigation of cell physiology in the animal using transgenic technology." American Journal of Physiology-Cell Physiology 262, no. 2 (February 1, 1992): C261—C275. http://dx.doi.org/10.1152/ajpcell.1992.262.2.c261.

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Over the past 10 years significant progress has been made in techniques for manipulating the genome of the animal. Production of transgenic mice has led to important insights into the regulation of gene expression, the molecular basis of cancer, immunology, and developmental biology. The tools necessary to generate transgenic mice are becoming widely available, making it possible to study a variety of problems. In this review a description of the strategies being used to address problems of interest in cell physiology using transgenic mice is given. Elucidation of the rules governing the regulation of gene expression now permits the targeted expression of a protein to a particular organ or cell type within an organ. Overexpression of proteins, expression of foreign or mutant proteins, mislocalization of proteins, and directed elimination of proteins are all procedures that can now be used to generate interesting animal models for physiological studies. The applications of these techniques to a variety of problems in normal and abnormal physiology are discussed in this review.

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Aravalli, Rajagopal N., Clifford J. Steer, M. Behnan Sahin, and Erik N. K. Cressman. "Stem Cell Origins and Animal Models of Hepatocellular Carcinoma." Digestive Diseases and Sciences 55, no. 5 (June 10, 2009): 1241–50. http://dx.doi.org/10.1007/s10620-009-0861-x.

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Oth, Guirad, and Yrick John. "The Discovery and History of Animal and Human Physiology." Journal La Lifesci 1, no. 6 (December 31, 2020): 19–27. http://dx.doi.org/10.37899/journallalifesci.v1i6.289.

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This study discusses Nucleus, history of the discovery of the cell nucleus Structure and parts of the cell nucleus. All of them is the phisiology of animal and human. The cell nucleus (nucleus) can be defined as an organelle found in eukaryotic cells. Nucleoplasm The nucleoplasm is the liquid that is in the nucleus which is thick and transparent. The cell nucleus has many genes from DNA which are arranged and form structures called chromosomes. The endoplasmic reticulum consists of tubules, vesicles and flattened pockets that occupy the cytoplasmic space. The endoplasmic reticulum is a part of the cell that consists of a membrane system, which has a structure that resembles a multi-layered sac. These sacs are called cisternae.

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Barbe, Michael T., Hannah Monyer, and Roberto Bruzzone. "Cell-Cell Communication Beyond Connexins: The Pannexin Channels." Physiology 21, no. 2 (April 2006): 103–14. http://dx.doi.org/10.1152/physiol.00048.2005.

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Direct cell-to-cell communication through specialized intercellular channels is a characteristic feature of virtually all multi-cellular organisms. The remarkable functional conservation of cell-to-cell coupling throughout the animal kingdom, however, is not matched at the molecular level of the structural protein components. Thus protostomes (including nematodes and flies) and deuterostomes (including all vertebrates) utilize two unrelated families of gap-junction genes, innexins and connexins, respectively. The recent discovery that pannexins, a novel group of proteins expressed by several organisms, are able to form intercellular channels has started a quest to understand their evolutionary relationship and functional contribution to cell communication in vivo. There are three pannexin genes in mammals, two of which are co-expressed in the developing and adult brain. Of note, pannexin1 can also form Ca2+-activated hemichannels that open at physiological extracellular Ca2+ concentrations and exhibit distinct pharmacological properties.

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Leulier, François, Lesley T. MacNeil, Won-jae Lee, John F. Rawls, Patrice D. Cani, Martin Schwarzer, Liping Zhao, and Stephen J. Simpson. "Integrative Physiology: At the Crossroads of Nutrition, Microbiota, Animal Physiology, and Human Health." Cell Metabolism 25, no. 3 (March 2017): 522–34. http://dx.doi.org/10.1016/j.cmet.2017.02.001.

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Rasmussen, Leif, Hans Toftlund, and Peter Suhr-Jessen. "Utilization of iron complexes in an animal cell." Journal of Cellular Physiology 122, no. 1 (January 1985): 155–58. http://dx.doi.org/10.1002/jcp.1041220123.

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Lang, M. A. "Correlation between osmoregulation and cell volume regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 4 (April 1, 1987): R768—R773. http://dx.doi.org/10.1152/ajpregu.1987.252.4.r768.

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The euryhaline crab, Callinectes sapidus, behaves both as an osmoregulator when equilibrated in salines in the range of 800 mosM and below and an osmoconformer when equilibrated in salines above 800 mosM. There exists a close correlation between osmoregulation seen in the whole animal in vivo and cell volume regulation studied in vitro. Hyperregulation of the hemolymph osmotic pressure and cell volume regulation both occurred in salines at approximately 800 mosM and below. During long-term equilibration of the crabs to a wide range of saline environments, the total concentration of hemolymph amino acids plus taurine remained below 3 mM. During the first 6 h after an acute osmotic stress to the whole animal, the hemolymph osmotic pressure and Na activity gradually decreased, whereas the free amino acids remained below 3 mM. As the hemolymph osmotic pressure decreased below approximately 850 mosM, the amino acid level began to increase to 17-25 mM. This change was primarily due to increases in glycine, proline, taurine, and alanine. The likely source of the increase in hemolymph free amino acids in vivo is the free amino acid loss from muscle cells observed during cell volume regulation in vitro.

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Khan, Shaharyar M., Rafal M. Smigrodzki, and Russell H. Swerdlow. "Cell and animal models of mtDNA biology: progress and prospects." American Journal of Physiology-Cell Physiology 292, no. 2 (February 2007): C658—C669. http://dx.doi.org/10.1152/ajpcell.00224.2006.

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The past two decades have witnessed an evolving understanding of the mitochondrial genome’s (mtDNA) role in basic biology and disease. From the recognition that mutations in mtDNA can be responsible for human disease to recent efforts showing that mtDNA mutations accumulate over time and may be responsible for some phenotypes of aging, the field of mitochondrial genetics has greatly benefited from the creation of cell and animal models of mtDNA mutation. In this review, we critically discuss the past two decades of efforts and insights gained from cell and animal models of mtDNA mutation. We attempt to reconcile the varied and at times contradictory findings by highlighting the various methodologies employed and using human mtDNA disease as a guide to better understanding of cell and animal mtDNA models. We end with a discussion of scientific and therapeutic challenges and prospects for the future of mtDNA transfection and gene therapy.

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Cheng, Fan, Patricia J. McLaughlin, William A. Banks, and Ian S. Zagon. "Passive diffusion of naltrexone into human and animal cells and upregulation of cell proliferation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 3 (September 2009): R844—R852. http://dx.doi.org/10.1152/ajpregu.00311.2009.

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Naltrexone (NTX) is a potent opioid antagonist that promotes cell proliferation by upregulating DNA synthesis through displacement of the tonically active inhibitory peptide, opioid growth factor (OGF) from its receptor (OGFr). To investigate how NTX enters cells, NTX was fluorescently labeled [1-( N)-fluoresceinyl NTX thiosemicarbazone; FNTX] to study its uptake by living cultured cells. When human head and neck squamous cell carcinoma cell line (SCC-1) was incubated with FNTX for as little as 1 min, cells displayed nuclear and cytoplasmic staining of FNTX as determined by fluorescent deconvolution microscopy, with enrichment of fluorescent signal in the nucleus and nucleolus. The same temporal-spatial distribution of FNTX was detected in a human pancreatic cancer cell line (MIA PaCa-2), African green monkey kidney cell line (COS-7), and human mesenchymal stem cells (hMSCs). FNTX remained in cells for as long as 48 h. FNTX was internalized in SCC-1 cells when incubation occurred at 4°C, with the signal being comparable to that recorded at 37°C. A 100-fold excess of NTX or a variety of other opioid ligands did not alter the temporal-spatial distribution of FNTX. Neither fluorescein-labeled dextran nor fluorescein alone entered the cells. To study the effect of FNTX on DNA synthesis, cells incubated with FNTX at concentrations ranging from 10−5 to 10−8 M had a 5-bromo-2′-deoxyuridine index that was 39–82% greater than for vehicle-treated cells and was comparable to that of unlabeled NTX (37–70%). Taken together, these results suggested that NTX enters cells by passive diffusion in a nonsaturable manner.

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Grinstein, S., W. Furuya, and L. Bianchini. "Protein Kinases, Phosphatases, and the Control of Cell Volume." Physiology 7, no. 5 (October 1, 1992): 232–37. http://dx.doi.org/10.1152/physiologyonline.1992.7.5.232.

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Animal cells regulate their size in isotonic and anisotonic conditions by activating volume-sensitive solute transport systems. Recent evidence suggests that protein phosporylation/dephosphorylation is involved in volume control. These observations are integrated into a model consisting of a single volume-sensing device, a transducing element which may be a protein kinase, and two types of volume change effectors.

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Goldenberg, Hans, and Esther Schweinzer. "Transport of vitamin C in animal and human cells." Journal of Bioenergetics and Biomembranes 26, no. 4 (August 1994): 359–67. http://dx.doi.org/10.1007/bf00762776.

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Zwick, Rachel K., Benjamin Ohlstein, and Ophir D. Klein. "Intestinal renewal across the animal kingdom: comparing stem cell activity in mouse and Drosophila." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 3 (March 1, 2019): G313—G322. http://dx.doi.org/10.1152/ajpgi.00353.2018.

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The gastrointestinal (GI) tract renews frequently to sustain nutrient digestion and absorption in the face of consistent tissue stress. In many species, proliferative intestinal stem cells (ISCs) are responsible for the repair of the damage arising from chemical and mechanical aspects of food breakdown and exposure to pathogens. As the cellular source of all mature cell types of the intestinal epithelium throughout adulthood, ISCs hold tremendous therapeutic potential for understanding and treating GI disease in humans. This review focuses on recent advances in our understanding of ISC identity, behavior, and regulation during homeostasis and injury-induced repair, as revealed by two major animal models used to study regeneration of the small intestine: Drosophila melanogaster and Mus musculus. We emphasize recent findings from Drosophila that are likely to translate to the mammalian GI system, as well as challenging topics in mouse ISC biology that may be ideally suited for investigation in flies. For context, we begin by reviewing major physiological similarities and distinctions between the Drosophila midgut and mouse small intestine.

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Abdelli, Latifa S., Hilda Merino, Crystal M. Rocher, and Dinender K. Singla. "Cell therapy in the heart." Canadian Journal of Physiology and Pharmacology 90, no. 3 (March 2012): 307–15. http://dx.doi.org/10.1139/y11-130.

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Cell therapy is emerging as a new strategy to circumvent the adverse effects of heart disease. Many experimental and clinical studies investigating the transplantation of cells into the injured myocardium have yielded promising results. Moreover, data from these reports show that transplanted stem cells can engraft within the myocardium, differentiate into major cardiac cell types, and improve cardiac function. However, results from clinical trials show conflicting results. These trials demonstrate significant improvements in cardiac function for up to 6 months. However, these improved functions were diminished when examined at 18 months. In this review, we will discuss the current literature available on cell transplantation, covering studies ranging from animal models to clinical trials.

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Shinder, Michael E., and Jeffrey S. Taube. "Self-motion improves head direction cell tuning." Journal of Neurophysiology 111, no. 12 (June 15, 2014): 2479–92. http://dx.doi.org/10.1152/jn.00512.2013.

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Head direction (HD) cells respond when an animal faces a particular direction in the environment and form the basis for the animal's perceived directional heading. When an animal moves through its environment, accurate updating of the HD signal is required to reflect the current heading, but the cells still maintain a representation of HD even when the animal is motionless. This finding suggests that the HD system holds its current state in the absence of input, a view that we tested by rotating a head-restrained rat in the presence of a prominent visual landmark and then stopping it suddenly when facing the cell's preferred firing direction (PFD). Firing rates were unchanged for the first 100 ms, but then progressively decreased over the next 4 s and stabilized at ∼42% of their initial values. When the rat was stopped facing away from the PFD, there was no initial effect of braking, but the firing rate then increased steadily over 4 s and plateaued at ∼14% of its peak firing rate, substantially above initial background firing rates. In experiment 2, the rat was serially placed facing one of eight equidistant directions over 360° and held there for 30 s. Compared with the cell's peak firing rate during a passive rotation session, firing rates were reduced (51%) for in-PFD directions and increased (∼300%) from background levels for off-PFD directions, values comparable to those observed in the braking protocol. These differential HD cell responses demonstrate the importance of self-motion to the HD signal integrity.

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Fuster, J. J., P. Fernandez, H. Gonzalez-Navarro, C. Silvestre, Y. N. A. Nabah, and V. Andres. "Control of cell proliferation in atherosclerosis: insights from animal models and human studies." Cardiovascular Research 86, no. 2 (November 9, 2009): 254–64. http://dx.doi.org/10.1093/cvr/cvp363.

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de Verneuil, Hubert, Cécile Ged, Samia Boulechfar, and François Moreau-Gaudry. "Porphyrias: Animal models and prospects for cellular and gene therapy." Journal of Bioenergetics and Biomembranes 27, no. 2 (April 1995): 239–48. http://dx.doi.org/10.1007/bf02110039.

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Mowes, Anja, Beatriz E. de Jongh, Timothy Cox, Yan Zhu, and Thomas H. Shaffer. "A translational cellular model to study the impact of high-frequency oscillatory ventilation on human epithelial cell function." Journal of Applied Physiology 122, no. 1 (January 1, 2017): 198–205. http://dx.doi.org/10.1152/japplphysiol.00400.2016.

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High-frequency oscillatory ventilation (HFOV) has been proposed as gentle ventilation strategy to prevent lung injury in the preterm infant. High-frequency jet ventilation leads to dimensional and mechanical airway deformation in animal airway models, which is consistent with translational studies demonstrating the impact of oxygen and biophysical stresses on normal airway cellular function. There is an overall paucity of clinical and cellular data on the impact of HFOV on the conducting airway. We developed an innovative method to test the impact of the clinical HFO Ventilator (SensorMedics 3100A) on human epithelial cell function. In this translational model, we were able to study the differential effects of biophysical stress due to HFOV independently and in combination with hyperoxia on a direct cellular level of the conducting airway system. Additionally, we could demonstrate that hyperoxia and pressure by HFOV independently resulted in significant cell dysfunction and inflammation, while the combination of HFOV and hyperoxia had a synergistic effect, resulting in greater cell death. NEW & NOTEWORTHY Traditionally, large-animal models are used to analyze the impact of clinical ventilators on lung cellular function. In our dual-chamber model, we interface high-frequency oscillatory ventilation (HFOV) directly with airway cells to study the effects of HFOV independently and combined with hyperoxia. Therefore, it is possible to study the preclinical impact of interventional factors without the high cost of animal models, thus reducing staff, time, as well as animal sparing.

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Kenneth Scott, G. "Proteinases and proteinase inhibitors as modulators of animal cell growth." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 103, no. 4 (December 1992): 785–93. http://dx.doi.org/10.1016/0305-0491(92)90195-w.

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Lee, Su-Jin, and Hyang-Ae Lee. "Trends in the development of human stem cell-based non-animal drug testing models." Korean Journal of Physiology & Pharmacology 24, no. 6 (November 1, 2020): 441–52. http://dx.doi.org/10.4196/kjpp.2020.24.6.441.

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Vance, Dennis E., Zhaoyu Li, and René L. Jacobs. "Hepatic Phosphatidylethanolamine N-Methyltransferase, Unexpected Roles in Animal Biochemistry and Physiology." Journal of Biological Chemistry 282, no. 46 (September 19, 2007): 33237–41. http://dx.doi.org/10.1074/jbc.r700028200.

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Chen, Chiao-nan Joyce, Ted G. Graber, Wendy M. Bratten, Deborah A. Ferrington, and LaDora V. Thompson. "Immunoproteasome in animal models of Duchenne muscular dystrophy." Journal of Muscle Research and Cell Motility 35, no. 2 (April 2014): 191–201. http://dx.doi.org/10.1007/s10974-014-9385-x.

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White, Martyn K., Jennifer Gordon, Joseph R. Berger, and Kamel Khalili. "Animal Models for Progressive Multifocal Leukoencephalopathy." Journal of Cellular Physiology 230, no. 12 (August 24, 2015): 2869–74. http://dx.doi.org/10.1002/jcp.25047.

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Mizgerd, Joseph P., and Shawn J. Skerrett. "Animal models of human pneumonia." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 3 (March 2008): L387—L398. http://dx.doi.org/10.1152/ajplung.00330.2007.

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Pneumonia is a medical and public health priority, and advances against this disease will require improved knowledge of biological mechanisms. Human pneumonia is modeled with experimental infections of animals, most frequently mice. Mouse models are leading to important discoveries relevant to pneumonia, but their limitations must be carefully considered. Several approaches to establishing pneumonia in mice have been developed, and each has specific strengths and weaknesses. Similarly, procedures for characterizing microbial and host responses to infection have unique advantages and disadvantages. Mice are not small humans, and the applicability of results from murine models to human disease depends on understanding the similarities and differences between species. Additional considerations such as mouse strain, microbe strain, and prior mouse-microbe interactions also influence the design and interpretation of experiments. Results from studies of pneumonia in animals, combined with complementary basic and translational studies, are elucidating mechanisms responsible for susceptibility to and pathophysiology of lung infection.

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Keeley, Thomas P., and Giovanni E. Mann. "Defining Physiological Normoxia for Improved Translation of Cell Physiology to Animal Models and Humans." Physiological Reviews 99, no. 1 (January 1, 2019): 161–234. http://dx.doi.org/10.1152/physrev.00041.2017.

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The extensive oxygen gradient between the air we breathe (Po2~21 kPa) and its ultimate distribution within mitochondria (as low as ~0.5–1 kPa) is testament to the efforts expended in limiting its inherent toxicity. It has long been recognized that cell culture undertaken under room air conditions falls short of replicating this protection in vitro. Despite this, difficulty in accurately determining the appropriate O2levels in which to culture cells, coupled with a lack of the technology to replicate and maintain a physiological O2environment in vitro, has hindered addressing this issue thus far. In this review, we aim to address the current understanding of tissue Po2distribution in vivo and summarize the attempts made to replicate these conditions in vitro. The state-of-the-art techniques employed to accurately determine O2levels, as well as the issues associated with reproducing physiological O2levels in vitro, are also critically reviewed. We aim to provide the framework for researchers to undertake cell culture under O2levels relevant to specific tissues and organs. We envisage that this review will facilitate a paradigm shift, enabling translation of findings under physiological conditions in vitro to disease pathology and the design of novel therapeutics.

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Miller, R. Lance. "Transgenic mice: beyond the knockout." American Journal of Physiology-Renal Physiology 300, no. 2 (February 2011): F291—F300. http://dx.doi.org/10.1152/ajprenal.00082.2010.

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Transgenic mice have had a tremendous impact on biomedical research. Most researchers are familiar with transgenic mice that carry Cre recombinase (Cre) and how they are used to create conditional knockouts. However, some researchers are less familiar with many of the other types of transgenic mice and their applications. For example, transgenic mice can be used to study biochemical and molecular pathways in primary cultures and cell suspensions derived from transgenic mice, cell-cell interactions using multiple fluorescent proteins in the same mouse, and the cell cycle in real time and in the whole animal, and they can be used to perform deep tissue imaging in the whole animal, follow cell lineage during development and disease, and isolate large quantities of a pure cell type directly from organs. These novel transgenic mice and their applications provide the means for studying of molecular and biochemical events in the whole animal that was previously limited to cell cultures. In conclusion, transgenic mice are not just for generating knockouts.

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Yang, Shao-Hua, Evelyn Perez, Jason Cutright, Ran Liu, Zhen He, Arthur L. Day, and James W. Simpkins. "Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model." Journal of Applied Physiology 92, no. 1 (January 1, 2002): 195–201. http://dx.doi.org/10.1152/jappl.2002.92.1.195.

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Increasing evidence has demonstrated striking sex differences in the outcome of neurological injury. Whereas estrogens contribute to these differences by attenuating neurotoxicity and ischemia-reperfusion injury, the effects of testosterone are unclear. The present study was undertaken to determine the effects of testosterone on neuronal injury in both a cell-culture model and a rodent ischemia-reperfusion model. Glutamate-induced HT-22 cell-death model was used to evaluate the effects of testosterone on cell survival. Testosterone was shown to significantly increase the toxicity of glutamate at a 10 μM concentration, whereas 17β-estradiol significantly attenuated the toxicity at the same concentration. In a rodent stroke model, ischemia-reperfusion injury was induced by temporal middle cerebral artery occlusion (MCAO) for 1 h and reperfusion for 24 h. To avoid the stress-related testosterone reduction, male rats were castrated and testosterone was replaced by testosterone pellet implantation. Testosterone pellets were removed at 1, 2, 4, or 6 h before MCAO to determine the duration of acute testosterone depletion effects on infarct volume. Ischemic lesion volume was significantly decreased from 239.6 ± 25.9 mm3 in control to 122.5 ± 28.6 mm3 when testosterone pellets were removed at 6 h before MCAO. Reduction of lesion volume was associated with amelioration of the hyperemia during reperfusion. Our in vitro and in vivo studies suggest that sex differences in response to brain injury are partly due to the consequence of damaging effects of testosterone.

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Schulte-Merker, Stefan, Amélie Sabine, and Tatiana V. Petrova. "Lymphatic vascular morphogenesis in development, physiology, and disease." Journal of Cell Biology 193, no. 4 (May 16, 2011): 607–18. http://dx.doi.org/10.1083/jcb.201012094.

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The lymphatic vasculature constitutes a highly specialized part of the vascular system that is essential for the maintenance of interstitial fluid balance, uptake of dietary fat, and immune response. Recently, there has been an increased awareness of the importance of lymphatic vessels in many common pathological conditions, such as tumor cell dissemination and chronic inflammation. Studies of embryonic development and genetically engineered animal models coupled with the discovery of mutations underlying human lymphedema syndromes have contributed to our understanding of mechanisms regulating normal and pathological lymphatic morphogenesis. It is now crucial to use this knowledge for the development of novel therapies for human diseases.

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Goldenring, James R., and Sachiyo Nomura. "Differentiation of the Gastric Mucosa III. Animal models of oxyntic atrophy and metaplasia." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 6 (December 2006): G999—G1004. http://dx.doi.org/10.1152/ajpgi.00187.2006.

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Gastric cancer in humans arises in the setting of oxyntic atrophy (parietal cell loss) and attendant hyperplastic and metaplastic lineage changes within the gastric mucosa. Helicobacter infection in mice and humans leads to spasmolytic polypeptide-expressing metaplasia (SPEM). In a number of mouse models, SPEM arises after oxyntic atrophy. In mice treated with the parietal cell toxic protonophore DMP-777, SPEM appears to arise from the transdifferentiation of chief cells. These results support the concept that intrinsic mucosal influences regulate and modulate the appearance of gastric metaplasia even in the absence of significant inflammation, whereas chronic inflammation is required for the further neoplastic transition.

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Doucet, Christelle, Isabelle Ernou, Yizhou Zhang, Jean-Roch Llense, Laurent Begot, Xavier Holy, and Jean-Jacques Lataillade. "Platelet lysates promote mesenchymal stem cell expansion: A safety substitute for animal serum in cell-based therapy applications." Journal of Cellular Physiology 205, no. 2 (2005): 228–36. http://dx.doi.org/10.1002/jcp.20391.

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Rivers, Angela, Ramasamy Jagadeeswaran, and Donald Lavelle. "Potential role of LSD1 inhibitors in the treatment of sickle cell disease: a review of preclinical animal model data." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 4 (October 1, 2018): R840—R847. http://dx.doi.org/10.1152/ajpregu.00440.2017.

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Sickle cell disease (SCD) is caused by a mutation of the β-globin gene (Ingram VM. Nature 180: 326–328, 1957), which triggers the polymerization of deoxygenated sickle hemoglobin (HbS). Approximately 100,000 SCD patients in the United States and millions worldwide (Piel FB, et al. PLoS Med 10: e1001484, 2013) suffer from chronic hemolytic anemia, painful crises, multisystem organ damage, and reduced life expectancy (Rees DC, et al. Lancet 376: 2018–2031, 2010; Serjeant GR. Cold Spring Harb Perspect Med 3: a011783, 2013). Hematopoietic stem cell transplantation can be curative, but the majority of patients do not have a suitable donor (Talano JA, Cairo MS. Eur J Haematol 94: 391–399, 2015). Advanced gene-editing technologies also offer the possibility of a cure (Goodman MA, Malik P. Ther Adv Hematol 7: 302–315, 2016; Lettre G, Bauer DE. Lancet 387: 2554–2564, 2016), but the likelihood that these strategies can be mobilized to treat the large numbers of patients residing in developing countries is remote. A pharmacological treatment to increase fetal hemoglobin (HbF) as a therapy for SCD has been a long-sought goal, because increased levels of HbF (α2γ2) inhibit the polymerization of HbS (Poillin WN, et al. Proc Natl Acad Sci USA 90: 5039–5043, 1993; Sunshine HR, et al. J Mol Biol 133: 435–467, 1979) and are associated with reduced symptoms and increased lifespan of SCD patients (Platt OS, et al. N Engl J Med 330: 1639–1644, 1994; Platt OS, et al. N Engl J Med 325: 11–16, 1991). Only two drugs, hydroxyurea and l-glutamine, are approved by the US Food and Drug Administration for treatment of SCD. Hydroxyurea is ineffective at HbF induction in ~50% of patients (Charache S, et al. N Engl J Med 332: 1317–1322, 1995). While polymerization of HbS has been traditionally considered the driving force in the hemolysis of SCD, the excessive reactive oxygen species generated from red blood cells, with further amplification by intravascular hemolysis, also are a major contributor to SCD pathology. This review highlights a new class of drugs, lysine-specific demethylase (LSD1) inhibitors, that induce HbF and reduce reactive oxygen species.

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Kvietys, Peter R., and D. Neil Granger. "Endothelial cell monolayers as a tool for studying microvascular pathophysiology." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 6 (December 1, 1997): G1189—G1199. http://dx.doi.org/10.1152/ajpgi.1997.273.6.g1189.

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Endothelial cells contribute to a variety of biological responses that facilitate organ function. This critical role of the endothelial cell has resulted in the development of different in vitro models that utilize monolayers of cultured cells to simulate conditions that exist in the intact animal. This review focuses on endothelial cell monolayers as a model system for research on certain pathophysiological conditions affecting the gastrointestinal tract. The advantages and limitations of endothelial cell monolayers are addressed, along with evolving technologies and strategies that hold promise for extending the utility of this in vitro model for studies of gastrointestinal function and disease.

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Ryter, Stefan W., Kevin C. Ma, and Augustine M. K. Choi. "Carbon monoxide in lung cell physiology and disease." American Journal of Physiology-Cell Physiology 314, no. 2 (February 1, 2018): C211—C227. http://dx.doi.org/10.1152/ajpcell.00022.2017.

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Carbon monoxide (CO) is an endogenously produced gas that has gained recognition as a biological signal transduction effector with properties similar, but not identical, to that of nitric oxide (NO). CO, which binds primarily to heme iron, may activate the hemoprotein guanylate cyclase, although with lower potency than NO. Furthermore, CO can modulate the activities of several cellular signaling molecules such as p38 MAPK, ERK1/2, JNK, Akt, NF-κB, and others. Emerging studies suggest that mitochondria, the energy-generating organelle of cells, represent a key target of CO action in eukaryotes. Dose-dependent modulation of mitochondrial function by CO can result in alteration of mitochondrial membrane potential, mitochondrial reactive oxygen species production, release of proapoptotic and proinflammatory mediators, as well as the inhibition of respiration at high concentration. CO, through modulation of signaling pathways, can impact key biological processes including autophagy, mitochondrial biogenesis, programmed cell death (apoptosis), cellular proliferation, inflammation, and innate immune responses. Inhaled CO is widely known as an inhalation hazard due to its rapid complexation with hemoglobin, resulting in impaired oxygen delivery to tissues and hypoxemia. Despite systemic and cellular toxicity at high concentrations, CO has demonstrated cyto- and tissue-protective effects at low concentration in animal models of organ injury and disease. These include models of acute lung injury (e.g., hyperoxia, hypoxia, ischemia-reperfusion, mechanical ventilation, bleomycin) and sepsis. The success of CO as a candidate therapeutic in preclinical models suggests potential clinical application in inflammatory and proliferative disorders, which is currently under evaluation in clinical trials.

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Yang, Xiaoping, Kwame Oteng Darko, Yanjun Huang, Caimei He, Huansheng Yang, Shanping He, Jianzhong Li, Jian Li, Berthold Hocher, and Yulong Yin. "Resistant Starch Regulates Gut Microbiota: Structure, Biochemistry and Cell Signalling." Cellular Physiology and Biochemistry 42, no. 1 (2017): 306–18. http://dx.doi.org/10.1159/000477386.

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Starch is one of the most popular nutritional sources for both human and animals. Due to the variation of its nutritional traits and biochemical specificities, starch has been classified into rapidly digestible, slowly digestible and resistant starch. Resistant starch has its own unique chemical structure, and various forms of resistant starch are commercially available. It has been found being a multiple-functional regulator for treating metabolic dysfunction. Different functions of resistant starch such as modulation of the gut microbiota, gut peptides, circulating growth factors, circulating inflammatory mediators have been characterized by animal studies and clinical trials. In this mini-review, recent remarkable progress in resistant starch on gut microbiota, particularly the effect of structure, biochemistry and cell signaling on nutrition has been summarized, with highlights on its regulatory effect on gut microbiota.

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Temkin, Alexis M., and Demetri D. Spyropoulos. "Induced pluripotent stem cell technology and aquatic animal species." Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 163 (June 2014): 3–13. http://dx.doi.org/10.1016/j.cbpc.2014.02.003.

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Wajner, Moacir, and Stephen I. Goodman. "Disruption of mitochondrial homeostasis in organic acidurias: insights from human and animal studies." Journal of Bioenergetics and Biomembranes 43, no. 1 (January 20, 2011): 31–38. http://dx.doi.org/10.1007/s10863-011-9324-0.

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Ma, Siyuan, Xiaohua Chen, Quanhui Tan, Shenglan Dai, Dan Li, Shanshan Wu, Yongsheng Yu, Guoqing Zang, and Zhenghao Tang. "An Engineered DC-Targeting Lentivector Induces Robust T Cell Responses and Inhibits HBV Replication in HBV Transgenic Mice via Upregulating T Cell Autophagy." Cellular Physiology and Biochemistry 48, no. 3 (2018): 1041–59. http://dx.doi.org/10.1159/000491972.

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Background/Aims: Developing engineered dendritic cell (DC)-targeting lentivectors (LVs) have been the target of intense research for their potential to create antigen-directed immunotherapeutics which can be safely administered to patients. In this study, we constructed a DC-directed LV (LVDC-UbHBcAg-LIGHT) as a potential vaccine to induce anti-HBV immune responses. Methods: Specificity of LVDC-UbHBcAg-LIGHT for DCs in vivo was confirmed through live animal imaging studies. The levels of cytokine production in T cells were assessed by flow cytometry. The HBcAg-specific cytotoxic T lymphocyte (CTL) responses and antibody responses induced by direct administration of the LVs were detected by LDH release assay and ELISA respectively. The levels of serum HBsAg and HBV DNA were evaluated by Abbott kits and quantitative PCR respectively. The expression levels of HBsAg and HBcAg in liver tissues of HBV transgenic mice were examined by immunohistochemistry. In addition, molecular mechanism underlying the activation of CD8+ T cells was explored. Results: Live animal imaging studies showed that following subcutaneous administration of LVDC-UbHBcAg-LIGHT, no obvious luminescence signal was detected at the injection site. Immunization with LVDC-UbHBcAg-LIGHT elicited potent T cell responses in HBV transgenic mice evidenced by increased percentages of IFN-γ, TNF-α and GzmB producing CD8+ T cells as well as IFN-γ producing CD4+ T cells, improved HBcAg-specific CTL activities and antibody responses. Additionally, vaccination with LVDC-UbHBcAg-LIGHT efficiently reduced serum HBsAg, HBV DNA levels and the expression of HBsAg and HBcAg in liver tissues of HBV transgenic mice. More importantly, autophagy was induced in the activated CD8+ T cells, and the induced autophagy noticeably promoted the proliferation of T cells and decreased the frequencies of apoptotic CD8+ T cells by selectively degrading ubiquitinated apoptosis and cell cycle-associated protein aggregates. Futhermore, we confirmed the interaction between autophagosomes and ubiquitinated aggregates by confocal microscopy and immunoprecipitation analysis. Conclusions: These results demonstrated that LVDC-UbHBcAg-LIGHT provided a simple method of eliciting effective antiviral immune responses in HBV transgenic mice and might potentially be used as a therapeutic strategy to eradicate HBV with more safety and efficiency. Moreover, our results revealed a direct role of autophagy in promoting the survival and proliferation of activated CD8+ T cells.

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Matute-Bello, Gustavo, Charles W. Frevert, and Thomas R. Martin. "Animal models of acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 3 (September 2008): L379—L399. http://dx.doi.org/10.1152/ajplung.00010.2008.

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Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.

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Barclay, Robert L., Partosh K. Dinda, Gerald P. Morris, and William G. Paterson. "Morphological evidence of mast cell degranulation in an animal model of acid-induced esophageal mucosal injury." Digestive Diseases and Sciences 40, no. 8 (August 1995): 1651–58. http://dx.doi.org/10.1007/bf02212685.

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Kamdar, Forum, Mohammad Nurulqadr Jameel, Paul Score, and Jianyi Zhang. "Cellular therapy promotes endogenous stem cell repair." Canadian Journal of Physiology and Pharmacology 90, no. 10 (October 2012): 1335–44. http://dx.doi.org/10.1139/y2012-115.

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Cellular transplantation for cardiac repair has emerged as an exciting treatment option for patients with myocardial infarction (MI) and heart failure. Animal models of post-infarction left ventricular remodeling have demonstrated an improvement in left ventricular (LV) function, decrease in scar size, and amelioration of adverse cardiac remodeling after stem cell transplantation. These beneficial effects occur despite minimal engraftment and negligible differentiation of transplanted cells. Evidence of the heart capability to self-renew continues to mount; however, the extent to which this occurs is still unclear. Although there is a specific population of cardiac stem cells capable of differentiating into cardiomyocytes, they alone are not capable of fully regenerating tissue damaged by MI. Therefore, paracrine mechanisms may be responsible for activating endogenous stem cells to promote regeneration and prevent apoptosis. These structural beneficial effects may reduce regional wall stresses, consequently leading to long-term host myocardium gene/protein expression changes, which may subsequently result in improvement in LV function.

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Mullins, Olivia J., John T. Hackett, and W. Otto Friesen. "Local-Distributed Integration by a Novel Neuron Ensures Rapid Initiation of Animal Locomotion." Journal of Neurophysiology 105, no. 1 (January 2011): 130–44. http://dx.doi.org/10.1152/jn.00507.2010.

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Animals are adapted to respond quickly to threats in their environment. In many invertebrate and some vertebrate species, the evolutionary pressures have resulted in rapidly conducting giant axons, which allow short response times. Although neural circuits mediating escape behavior are identified in several species, little attention has been paid to this behavior in the medicinal leech, a model organism whose neuronal circuits are well known. We present data that suggest an alternative to giant axons for the rapid initiation of locomotion. A novel individual neuron, cell E21, appears to be one mediator of this short-latency action in the leech. In isolated nerve cord and semi-intact preparations, cell E21 excitation initiates and extends swimming and reduces the cycle period. The soma of this cell is located caudally, but its axon extends nearly the entire length of the nerve cord. We found that cell E21 fires impulses following local sensory inputs anywhere along the body and makes excitatory synapses onto the gating cells that drive swimming behavior. These distributed input–output sites minimize the distance information travels to initiate swimming behavior, thus minimizing the latency between sensory input and motor output. We propose that this single cell E21 functions to rapidly initiate or modulate locomotion through its distributed synaptic connections.

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Duchen, Michael R. "Contributions of mitochondria to animal physiology: from homeostatic sensor to calcium signalling and cell death." Journal of Physiology 516, no. 1 (April 1999): 1–17. http://dx.doi.org/10.1111/j.1469-7793.1999.001aa.x.

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Willecke, Klaus, and Sandra Haubrich. "Connexin expression systems: To what extent do they reflect the situation in the animal?" Journal of Bioenergetics and Biomembranes 28, no. 4 (August 1996): 319–26. http://dx.doi.org/10.1007/bf02110108.

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LI, C., T. WRIGHT, M. DONG, Y. DOMMELS, L. TRUDEL, P. DEDON, S. TANNENBAUM, and G. WOGAN. "Biological role of glutathione in nitric oxide-induced toxicity in cell culture and animal models." Free Radical Biology and Medicine 39, no. 11 (December 1, 2005): 1489–98. http://dx.doi.org/10.1016/j.freeradbiomed.2005.07.011.

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Mohan, Ramkumar, Daniel Baumann, and Emilyn Uy Alejandro. "Fetal undernutrition, placental insufficiency, and pancreatic β-cell development programming in utero." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 5 (November 1, 2018): R867—R878. http://dx.doi.org/10.1152/ajpregu.00072.2018.

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The prevalence of obesity and type 2 (T2D) diabetes is a major health concern in the United States and around the world. T2D is a complex disease characterized by pancreatic β-cell failure in association with obesity and insulin resistance in peripheral tissues. Although several genes associated with T2D have been identified, it is speculated that genetic variants account for only <10% of the risk for this disease. A strong body of data from both human epidemiological and animal studies shows that fetal nutrient factors in utero confer significant susceptibility to T2D. Numerous studies done in animals have shown that suboptimal maternal environment or placental insufficiency causes intrauterine growth restriction (IUGR) in the fetus, a critical factor known to predispose offspring to obesity and T2D, in part by causing permanent consequences in total functional β-cell mass. This review will focus on the potential contribution of the placenta in fetal programming of obesity and TD and its likely impact on pancreatic β-cell development and growth.

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Fasolo, Francesca, Karina Di Gregoli, Lars Maegdefessel, and Jason L. Johnson. "Non-coding RNAs in cardiovascular cell biology and atherosclerosis." Cardiovascular Research 115, no. 12 (August 7, 2019): 1732–56. http://dx.doi.org/10.1093/cvr/cvz203.

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Abstract Atherosclerosis underlies the predominant number of cardiovascular diseases and remains a leading cause of morbidity and mortality worldwide. The development, progression and formation of clinically relevant atherosclerotic plaques involves the interaction of distinct and over-lapping mechanisms which dictate the roles and actions of multiple resident and recruited cell types including endothelial cells, vascular smooth muscle cells, and monocyte/macrophages. The discovery of non-coding RNAs (ncRNAs) including microRNAs, long non-coding RNAs, and circular RNAs, and their identification as key mechanistic regulators of mRNA and protein expression has piqued interest in their potential contribution to atherosclerosis. Accruing evidence has revealed ncRNAs regulate pivotal cellular and molecular processes during all stages of atherosclerosis including cell invasion, growth, and survival; cellular uptake and efflux of lipids, expression and release of pro- and anti-inflammatory intermediaries, and proteolytic balance. The expression profile of ncRNAs within atherosclerotic lesions and the circulation have been determined with the aim of identifying individual or clusters of ncRNAs which may be viable therapeutic targets alongside deployment as biomarkers of atherosclerotic plaque progression. Consequently, numerous in vivo studies have been convened to determine the effects of moderating the function or expression of select ncRNAs in well-characterized animal models of atherosclerosis. Together, clinicopathological findings and studies in animal models have elucidated the multifaceted and frequently divergent effects ncRNAs impose both directly and indirectly on the formation and progression of atherosclerosis. From these findings’ potential novel therapeutic targets and strategies have been discovered which may pave the way for further translational studies and possibly taken forward for clinical application.

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Hawke, Thomas J., and Daniel J. Garry. "Myogenic satellite cells: physiology to molecular biology." Journal of Applied Physiology 91, no. 2 (August 1, 2001): 534–51. http://dx.doi.org/10.1152/jappl.2001.91.2.534.

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Adult skeletal muscle has a remarkable ability to regenerate following myotrauma. Because adult myofibers are terminally differentiated, the regeneration of skeletal muscle is largely dependent on a small population of resident cells termed satellite cells. Although this population of cells was identified 40 years ago, little is known regarding the molecular phenotype or regulation of the satellite cell. The use of cell culture techniques and transgenic animal models has improved our understanding of this unique cell population; however, the capacity and potential of these cells remain ill-defined. This review will highlight the origin and unique markers of the satellite cell population, the regulation by growth factors, and the response to physiological and pathological stimuli. We conclude by highlighting the potential therapeutic uses of satellite cells and identifying future research goals for the study of satellite cell biology.

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Yang, Chun, Wei Xiong, Qian Qiu, Zuo Shao, David Hamel, Houda Tahiri, Grégoire Leclair, Pierre Lachapelle, Sylvain Chemtob, and Pierre Hardy. "Role of receptor-mediated endocytosis in the antiangiogenic effects of human T lymphoblastic cell-derived microparticles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 8 (April 15, 2012): R941—R949. http://dx.doi.org/10.1152/ajpregu.00527.2011.

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Microparticles possess therapeutic potential regarding angiogenesis. We have demonstrated the contribution of apoptotic human CEM T lymphocyte-derived microparticles (LMPs) as inhibitors of angiogenic responses in animal models of inflammation and tumor growth. In the present study, we characterized the antivascular endothelial growth factor (VEGF) effects of LMPs on pathological angiogenesis in an animal model of oxygen-induced retinopathy and explored the role of receptor-mediated endocytosis in the effects of LMPs on human retinal endothelial cells (HRECs). LMPs dramatically inhibited cell growth of HRECs, suppressed VEGF-induced cell migration in vitro experiments, and attenuated VEGF-induced retinal vascular leakage in vivo. Intravitreal injections of fluorescently labeled LMPs revealed accumulation of LMPs in retinal tissue, with more than 60% reductions of the vascular density in retinas of rats with oxygen-induced neovascularization. LMP uptake experiments demonstrated that the interaction between LMPs and HRECs is dependent on temperature. In addition, endocytosis is partially dependent on extracellular calcium. RNAi-mediated knockdown of low-density lipoprotein receptor (LDLR) reduced the uptake of LMPs and attenuated the inhibitory effects of LMPs on VEGF-A protein expression and HRECs cell growth. Intravitreal injection of lentivirus-mediated RNA interference reduced LDLR protein expression in retina by 53% and significantly blocked the antiangiogenic effects of LMPs on pathological vascularization. In summary, the potent antiangiogenic LMPs lead to a significant reduction of pathological retinal angiogenesis through modulation of VEGF signaling, whereas LDLR-mediated endocytosis plays a partial, but pivotal, role in the uptake of LMPs in HRECs.

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Journal articles on the topic '060602 Animal Physiology - Cell'

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