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1. Full Text Systemic peripheral artery relaxation by KCNQ channel openers and hydrogen sulfide
by Schleifenbaum, Johanna and Köhn, Carolin and Voblova, Nadezda and Dubrovska, Galyna and Zavarirskaya, Olga and Gloe, Torsten and Crean, Christopher S and Luft, Friedrich C and Huang, Yu and Schubert, Rudolf and Gollasch, Maik
Journal of Hypertension, ISSN 0263-6352, 09/2010, Volume 28, Issue 9, pp. 1875 - 1882
Background Perivascular adipose tissue secretes an adipocyte-derived relaxing factor (ADRF) that opens voltage-dependent K+ (K-v) channels in peripheral... 
perivascular fat | ADRF | KCNQ channels | obesity hypertension | adipocyte-derived relaxing factor | SPONTANEOUSLY HYPERTENSIVE-RATS | POTASSIUM CHANNELS | ANTICONVULSANT | FLUPIRTINE | SMOOTH-MUSCLE | ACTIVATOR | PROFILE | TONE | VASCULAR FUNCTION | PERIPHERAL VASCULAR DISEASE | PERIVASCULAR ADIPOSE-TISSUE | Hydrogen Sulfide - metabolism | Mesenteric Arteries - physiology | Adipose Tissue - physiology | Isometric Contraction - drug effects | Male | Mesenteric Arteries - drug effects | KCNQ Potassium Channels - antagonists & inhibitors | Paracrine Communication - physiology | Arteries - physiology | Vasodilation - physiology | Isometric Contraction - physiology | Carbamates - pharmacology | Aorta - drug effects | Mice, Inbred C57BL | KCNQ Potassium Channels - agonists | Rats | Arteries - drug effects | Rats, Sprague-Dawley | Anthracenes - pharmacology | Animals | Paracrine Communication - drug effects | Phenylenediamines - pharmacology | KCNQ Potassium Channels - physiology | Mice | Vasodilation - drug effects | In Vitro Techniques | Aorta - physiology
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2. Full Text Human TH9 cells are skin-tropic and have autocrine and paracrine proinflammatory capacity
by Schlapbach, Christoph and Gehad, Ahmed and Yang, Chao and Watanabe, Rei and Guenova, Emmanuella and Teague, Jessica E and Campbell, Laura and Yawalkar, Nikhil and Kupper, Thomas S and Clark, Rachael A
Science Translational Medicine, ISSN 1946-6234, 01/2014, Volume 6, Issue 219, pp. 219ra8 - 219ra8
T helper type 9 (TH9) cells can mediate tumor immunity and participate in autoimmune and allergic inflammation in mice, but little is known about the TH9 cells... 
T-Lymphocytes, Helper-Inducer - microbiology | Inflammation - pathology | Humans | Autocrine Communication - drug effects | Paracrine Communication - immunology | T-Lymphocytes, Helper-Inducer - drug effects | Lymphocyte Activation - immunology | Candida albicans - drug effects | Autocrine Communication - immunology | Psoriasis - pathology | T-Lymphocytes, Helper-Inducer - immunology | Dermatitis, Atopic - immunology | Interleukin-9 - metabolism | Candida albicans - physiology | Skin - pathology | Skin - immunology | Psoriasis - immunology | Dermatitis, Atopic - pathology | Inflammation - immunology | Transforming Growth Factor beta - pharmacology | Animals | Lymphocyte Activation - drug effects | Paracrine Communication - drug effects | Interleukin-2 - pharmacology | Mice | Skin - drug effects
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3. Full Text Composite scaffolds of nano-hydroxyapatite and silk fibroin enhance mesenchymal stem cell-based bone regeneration via the interleukin 1 alpha autocrine/paracrine signaling loop
by Liu, Hua and Xu, Guo Wei and Wang, Ya Fei and Zhao, Hong Shi and Xiong, Si and Wu, Yan and Heng, Boon Chin and An, Cheng Rui and Zhu, Gang Hua and Xie, Ding Hua
Biomaterials, ISSN 0142-9612, 2015, Volume 49, pp. 103 - 112
Abstract Composite scaffolds of nano-hydroxyapatite (nHAp) and silk fibroin (SF) have been reported to promote bone regeneration mainly through signaling... 
Advanced Basic Science | Dentistry | Silk | Hydroxyapatite | Bone regeneration | Stem cell | Interleukin | Osteogenesis | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | PARTICLES | ENGINEERING, BIOMEDICAL | OSTEOGENIC DIFFERENTIATION | ADIPOGENESIS | IN-VITRO | GENE-EXPRESSION | PPAR-GAMMA | FABRICATION | STROMAL CELLS | OSTEOINDUCTIVITY | Receptors, Interleukin-1 Type II - metabolism | Nanoparticles - chemistry | Interleukin-1alpha - metabolism | Male | Autocrine Communication - drug effects | Tissue Scaffolds - chemistry | Mesenchymal Stromal Cells - cytology | Mesenchymal Stromal Cells - ultrastructure | Skull - pathology | Bone Morphogenetic Protein 2 - metabolism | Durapatite - pharmacology | Female | Skull - drug effects | Disease Models, Animal | Bone Regeneration - drug effects | Mesenchymal Stromal Cells - drug effects | Bone Marrow Cells - cytology | Osteogenesis - drug effects | Nanoparticles - ultrastructure | Fibroins - pharmacology | Biocompatible Materials - pharmacology | Rats, Sprague-Dawley | Cell Shape - drug effects | Animals | Signal Transduction - drug effects | Cell Differentiation - drug effects | Paracrine Communication - drug effects | Cluster Analysis | Biological products | Interleukins | Tissue engineering | Analysis | Stem cells | Bone morphogenetic proteins | Gene expression | Surgical implants | Regeneration | Biomedical materials | Biocompatibility | Bones | Nanostructure | Scaffolds | Biomaterials
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4. Full Text Retinoic Acid–Induced Pancreatic Stellate Cell Quiescence Reduces Paracrine Wnt–β-Catenin Signaling to Slow Tumor Progression
by Froeling, Fieke E.M and Feig, Christine and Chelala, Claude and Dobson, Richard and Mein, Charles E and Tuveson, David A and Clevers, Hans and Hart, Ian R and Kocher, Hemant M
Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 4, pp. 1486 - 1497.e14
Background & Aims Patients with pancreatic ductal adenocarcinoma are deficient in vitamin A, resulting in activation of pancreatic stellate cells (PSCs). We... 
Gastroenterology and Hepatology | 9RA | Therapy | Secreted Frizzled-Related Protein 4 | 13RA | Mouse Model | ACTIVATION | CANCER CELLS | TRANSCRIPTOME | ADENOCARCINOMA | STABILIZATION | MODEL | CULTURE | IN-VITRO | GASTROENTEROLOGY & HEPATOLOGY | IMMORTALIZATION | EXPRESSION | Transcription, Genetic - drug effects | Pancreatic Neoplasms - metabolism | Apoptosis - drug effects | Humans | Pancreatic Stellate Cells - drug effects | Carcinoma, Pancreatic Ductal - metabolism | Cellular Senescence - drug effects | Wnt Proteins - metabolism | Carcinoma, Pancreatic Ductal - genetics | Dose-Response Relationship, Drug | Pancreatic Neoplasms - drug therapy | RNA Interference | Time Factors | Mice, Mutant Strains | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Pancreatic Stellate Cells - pathology | Disease Models, Animal | Tretinoin - pharmacology | Proto-Oncogene Proteins - metabolism | Isotretinoin - pharmacology | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - pathology | beta Catenin - metabolism | Disease Progression | Carcinoma, Pancreatic Ductal - drug therapy | Cell Movement - drug effects | Animals | Signal Transduction - drug effects | Paracrine Communication - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Pancreatic Stellate Cells - metabolism
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5. Full Text Fibroblast-derived exosomes contribute to chemoresistance through priming cancer stem cells in colorectal cancer
by Hu, Yibing and Yan, Chang and Mu, Lei and Huang, Kaiyu and Li, Xiaolan and Tao, Deding and Wu, Yaqun and Qin, Jichao
PLoS ONE, ISSN 1932-6203, 05/2015, Volume 10, Issue 5, p. e0125625
Chemotherapy resistance observed in patients with colorectal cancer (CRC) may be related to the presence of cancer stem cells (CSCs), but the underlying... 
POPULATION | MECHANISM | MULTIDISCIPLINARY SCIENCES | ACTIVATION PROTEIN | PHENOTYPE | DRUG-RESISTANCE | BETA-CATENIN | EXCHANGE | TUMOR-GROWTH | EXPRESSION | CHEMOTHERAPY | Exosomes - drug effects | Exosomes - metabolism | Neoplastic Stem Cells - drug effects | Humans | Glycoproteins - metabolism | Culture Media, Conditioned - pharmacology | AC133 Antigen | Antigens, CD - metabolism | Xenograft Model Antitumor Assays | Animals | Peptides - metabolism | Wnt Signaling Pathway - drug effects | Mice, Nude | Fibroblasts - drug effects | Paracrine Communication - drug effects | Cell Line, Tumor | Neoplastic Stem Cells - pathology | Female | Colorectal Neoplasms - pathology | Colorectal Neoplasms - metabolism | Drug Resistance, Neoplasm - drug effects | Exosomes - ultrastructure | Fibroblasts - metabolism | Complications and side effects | Stem cell research | Care and treatment | Chemotherapy | Usage | Colorectal cancer | Research | Health aspects | Cancer | 5-Fluorouracil | Colorectal carcinoma | Chemoresistance | Science | Biology | Metastasis | Exosomes | Drug resistance | Blood | Oxaliplatin | Surgery | Xenografts | Fibroblasts | Bone marrow | Conditioning | Medical research | Secretion | Priming | Patients | Medicine | Hospitals | Cell death | Cell lines | Stem cells | Tumors
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6. Full Text Exosomal miR‐146a Contributes to the Enhanced Therapeutic Efficacy of Interleukin‐1β‐Primed Mesenchymal Stem Cells Against Sepsis
by Song, Yuxian and Dou, Huan and Li, Xiujun and Zhao, Xiaoyin and Li, Yi and Liu, Dan and Ji, Jianjian and Liu, Fei and Ding, Liang and Ni, Yanhong and Hou, Yayi
STEM CELLS, ISSN 1066-5099, 05/2017, Volume 35, Issue 5, pp. 1208 - 1221
Improving the immunomodulatory efficacy of mesenchymal stem cells (MSCs) through pretreatment with pro‐inflammatory cytokines is an evolving field of... 
IL‐1β | Sepsis | Macrophage polarization | miR‐146a | Exosome | Mesenchymal stem cells | miR-146a | IL-1β | Exosomes - metabolism | Immunomodulation - drug effects | Mesenchymal Stromal Cells - drug effects | Interleukin-1beta - pharmacology | Sepsis - prevention & control | Humans | Mice, Inbred C57BL | Mesenchymal Stromal Cells - metabolism | Male | MicroRNAs - metabolism | Treatment Outcome | Macrophages - cytology | Phenotype | Animals | Mesenchymal Stromal Cells - ultrastructure | Paracrine Communication - drug effects | Sepsis - therapy | Macrophages - drug effects | Cell Polarity - drug effects | Macrophage Activation - drug effects | Mesenchymal Stem Cell Transplantation | Disease Models, Animal | Exosomes - ultrastructure
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7. Full Text Carcinoma-astrocyte gap junctions promote brain metastasis by cGAMP transfer
by Chen, Qing and Boire, Adrienne and Jin, Xin and Valiente, Manuel and Er, Ekrem Emrah and Lopez-Soto, Alejandro and Jacob, Leni S and Patwa, Ruzeen and Shah, Hardik and Xu, Ke and Cross, Justin R and Massague, Joan
Nature, ISSN 0028-0836, 05/2016, Volume 533, Issue 7604, pp. 493 - 498
Brain metastasis represents a substantial source of morbidity and mortality in various cancers, and is characterized by high resistance to chemotherapy. Here... 
SURVIVAL | CADHERIN SUPERFAMILY | EXPRESSION ANALYSIS | CONNEXIN | RECOGNITION | PATHWAY | BREAST-CANCER METASTASIS | MULTIDISCIPLINARY SCIENCES | GENES | CLASSIFICATION | TUMOR-CELLS | Meclofenamic Acid - pharmacology | Meclofenamic Acid - therapeutic use | Nucleotides, Cyclic - metabolism | Gap Junctions - metabolism | Benzopyrans - therapeutic use | Cadherins - metabolism | Coculture Techniques | Humans | Brain Neoplasms - pathology | Drug Resistance, Neoplasm | Lung Neoplasms - pathology | NF-kappa B - metabolism | Brain Neoplasms - metabolism | Brain Neoplasms - secondary | STAT1 Transcription Factor - metabolism | Benzamides - therapeutic use | Female | Benzamides - pharmacology | Membrane Proteins - metabolism | Benzopyrans - pharmacology | Astrocytes - cytology | Astrocytes - drug effects | Interferon-alpha - metabolism | Connexin 43 - metabolism | Tumor Necrosis Factors - metabolism | Brain Neoplasms - drug therapy | Immunity, Innate | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - pathology | Paracrine Communication - drug effects | Cell Line, Tumor | Mice | Gap Junctions - drug effects | Astrocytes - metabolism | Astrocytes | Brain cancer | Physiological aspects | Metastasis | Observations | Adenylic acid | Health aspects | Proteins | Brain | Cytokines | Cells | Tumors | Cancer
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8. Full Text Inhibition of CXCL12/CXCR4 autocrine/paracrine loop reduces viability of human glioblastoma stem-like cells affecting self-renewal activity
by Gatti, Monica and Pattarozzi, Alessandra and Bajetto, Adriana and Würth, Roberto and Daga, Antonio and Fiaschi, Pietro and Zona, Gianluigi and Florio, Tullio and Barbieri, Federica
Toxicology, ISSN 0300-483X, 2013, Volume 314, Issue 2, pp. 209 - 220
Abstract Cancer stem cells (CSCs) or tumor initiating cells (TICs) drive glioblastoma (GBM) development, invasiveness and drug resistance. Distinct molecular... 
Emergency | CXCR4 | CXCL12 | Cancer stem cells | Intracellular signaling | Glioblastoma | SURVIVAL | CHEMOKINE RECEPTOR CXCR4 | PROLIFERATION | CANCER | TUMOR-INITIATING CELLS | BRAIN-TUMORS | IN-VITRO | GENE-EXPRESSION | HUMAN GLIOMAS | PHARMACOLOGY & PHARMACY | TOXICOLOGY | GROWTH-FACTOR | Cell Survival - drug effects | Neoplastic Stem Cells - drug effects | Receptors, CXCR4 - antagonists & inhibitors | Autocrine Communication - physiology | Humans | Heterocyclic Compounds - pharmacology | Autocrine Communication - drug effects | Down-Regulation - drug effects | Mice, SCID | Chemokine CXCL12 - antagonists & inhibitors | Down-Regulation - physiology | Paracrine Communication - physiology | Animals | Neoplastic Stem Cells - metabolism | Receptors, CXCR4 - biosynthesis | Glioblastoma - pathology | Paracrine Communication - drug effects | Cell Line, Tumor | Chemokine CXCL12 - biosynthesis | Glioblastoma - metabolism | Cell Proliferation - drug effects | Glioblastoma - drug therapy | Cell Survival - physiology | Drug resistance | Glioblastoma multiforme | Stem cells | Index Medicus
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9. Full Text Retinoic acid induces Sertoli cell paracrine signals for spermatogonia differentiation but cell autonomously drives spermatocyte meiosis
by Mathilde Raverdeau and Aurore Gely-Pernot and Betty Féret and Christine Dennefeld and Gérard Benoit and Irwin Davidson and Pierre Chambon and Manuel Mark and Norbert B. Ghyselinck
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2012, Volume 109, Issue 41, pp. 16582 - 16587
Direct evidence for a role of endogenous retinoic acid (RA), the active metabolite of vitamin A in the initial differentiation and meiotic entry of... 
Germ cells | Spermatocytes | Spermatogenesis | Spermatogonia | Stem cells | Meiosis | Testes | Seminiferous tubules | Cellular differentiation | Sertoli cells | Mouse | Mutagenesis | RAR/RXR heterodimer | Retinoid antagonist | MOUSE TESTIS | SPERMATOGENESIS | retinoid antagonist | UNDIFFERENTIATED SPERMATOGONIA | MULTIDISCIPLINARY SCIENCES | mutagenesis | VITAMIN-A | mouse | GENE | GERM-CELLS | SEX DETERMINATION | EXPRESSION PATTERN | TRANSGENIC MICE | KIT EXPRESSION | Immunohistochemistry | Spermatocytes - metabolism | Gene Expression - drug effects | Retinal Dehydrogenase - metabolism | Male | Mice, 129 Strain | Receptors, Retinoic Acid - genetics | Sertoli Cells - drug effects | Spermatogonia - metabolism | Cell Differentiation - genetics | Meiosis - drug effects | In Situ Hybridization | Spermatocytes - drug effects | Tretinoin - metabolism | Female | Spermatogonia - cytology | Aldehyde Dehydrogenase - metabolism | Tretinoin - pharmacology | Sertoli Cells - metabolism | Spermatogonia - drug effects | Mice, Inbred C57BL | Paracrine Communication - genetics | Aldehyde Dehydrogenase - genetics | Mice, Transgenic | Receptors, Retinoic Acid - metabolism | Retinal Dehydrogenase - genetics | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Meiosis - genetics | Animals | Cell Differentiation - drug effects | Paracrine Communication - drug effects | Mice | Physiological aspects | Research | Cell differentiation | Health aspects | Tretinoin | Life Sciences | Biochemistry, Molecular Biology | Biological Sciences | RAR | RXR heterodimer
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10. Full Text Progesterone induces adult mammary stem cell expansion
by Joshi, Purna A and Jackson, Hartland W and Beristain, Alexander G and Di Grappa, Marco A and Mote, Patricia A and Clarke, Christine L and Stingl, John and Waterhouse, Paul D and Khokha, Rama
Nature, ISSN 0028-0836, 06/2010, Volume 465, Issue 7299, pp. 803 - 807
Reproductive history is the strongest risk factor for breast cancer after age, genetics and breast density(1,2). Increased breast cancer risk is entwined with... 
BREAST-CANCER | MORPHOGENESIS | EPITHELIAL-CELLS | MULTIDISCIPLINARY SCIENCES | RISK | PROLIFERATION | DIFFERENTIATION | RECEPTOR-B | GLAND DEVELOPMENT | 17-BETA-ESTRADIOL | ESTROUS-CYCLE | Receptors, Estrogen - metabolism | Estrogens - pharmacology | RANK Ligand - metabolism | Estrous Cycle - physiology | Cell Count | Progesterone - blood | Stem Cells - cytology | Stem Cells - metabolism | Wnt Proteins - metabolism | Receptors, Progesterone - metabolism | Female | Homeostasis - drug effects | Progesterone - pharmacology | Ovariectomy | Stem Cell Niche - cytology | Cell Division - drug effects | Mammary Glands, Animal - cytology | Integrin alpha6 - metabolism | Animals | Aging - physiology | Cell Transformation, Neoplastic | Paracrine Communication - drug effects | Progesterone - metabolism | Stem Cell Niche - metabolism | Stem Cells - drug effects | Mice | Stem Cell Niche - drug effects | Estrous Cycle - blood | Wnt4 Protein | Stem cells | Physiological aspects | Breast cancer | Genetic aspects | Research | Progesterone | Health aspects | Risk factors | Cell division | Rodents | Cell cycle
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11. Full Text CD73-generated extracellular adenosine in chronic lymphocytic leukemia creates local conditions counteracting drug-induced cell death
by Serra, Sara and Horenstein, Alberto L and Vaisitti, Tiziana and Brusa, Davide and Rossi, Davide and Laurenti, Luca and D'Arena, Giovanni and Coscia, Marta and Tripodo, Claudio and Inghirami, Giorgio and Robson, Simon C and Gaidano, Gianluca and Malavasi, Fabio and Deaglio, Silvia
Blood, ISSN 0006-4971, 12/2011, Volume 118, Issue 23, pp. 6141 - 6152
Extracellular adenosine (ADO), generated from ATP or ADP through the concerted action of the ectoenzymes CD39 and CD73, elicits autocrine and paracrine effects... 
CD73 | ACTIVATION | MICROENVIRONMENT | IMMUNE SUPPRESSION | RECEPTOR | CD38 | ZAP-70 EXPRESSION | HEMATOLOGY | TUMOR-GROWTH | T-CELLS | DAMAGE-INDUCED APOPTOSIS | Humans | Autocrine Communication - drug effects | Cell Movement - physiology | Antigens, CD - metabolism | Paracrine Communication - physiology | Extracellular Space - metabolism | Adenosine Triphosphate - metabolism | Cell Death - drug effects | Tumor Cells, Cultured | Cell Differentiation - physiology | Cell Survival - physiology | Cell Survival - drug effects | Autocrine Communication - physiology | Apyrase - metabolism | Etoposide - pharmacology | Receptor, Adenosine A2A - metabolism | GPI-Linked Proteins - metabolism | Leukemia, Lymphocytic, Chronic, B-Cell - pathology | Cell Movement - drug effects | Cell Death - physiology | Cell Differentiation - drug effects | Leukemia, Lymphocytic, Chronic, B-Cell - metabolism | Paracrine Communication - drug effects | Adenosine - metabolism | Adenosine Diphosphate - metabolism | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | 5'-Nucleotidase - metabolism | Antineoplastic Agents, Phytogenic - pharmacology | Lymphoid Neoplasia | Immunobiology
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12. Full Text Lactate is a mediator of metabolic cooperation between stromal carcinoma associated fibroblasts and glycolytic tumor cells in the tumor microenvironment
by Rattigan, Yanique I and Patel, Brijesh B and Ackerstaff, Ellen and Sukenick, George and Koutcher, Jason A and Glod, John W and Banerjee, Debabrata
Experimental Cell Research, ISSN 0014-4827, 2012, Volume 318, Issue 4, pp. 326 - 335
Human mesenchymal stem cells (hMSCs) are bone marrow-derived stromal cells, which play a role in tumor progression. We have shown earlier that breast cancer... 
Lactate metabolism | Glycolytic tumor cells | Stromal carcinoma-associated fibroblasts (CAFs) | CANCER-CELLS | LACTIC-ACID | MONOCARBOXYLATE TRANSPORTERS | ACTIVATION | TRANSCRIPTION | HYALURONAN | OXIDATIVE-METABOLISM | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | LUNG-CANCER | ONCOLOGY | EXPRESSION | Fibroblasts - physiology | Stromal Cells - pathology | Humans | Cell Communication - physiology | Tumor Microenvironment - physiology | Glycolysis - drug effects | Breast Neoplasms - metabolism | Hypoxia - metabolism | Glycolysis - physiology | Paracrine Communication - physiology | Stromal Cells - drug effects | Female | Carcinoma - pathology | Lactic Acid - pharmacology | Fibroblasts - metabolism | Tumor Microenvironment - drug effects | Stromal Cells - metabolism | Mesenchymal Stromal Cells - metabolism | Fibroblasts - pathology | Breast Neoplasms - pathology | Hypoxia - pathology | Fibroblasts - drug effects | Paracrine Communication - drug effects | Cell Communication - drug effects | Cell Line, Tumor | Carcinoma - metabolism | Mesenchymal Stromal Cells - pathology | Metabolic Networks and Pathways - drug effects | Lactates | Carcinoma | RNA | Analysis | Stem cells | Development and progression | Cancer | Cellular biology | Metabolism | Tumors | CARBON 13 | MAMMARY GLANDS | NUCLEAR MAGNETIC RESONANCE | LACTATES | BONE MARROW | TUMOR CELLS | 60 APPLIED LIFE SCIENCES | FIBROBLASTS | MESSENGER-RNA | METABOLISM | ANOXIA | IN VITRO | CARCINOMAS | STEM CELLS | PROTEINS | Stromal carcinoma-associated | fibroblasts (CAFs)
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