24 results on '"Waterhouse PD"'
Search Results
2. Droplet-based proteomics reveals CD36 as a marker for progenitors in mammary basal epithelium.
- Author
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Waas M, Khoo A, Tharmapalan P, McCloskey CW, Govindarajan M, Zhang B, Khan S, Waterhouse PD, Khokha R, and Kislinger T
- Subjects
- Animals, Female, Epithelium metabolism, Mice, Humans, Mitochondria metabolism, Proteomics methods, CD36 Antigens metabolism, Stem Cells metabolism, Mammary Glands, Animal cytology, Mammary Glands, Animal metabolism, Biomarkers metabolism, Biomarkers analysis
- Abstract
Deep proteomic profiling of rare cell populations has been constrained by sample input requirements. Here, we present DROPPS (droplet-based one-pot preparation for proteomic samples), an accessible low-input platform that generates high-fidelity proteomic profiles of 100-2,500 cells. By applying DROPPS within the mammary epithelium, we elucidated the connection between mitochondrial activity and clonogenicity, identifying CD36 as a marker of progenitor capacity in the basal cell compartment. We anticipate that DROPPS will accelerate biology-driven proteomic research for a multitude of rare cell populations., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
- Published
- 2024
- Full Text
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3. Differential DNA damage repair and PARP inhibitor vulnerability of the mammary epithelial lineages.
- Author
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Kim H, Aliar K, Tharmapalan P, McCloskey CW, Kuttanamkuzhi A, Grünwald BT, Palomero L, Mahendralingam MJ, Waas M, Mer AS, Elliott MJ, Zhang B, Al-Zahrani KN, Langille ER, Parsons M, Narala S, Hofer S, Waterhouse PD, Hakem R, Haibe-Kains B, Kislinger T, Schramek D, Cescon DW, Pujana MA, Berman HK, and Khokha R
- Published
- 2023
- Full Text
- View/download PDF
4. Abnormal B-cell development in TIMP-deficient bone marrow.
- Author
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Weiss A, Saw S, Aiken A, Aliar K, Shao YW, Fang H, Narala S, Shetty R, Waterhouse PD, and Khokha R
- Subjects
- Animals, B-Lymphocytes, Hematopoiesis, Mice, Tissue Inhibitor of Metalloproteinases genetics, Bone Marrow, Bone Marrow Cells
- Abstract
Bone marrow (BM) is the primary site of hematopoiesis and is responsible for a lifelong supply of all blood cell lineages. The process of hematopoiesis follows key intrinsic programs that also integrate instructive signals from the BM niche. First identified as an erythropoietin-potentiating factor, the tissue inhibitor of metalloproteinase (TIMP) protein family has expanded to 4 members and has widely come to be viewed as a classical regulator of tissue homeostasis. By virtue of metalloprotease inhibition, TIMPs not only regulate extracellular matrix turnover but also control growth factor bioavailability. The 4 mammalian TIMPs possess overlapping enzyme-inhibition profiles and have never been studied for their cumulative role in hematopoiesis. Here, we show that TIMPs are critical for postnatal B lymphopoiesis in the BM. TIMP-deficient mice have defective B-cell development arising at the pro-B-cell stage. Expression analysis of TIMPless hematopoietic cell subsets pointed to an altered B-cell program in the Lineage-Sca-1+c-Kit+ (LSK) cell fraction. Serial and competitive BM transplants identified a defect in TIMP-deficient hematopoietic stem and progenitor cells for B lymphopoiesis. In parallel, reverse BM transplants uncovered the extrinsic role of stromal TIMPs in pro- and pre-B-cell development. TIMP deficiency disrupted CXCL12 localization to LepR+ cells, and increased soluble CXCL12 within the BM niche. It also compromised the number and morphology of LepR+ cells. These data provide new evidence that TIMPs control the cellular and biochemical makeup of the BM niche and influence the LSK transcriptional program required for optimal B lymphopoiesis., (© 2021 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)
- Published
- 2021
- Full Text
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5. Author Correction: Human somatic cell mutagenesis creates genetically tractable sarcomas.
- Author
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Molyneux SD, Waterhouse PD, Shelton D, Shao YW, Watling CM, Tang QL, Harris IS, Dickson BC, Tharmapalan P, Sandve GK, Zhang X, Bailey SD, Berman H, Wunder JS, Izsvák Z, Lupien M, Mak TW, and Khokha R
- Abstract
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
- Published
- 2020
- Full Text
- View/download PDF
6. Metalloproteases: On the Watch in the Hematopoietic Niche.
- Author
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Saw S, Weiss A, Khokha R, and Waterhouse PD
- Subjects
- Animals, Cell Differentiation, Cell Self Renewal, Hematopoiesis, Humans, Proteolysis, Stem Cell Niche, Extracellular Matrix metabolism, Hematopoietic Stem Cells physiology, Metalloproteases metabolism
- Abstract
Hematopoietic stem cells (HSCs) self-renew or differentiate into blood cell lineages following extrinsic cues propagated in specialized niches. Support cells and soluble factors in the niche respond to stress and enable progenitor activity. Metalloproteases (MMPs, ADAMs, ADAMTSs) and their inhibitors (TIMPs) control certain physical and biochemical features of the niche by altering protease-dependent bioavailability of local niche factors (e.g., CXCL12, SCF, TGFβ, VEGF), matrix turnover, and cellular interactions. With over 40 examples of diverse metalloprotease substrates known to trigger fate-changing decisions, the spatially confined activity of this multi-member protease family is ideally positioned to constitute a higher order control over hematopoiesis. Comprehension of regulated proteolysis in the bone marrow may fuel innovative strategies to harness HSC fate and function., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
7. Metalloprotease inhibitor TIMP proteins control FGF-2 bioavailability and regulate skeletal growth.
- Author
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Saw S, Aiken A, Fang H, McKee TD, Bregant S, Sanchez O, Chen Y, Weiss A, Dickson BC, Czarny B, Sinha A, Fosang A, Dive V, Waterhouse PD, Kislinger T, and Khokha R
- Subjects
- Animals, Fibroblast Growth Factor 2 genetics, Mice, Mice, Knockout, Tissue Inhibitor of Metalloproteinases genetics, Bone Development, Bone and Bones metabolism, Chondrocytes metabolism, Fibroblast Growth Factor 2 metabolism, Growth Plate metabolism, Tissue Inhibitor of Metalloproteinases metabolism
- Abstract
Regulated growth plate activity is essential for postnatal bone development and body stature, yet the systems regulating epiphyseal fusion are poorly understood. Here, we show that the tissue inhibitors of metalloprotease (TIMP) gene family is essential for normal bone growth after birth. Whole-body quadruple-knockout mice lacking all four TIMPs have growth plate closure in long bones, precipitating limb shortening, epiphyseal distortion, and widespread chondrodysplasia. We identify TIMP/FGF-2/IHH as a novel nexus underlying bone lengthening where TIMPs negatively regulate the release of FGF-2 from chondrocytes to allow IHH expression. Using a knock-in approach that combines MMP-resistant or ADAMTS-resistant aggrecans with TIMP deficiency, we uncouple growth plate activity in axial and appendicular bones. Thus, natural metalloprotease inhibitors are crucial regulators of chondrocyte maturation program, growth plate integrity, and skeletal proportionality. Furthermore, individual and combinatorial TIMP-deficient mice demonstrate the redundancy of metalloprotease inhibitor function in embryonic and postnatal development., (© 2019 Saw et al.)
- Published
- 2019
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8. Identifying the murine mammary cell target of metformin exposure.
- Author
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Shehata M, Kim H, Vellanki R, Waterhouse PD, Mahendralingam M, Casey AE, Koritzinsky M, and Khokha R
- Subjects
- Animals, Apoptosis, Cell Cycle, Cell Lineage, Cell Separation, DNA Damage, Female, Flow Cytometry, Mice, Receptors, Estrogen metabolism, Hypoglycemic Agents pharmacology, Mammary Glands, Animal drug effects, Mammary Neoplasms, Animal drug therapy, Mammary Neoplasms, Experimental drug therapy, Metformin pharmacology
- Abstract
The heterogeneity of breast cancer makes current therapies challenging. Metformin, the anti-diabetic drug, has shown promising anti-cancer activities in epidemiological studies and breast cancer models. Yet, how metformin alters the normal adult breast tissue remains elusive. We demonstrate metformin intake at a clinically relevant dose impacts the hormone receptor positive (HR+) luminal cells in the normal murine mammary gland. Metformin decreases total cell number, progenitor capacity and specifically reduces DNA damage in normal HR+ luminal cells, decreases oxygen consumption rate and increases cell cycle length of luminal cells. HR+ luminal cells demonstrate the lowest levels of mitochondrial respiration and capacity to handle oxidative stress compared to the other fractions, suggesting their intrinsic susceptibility to long-term metformin exposure. Uncovering HR+ luminal cells in the normal mammary gland as the major cell target of metformin exposure could identify patients that would most benefit from repurposing this anti-diabetic drug for cancer prevention/therapy purposes., Competing Interests: Competing interestsThe authors declare no competing interests.
- Published
- 2019
- Full Text
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9. PDGFRα + stromal adipocyte progenitors transition into epithelial cells during lobulo-alveologenesis in the murine mammary gland.
- Author
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Joshi PA, Waterhouse PD, Kasaian K, Fang H, Gulyaeva O, Sul HS, Boutros PC, and Khokha R
- Subjects
- Animals, Cell Differentiation, Cell Lineage, Epithelial Cells, Humans, Mammary Glands, Animal growth & development, Mice, Adipocytes cytology, Mammary Glands, Animal cytology, Receptor, Platelet-Derived Growth Factor alpha metabolism, Stromal Cells cytology
- Abstract
The mammary gland experiences substantial remodeling and regeneration during development and reproductive life, facilitated by stem cells and progenitors that act in concert with physiological stimuli. While studies have focused on deciphering regenerative cells within the parenchymal epithelium, cell lineages in the stroma that may directly contribute to epithelial biology is unknown. Here we identify, in mouse, the transition of a PDGFRα
+ mesenchymal cell population into mammary epithelial progenitors. In addition to being adipocyte progenitors, PDGFRα+ cells make a de novo contribution to luminal and basal epithelia during mammary morphogenesis. In the adult, this mesenchymal lineage primarily generates luminal progenitors within lobuloalveoli during sex hormone exposure or pregnancy. We identify cell migration as a key molecular event that is activated in mesenchymal progenitors in response to epithelium-derived chemoattractant. These findings demonstrate a stromal reservoir of epithelial progenitors and provide insight into cell origins and plasticity during mammary tissue growth.- Published
- 2019
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10. Proliferative heterogeneity of murine epithelial cells in the adult mammary gland.
- Author
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Shehata M, Waterhouse PD, Casey AE, Fang H, Hazelwood L, and Khokha R
- Abstract
Breast cancer is the most common cancer in females. The number of years menstruating and length of an individual menstrual cycle have been implicated in increased breast cancer risk. At present, the proliferative changes within an individual reproductive cycle or variations in the estrous cycle in the normal mammary gland are poorly understood. Here we use Fucci2 reporter mice to demonstrate actively proliferating mammary epithelial cells have shorter G1 lengths, whereas more differentiated/non-proliferating cells have extended G1 lengths. We find that cells enter into the cell cycle mainly during diestrus, yet the expansion is erratic and does not take place every reproductive cycle. Single cell expression analyses feature expected proliferation markers ( Birc5, Top2a ), while HR+ luminal cells exhibit fluctuations of key differentiation genes ( ER, Gata3 ) during the cell cycle. We highlight the proliferative heterogeneity occurring within the normal mammary gland during a single-estrous cycle, indicating that the mammary gland undergoes continual dynamic proliferative changes., Competing Interests: The authors declare no competing interests.
- Published
- 2018
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11. RANK Signaling Amplifies WNT-Responsive Mammary Progenitors through R-SPONDIN1.
- Author
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Joshi PA, Waterhouse PD, Kannan N, Narala S, Fang H, Di Grappa MA, Jackson HW, Penninger JM, Eaves C, and Khokha R
- Subjects
- Animals, Cell Proliferation genetics, Female, Humans, Mammary Glands, Animal growth & development, Mice, Receptor Activator of Nuclear Factor-kappa B antagonists & inhibitors, Thrombospondins biosynthesis, Wnt Signaling Pathway genetics, Mammary Glands, Animal metabolism, Receptor Activator of Nuclear Factor-kappa B genetics, Stem Cells cytology, Thrombospondins genetics
- Abstract
Systemic and local signals must be integrated by mammary stem and progenitor cells to regulate their cyclic growth and turnover in the adult gland. Here, we show RANK-positive luminal progenitors exhibiting WNT pathway activation are selectively expanded in the human breast during the progesterone-high menstrual phase. To investigate underlying mechanisms, we examined mouse models and found that loss of RANK prevents the proliferation of hormone receptor-negative luminal mammary progenitors and basal cells, an accompanying loss of WNT activation, and, hence, a suppression of lobuloalveologenesis. We also show that R-spondin1 is depleted in RANK-null progenitors, and that its exogenous administration rescues key aspects of RANK deficiency by reinstating a WNT response and mammary cell expansion. Our findings point to a novel role of RANK in dictating WNT responsiveness to mediate hormone-induced changes in the growth dynamics of adult mammary cells., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2015
- Full Text
- View/download PDF
12. A Progesterone-CXCR4 Axis Controls Mammary Progenitor Cell Fate in the Adult Gland.
- Author
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Shiah YJ, Tharmapalan P, Casey AE, Joshi PA, McKee TD, Jackson HW, Beristain AG, Chan-Seng-Yue MA, Bader GD, Lydon JP, Waterhouse PD, Boutros PC, and Khokha R
- Abstract
Progesterone drives mammary stem and progenitor cell dynamics through paracrine mechanisms that are currently not well understood. Here, we demonstrate that CXCR4, the receptor for stromal-derived factor 1 (SDF-1; CXC12), is a crucial instructor of hormone-induced mammary stem and progenitor cell function. Progesterone elicits specific changes in the transcriptome of basal and luminal mammary epithelial populations, where CXCL12 and CXCR4 represent a putative ligand-receptor pair. In situ, CXCL12 localizes to progesterone-receptor-positive luminal cells, whereas CXCR4 is induced in both basal and luminal compartments in a progesterone-dependent manner. Pharmacological inhibition of CXCR4 signaling abrogates progesterone-directed expansion of basal (CD24
+ CD49fhi ) and luminal (CD24+ CD49flo ) subsets. This is accompanied by a marked reduction in CD49b+ SCA-1- luminal progenitors, their functional capacity, and lobuloalveologenesis. These findings uncover CXCL12 and CXCR4 as novel paracrine effectors of hormone signaling in the adult mammary gland, and present a new avenue for potentially targeting progenitor cell growth and malignant transformation in breast cancer., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2015
- Full Text
- View/download PDF
13. Human somatic cell mutagenesis creates genetically tractable sarcomas.
- Author
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Molyneux SD, Waterhouse PD, Shelton D, Shao YW, Watling CM, Tang QL, Harris IS, Dickson BC, Tharmapalan P, Sandve GK, Zhang X, Bailey SD, Berman H, Wunder JS, Izsvák Z, Lupien M, Mak TW, and Khokha R
- Subjects
- Cell Line, DNA Transposable Elements, Genetic Vectors genetics, Genome, Human, HEK293 Cells, Humans, RNA-Binding Proteins genetics, Retroviridae genetics, Mutagenesis, Insertional, Sarcoma genetics
- Abstract
Creating spontaneous yet genetically tractable human tumors from normal cells presents a fundamental challenge. Here we combined retroviral and transposon insertional mutagenesis to enable cancer gene discovery starting with human primary cells. We used lentiviruses to seed gain- and loss-of-function gene disruption elements, which were further deployed by Sleeping Beauty transposons throughout the genome of human bone explant mesenchymal cells. De novo tumors generated rapidly in this context were high-grade myxofibrosarcomas. Tumor insertion sites were enriched in recurrent somatic copy-number aberration regions from multiple cancer types and could be used to pinpoint new driver genes that sustain somatic alterations in patients. We identified HDLBP, which encodes the RNA-binding protein vigilin, as a candidate tumor suppressor deleted at 2q37.3 in greater than one out of ten tumors across multiple tissues of origin. Hybrid viral-transposon systems may accelerate the functional annotation of cancer genomes by enabling insertional mutagenesis screens in higher eukaryotes that are not amenable to germline transgenesis.
- Published
- 2014
- Full Text
- View/download PDF
14. Loss of the Timp gene family is sufficient for the acquisition of the CAF-like cell state.
- Author
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Shimoda M, Principe S, Jackson HW, Luga V, Fang H, Molyneux SD, Shao YW, Aiken A, Waterhouse PD, Karamboulas C, Hess FM, Ohtsuka T, Okada Y, Ailles L, Ludwig A, Wrana JL, Kislinger T, and Khokha R
- Subjects
- ADAM Proteins metabolism, ADAM10 Protein, Amyloid Precursor Protein Secretases metabolism, Animals, Cell Line, Tumor, Cell Movement, Exosomes physiology, Female, Fibroblasts pathology, Humans, Lung Neoplasms enzymology, Mammary Neoplasms, Experimental enzymology, Membrane Proteins metabolism, Metalloendopeptidases metabolism, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Neoplasm Transplantation, Phenotype, Signal Transduction, Tissue Inhibitor of Metalloproteinases deficiency, Tumor Burden, Fibroblasts metabolism, Lung Neoplasms secondary, Mammary Neoplasms, Experimental pathology, Tissue Inhibitor of Metalloproteinases genetics
- Abstract
Cancer-associated fibroblasts (CAFs) drive tumour progression, but the emergence of this cell state is poorly understood. A broad spectrum of metalloproteinases, controlled by the Timp gene family, influence the tumour microenvironment in human cancers. Here, we generate quadruple TIMP knockout (TIMPless) fibroblasts to unleash metalloproteinase activity within the tumour-stromal compartment and show that complete Timp loss is sufficient for the acquisition of hallmark CAF functions. Exosomes produced by TIMPless fibroblasts induce cancer cell motility and cancer stem cell markers. The proteome of these exosomes is enriched in extracellular matrix proteins and the metalloproteinase ADAM10. Exosomal ADAM10 increases aldehyde dehydrogenase expression in breast cancer cells through Notch receptor activation and enhances motility through the GTPase RhoA. Moreover, ADAM10 knockdown in TIMPless fibroblasts abrogates their CAF function. Importantly, human CAFs secrete ADAM10-rich exosomes that promote cell motility and activate RhoA and Notch signalling in cancer cells. Thus, Timps suppress cancer stroma where activated-fibroblast-secreted exosomes impact tumour progression.
- Published
- 2014
- Full Text
- View/download PDF
15. Progesterone induces adult mammary stem cell expansion.
- Author
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Joshi PA, Jackson HW, Beristain AG, Di Grappa MA, Mote PA, Clarke CL, Stingl J, Waterhouse PD, and Khokha R
- Subjects
- Animals, Cell Count, Cell Division drug effects, Cell Transformation, Neoplastic, Estrogens pharmacology, Estrous Cycle blood, Estrous Cycle physiology, Female, Homeostasis drug effects, Integrin alpha6 metabolism, Mice, Ovariectomy, Paracrine Communication drug effects, Progesterone blood, Progesterone metabolism, RANK Ligand metabolism, Receptors, Estrogen metabolism, Receptors, Progesterone metabolism, Stem Cell Niche cytology, Stem Cell Niche drug effects, Stem Cell Niche metabolism, Stem Cells metabolism, Wnt Proteins metabolism, Wnt4 Protein, Aging physiology, Mammary Glands, Animal cytology, Progesterone pharmacology, Stem Cells cytology, Stem Cells drug effects
- Abstract
Reproductive history is the strongest risk factor for breast cancer after age, genetics and breast density. Increased breast cancer risk is entwined with a greater number of ovarian hormone-dependent reproductive cycles, yet the basis for this predisposition is unknown. Mammary stem cells (MaSCs) are located within a specialized niche in the basal epithelial compartment that is under local and systemic regulation. The emerging role of MaSCs in cancer initiation warrants the study of ovarian hormones in MaSC homeostasis. Here we show that the MaSC pool increases 14-fold during maximal progesterone levels at the luteal dioestrus phase of the mouse. Stem-cell-enriched CD49fhi cells amplify at dioestrus, or with exogenous progesterone, demonstrating a key role for progesterone in propelling this expansion. In aged mice, CD49fhi cells display stasis upon cessation of the reproductive cycle. Progesterone drives a series of events where luminal cells probably provide Wnt4 and RANKL signals to basal cells which in turn respond by upregulating their cognate receptors, transcriptional targets and cell cycle markers. Our findings uncover a dynamic role for progesterone in activating adult MaSCs within the mammary stem cell niche during the reproductive cycle, where MaSCs are putative targets for cell transformation events leading to breast cancer.
- Published
- 2010
- Full Text
- View/download PDF
16. Inhibition of surface immunoglobulin capping on mouse splenic lymphocytes by cetyltrimethylammonium bromide.
- Author
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Paatero GI, Brown DL, and Waterhouse PD
- Subjects
- Animals, Cetrimonium, Lymphocytes drug effects, Mice, Mice, Inbred BALB C, Mice, Inbred Strains, Spleen immunology, Cetrimonium Compounds pharmacology, Detergents pharmacology, Immunologic Capping drug effects, Lymphocytes immunology, Quaternary Ammonium Compounds pharmacology, Surface-Active Agents pharmacology
- Published
- 1986
17. Increases in microtubule assembly and in tubulin content in mitogenically stimulated mouse splenic T lymphocytes.
- Author
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Waterhouse PD, Anderson PJ, and Brown DL
- Subjects
- Actins metabolism, Animals, B-Lymphocytes metabolism, Cell Nucleus ultrastructure, Concanavalin A pharmacology, Cytoplasm ultrastructure, Mice, Mice, Inbred BALB C, Microscopy, Electron, Microtubules ultrastructure, Spleen cytology, T-Lymphocytes ultrastructure, Lymphocyte Activation, Microtubules metabolism, T-Lymphocytes metabolism, Tubulin metabolism
- Abstract
We have examined the changes in the microtubule and tubulin contents in populations of mouse splenic T lymphocytes stimulated by the mitogen concanavalin A. Indirect immunofluorescence staining with antiserum to tubulin indicated that a more extensive microtubule network was assembled from the centrosome in those cells which had increased in size in response to the mitogen. Direct counts of microtubules from electron micrographs of the centrosome regions of cells showed approximately a 2-fold increase in microtubule number in 48 h stimulated populations and up to a 5-fold increase in the large, fully stimulated, blast cells. Determinations of tubulin and actin contents were made by the measurement of peptides specific to those proteins. As a percentage of total cell protein both of these cytoskeletal proteins increased during the first 24 h of stimulation. Tubulin increased 50% by 24 h and remained high in populations stimulated for 48 h. The tubulin content per cell increased 2.5-fold, from 0.20 to 0.51 microgram/10(6) cells, in the 48 h stimulated population. An increase in tubulin content was also seen following the stimulation of nude mouse B lymphocyte populations and of total splenic lymphocyte populations. Our results show that during lymphocyte stimulation there is a large increase in the numbers of microtubules assembled which is correlated with, and appears dependent on, a similar large increase in the cellular tubulin content.
- Published
- 1983
- Full Text
- View/download PDF
18. The analgesic and antipyretic properties of some derivatives of salicylamide.
- Author
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BAVIN EM, MACRAE FJ, SEYMOUR DE, and WATERHOUSE PD
- Subjects
- Analgesics, Antipyretics, Salicylamides, Salicylates
- Published
- 1952
- Full Text
- View/download PDF
19. Anti-inflammatory compounds. I. The activity of a series of new compounds compared with phenylbutazone and cortisone.
- Author
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BAVIN EM, DRAIN DJ, SEYMOUR DE, and WATERHOUSE PD
- Subjects
- Analgesics pharmacology, Anti-Inflammatory Agents, Cortisone pharmacology, Inflammation, Phenylbutazone, Sulfhydryl Compounds pharmacology
- Published
- 1955
- Full Text
- View/download PDF
20. Studies in the chemotherapy of cholera. IV. Antagonism of the antibacterial activities of 2:4-diaminopteridines, sulphaguanidine, and their mixtures.
- Author
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COLLIER HO and WATERHOUSE PD
- Subjects
- Humans, Anti-Bacterial Agents, Cholera, Pteridines, Sulfaguanidine
- Published
- 1950
- Full Text
- View/download PDF
21. Studies in the chemotherapy of cholera. II. In vitro vibriostatic properties of certain 2:4-diaminopteridines.
- Author
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COLLIER HO and WATERHOUSE PD
- Subjects
- Humans, In Vitro Techniques, Cholera, Pteridines
- Published
- 1950
- Full Text
- View/download PDF
22. The laboratory evaluation of remedies for cholera.
- Author
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COLLIER HO, HALL IF, and WATERHOUSE PD
- Subjects
- Humans, Cholera, Laboratories
- Published
- 1949
- Full Text
- View/download PDF
23. Studies in the chemotherapy of cholera. III. The action of pteridinesulphonamide mixtures upon Vibrio cholerae and upon the mouse.
- Author
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COLLIER HO, HALL IF, and WATERHOUSE PD
- Subjects
- Animals, Mice, Sulfanilamide, Sulfanilamides, Cholera, Pteridines, Sulfonamides, Vibrio cholerae
- Published
- 1950
- Full Text
- View/download PDF
24. The activities of some 2 : 4-diaminopteridines and sulphathiazole against Streptococcus faecalis and Staphylococcus aureus.
- Author
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COLLIER HO and WATERHOUSE PD
- Subjects
- Folic Acid analogs & derivatives, Humans, Sulfathiazole, Antimetabolites, Enterococcus faecalis, Micrococcus drug effects, Staphylococcal Infections, Staphylococcus aureus, Streptococcus drug effects, Sulfathiazoles pharmacology
- Published
- 1952
- Full Text
- View/download PDF
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