Academic literature on the topic 'Hypoxická translace'
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Journal articles on the topic "Hypoxická translace"
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Blais, Jaime D., Vasilisa Filipenko, Meixia Bi, Heather P. Harding, David Ron, Costas Koumenis, Bradly G. Wouters, and John C. Bell. "Activating Transcription Factor 4 Is Translationally Regulated by Hypoxic Stress." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7469–82. http://dx.doi.org/10.1128/mcb.24.17.7469-7482.2004.
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ABSTRACT Hypoxic stress results in a rapid and sustained inhibition of protein synthesis that is at least partially mediated by eukaryotic initiation factor 2α (eIF2α) phosphorylation by the endoplasmic reticulum (ER) kinase PERK. Here we show through microarray analysis of polysome-bound RNA in aerobic and hypoxic HeLa cells that a subset of transcripts are preferentially translated during hypoxia, including activating transcription factor 4 (ATF4), an important mediator of the unfolded protein response. Changes in mRNA translation during the unfolded protein response are mediated by PERK phosphorylation of the translation initiation factor eIF2α at Ser-51. Similarly, PERK is activated and is responsible for translational regulation under hypoxic conditions, while inducing the translation of ATF4. The overexpression of a C-terminal fragment of GADD34 that constitutively dephosphorylates eIF2α was able to attenuate the phosphorylation of eIF2α and severely inhibit the induction of ATF4 in response to hypoxic stress. These studies demonstrate the essential role of ATF4 in the response to hypoxic stress, define the pathway for its induction, and reveal that GADD34, a target of ATF4 activation, negatively regulates the eIF2α-mediated inhibition of translation. Taken with the concomitant induction of additional ER-resident proteins identified by our microarray analysis, this study suggests an important integrated response between ER signaling and the cellular adaptation to hypoxic stress.
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Sotiridis, Alexandros, Tadej Debevec, Adam C. McDonnell, Urša Ciuha, Ola Eiken, and Igor B. Mekjavic. "Exercise cardiorespiratory and thermoregulatory responses in normoxic, hypoxic, and hot environment following 10-day continuous hypoxic exposure." Journal of Applied Physiology 125, no. 4 (October 1, 2018): 1284–95. http://dx.doi.org/10.1152/japplphysiol.01114.2017.
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We examined the effects of acclimatization to normobaric hypoxia on aerobic performance and exercise thermoregulatory responses under normoxic, hypoxic, and hot conditions. Twelve men performed tests of maximal oxygen uptake (V̇O2max) in normoxic (NOR), hypoxic [HYP; 13.5% fraction of inspired oxygen (FiO2)], and hot (HE; 35°C, 50% relative humidity) conditions in a randomized manner before and after a 10-day continuous normobaric hypoxic exposure [FiO2 = 13.65 (0.35)%, inspired partial pressure of oxygen = 87 (3) mmHg]. The acclimatization protocol included daily exercise [60 min at 50% hypoxia-specific peak power output (Wpeak)]. All maximal tests were preceded by a steady-state exercise (30 min at 40% Wpeak) to assess the sweating response. Hematological data were assessed from venous blood samples obtained before and after acclimatization. V̇o2max increased by 10.7% ( P = 0.002) and 7.9% ( P = 0.03) from pre-acclimatization to post acclimatization in NOR and HE, respectively, whereas no differences were found in HYP [pre: 39.9 (3.8) vs. post: 39.4 (5.1) ml·kg−1·min−1, P = 1.0]. However, the increase in V̇O2max did not translate into increased Wpeak in either NOR or HE. Maximal heart rate and ventilation remained unchanged following acclimatization. Νo differences were noted in the sweating gain and thresholds independent of the acclimatization or environmental conditions. Hypoxic acclimatization markedly increased hemoglobin ( P < 0.001), hematocrit ( P < 0.001), and extracellular HSP72 ( P = 0.01). These data suggest that 10 days of normobaric hypoxic acclimatization combined with moderate-intensity exercise training improves V̇o2max in NOR and HE, but does not seem to affect exercise performance or thermoregulatory responses in any of the tested environmental conditions. NEW & NOTEWORTHY The potential crossover effect of hypoxic acclimatization on performance in the heat remains unexplored. Here we show that 10-day continuous hypoxic acclimatization combined with moderate-intensity exercise training can increase maximal oxygen uptake in hot conditions.
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Blais, Jaime D., Christina L. Addison, Robert Edge, Theresa Falls, Huijun Zhao, Kishore Wary, Costas Koumenis, et al. "Perk-Dependent Translational Regulation Promotes Tumor Cell Adaptation and Angiogenesis in Response to Hypoxic Stress." Molecular and Cellular Biology 26, no. 24 (October 9, 2006): 9517–32. http://dx.doi.org/10.1128/mcb.01145-06.
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ABSTRACT It has been well established that the tumor microenvironment can promote tumor cell adaptation and survival. However, the mechanisms that influence malignant progression have not been clearly elucidated. We have previously demonstrated that cells cultured under hypoxic/anoxic conditions and transformed cells in hypoxic areas of tumors activate a translational control program known as the integrated stress response (ISR). Here, we show that tumors derived from K-Ras-transformed Perk−/− mouse embryonic fibroblasts (MEFs) are smaller and exhibit less angiogenesis than tumors with an intact ISR. Furthermore, Perk promotes a tumor microenvironment that favors the formation of functional microvessels. These observations were corroborated by a microarray analysis of polysome-bound RNA in aerobic and hypoxic Perk+/+ and Perk−/− MEFs. This analysis revealed that a subset of proangiogenic transcripts is preferentially translated in a Perk-dependent manner; these transcripts include VCIP, an adhesion molecule that promotes cellular adhesion, integrin binding, and capillary morphogenesis. Taken with the concomitant Perk-dependent translational induction of additional proangiogenic genes identified by our microarray analysis, this study suggests that Perk plays a role in tumor cell adaptation to hypoxic stress by regulating the translation of angiogenic factors necessary for the development of functional microvessels and further supports the contention that the Perk pathway could be an attractive target for novel antitumor modalities.
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Harper, Kelly, Anna Yatsyna, Martine Charbonneau, Karine Brochu-Gaudreau, Alexis Perreault, Claudio Jeldres, Patrick P. McDonald, and Claire M. Dubois. "The Chicken Chorioallantoic Membrane Tumor Assay as a Relevant In Vivo Model to Study the Impact of Hypoxia on Tumor Progression and Metastasis." Cancers 13, no. 5 (March 4, 2021): 1093. http://dx.doi.org/10.3390/cancers13051093.
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Hypoxia in the tumor microenvironment is a negative prognostic factor associated with tumor progression and metastasis, and therefore represents an attractive therapeutic target for anti-tumor therapy. To test the effectiveness of novel hypoxia-targeting drugs, appropriate preclinical models that recreate tumor hypoxia are essential. The chicken ChorioAllantoic Membrane (CAM) assay is increasingly used as a rapid cost-effective in vivo drug-testing platform that recapitulates many aspects of human cancers. However, it remains to be determined whether this model recreates the hypoxic microenvironment of solid tumors. To detect hypoxia in the CAM model, the hypoxic marker pimonidazole was injected into the vasculature of tumor-bearing CAM, and hypoxia-dependent gene expression was analyzed. We observed that the CAM model effectively supports the development of hypoxic zones in a variety of human tumor cell line-derived and patient’s tumor fragment-derived xenografts. The treatment of both patient and cell line-derived CAM xenografts with modulators of angiogenesis significantly altered the formation of hypoxic zones within the xenografts. Furthermore, the changes in hypoxia translated into modulated levels of chick liver metastasis as measured by Alu-based assay. These findings demonstrate that the CAM xenograft model is a valuable in vivo platform for studying hypoxia that could facilitate the identification and testing of drugs targeting this tumor microenvironment.
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Patil, Deepak. "Does culture condition of reduced oxygen pressure helps in embryo quality? A prospective randomized study." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 10, no. 6 (May 27, 2021): 2239. http://dx.doi.org/10.18203/2320-1770.ijrcog20212154.
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Background: Embryo quality is of paramount importance in an in vitro fertilization and embryo transfer (IVF-ET) cycle. A healthy embryo leads to a robust pregnancy. Incubation in an ideal atmosphere is essential requirement in an IVF-ET cycle.Methods: Traditionally carbon dioxide incubator with sensors for carbon dioxide levels and temperature has been used widely. We compared the quality of these embryos to incubation in hypoxic condition by addition of nitrogen. Oxygen levels were brought to 5% as compared to 21% in room air.Results: Ladies with high body mass index (BMI) and advanced age had more embryos available for transfer. More embryos reached day 3 and day 5, thus increasing availability for cryopreservation. The fragmentation rate and fertilization failure were less. Pregnancy rate was definitely improved as compared to traditional incubation.Conclusions: Hypoxic incubation condition leads to better embryo health. This translates into improved and efficient cycle outcome.
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Joyner-Matos, J., H. Richardson, T. Sammeli, and L. J. Chapman. "A fingernail clam (Sphaerium sp.) shows higher reproductive success in hypoxic waters." Canadian Journal of Zoology 89, no. 3 (March 2011): 161–68. http://dx.doi.org/10.1139/z10-106.
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Low dissolved O2, or hypoxia, is becoming increasingly prevalent in aquatic habitats and is considered to be stressful for aerobic organisms. However, hypoxia also can be beneficial by decreasing cellular stress, particularly that related to free radicals. Therefore, an animal’s ideal habitat may have the minimum O2 necessary to sustain aerobic metabolism, with excess O2 increasing the need to scavenge free radicals and repair free radical damage. Here we show that a natural population of small (<9 mm shell length) freshwater clams (genus Sphaerium Scopoli, 1777) lives along a dissolved O2 gradient from extreme hypoxia to moderate hypoxia. We tested the hypothesis that clams living in extreme hypoxia would have higher reproductive success than clams that live in moderate hypoxia. Clam abundance was highest in water with very low dissolved O2, conditions previously demonstrated to decrease cellular stress. The internally brooding clams reproduced year-round and had higher reproductive output in extreme hypoxia than in moderate hypoxia. The findings demonstrate that the apparent cellular-level benefits of hypoxia may translate into increased fitness, especially for small organisms.
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Burtscher, Johannes, Vittorio Maglione, Alba Di Pardo, Grégoire P. Millet, Christoph Schwarzer, and Luca Zangrandi. "A Rationale for Hypoxic and Chemical Conditioning in Huntington’s Disease." International Journal of Molecular Sciences 22, no. 2 (January 8, 2021): 582. http://dx.doi.org/10.3390/ijms22020582.
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Neurodegenerative diseases are characterized by adverse cellular environments and pathological alterations causing neurodegeneration in distinct brain regions. This development is triggered or facilitated by conditions such as hypoxia, ischemia or inflammation and is associated with disruptions of fundamental cellular functions, including metabolic and ion homeostasis. Targeting intracellular downstream consequences to specifically reverse these pathological changes proved difficult to translate to clinical settings. Here, we discuss the potential of more holistic approaches with the purpose to re-establish a healthy cellular environment and to promote cellular resilience. We review the involvement of important molecular pathways (e.g., the sphingosine, δ-opioid receptor or N-Methyl-D-aspartate (NMDA) receptor pathways) in neuroprotective hypoxic conditioning effects and how these pathways can be targeted for chemical conditioning. Despite the present scarcity of knowledge on the efficacy of such approaches in neurodegeneration, the specific characteristics of Huntington’s disease may make it particularly amenable for such conditioning techniques. Not only do classical features of neurodegenerative diseases like mitochondrial dysfunction, oxidative stress and inflammation support this assumption, but also specific Huntington’s disease characteristics: a relatively young age of neurodegeneration, molecular overlap of related pathologies with hypoxic adaptations and sensitivity to brain hypoxia. The aim of this review is to discuss several molecular pathways in relation to hypoxic adaptations that have potential as drug targets in neurodegenerative diseases. We will extract the relevance for Huntington’s disease from this knowledge base.
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Burtscher, Johannes, Vittorio Maglione, Alba Di Pardo, Grégoire P. Millet, Christoph Schwarzer, and Luca Zangrandi. "A Rationale for Hypoxic and Chemical Conditioning in Huntington’s Disease." International Journal of Molecular Sciences 22, no. 2 (January 8, 2021): 582. http://dx.doi.org/10.3390/ijms22020582.
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Neurodegenerative diseases are characterized by adverse cellular environments and pathological alterations causing neurodegeneration in distinct brain regions. This development is triggered or facilitated by conditions such as hypoxia, ischemia or inflammation and is associated with disruptions of fundamental cellular functions, including metabolic and ion homeostasis. Targeting intracellular downstream consequences to specifically reverse these pathological changes proved difficult to translate to clinical settings. Here, we discuss the potential of more holistic approaches with the purpose to re-establish a healthy cellular environment and to promote cellular resilience. We review the involvement of important molecular pathways (e.g., the sphingosine, δ-opioid receptor or N-Methyl-D-aspartate (NMDA) receptor pathways) in neuroprotective hypoxic conditioning effects and how these pathways can be targeted for chemical conditioning. Despite the present scarcity of knowledge on the efficacy of such approaches in neurodegeneration, the specific characteristics of Huntington’s disease may make it particularly amenable for such conditioning techniques. Not only do classical features of neurodegenerative diseases like mitochondrial dysfunction, oxidative stress and inflammation support this assumption, but also specific Huntington’s disease characteristics: a relatively young age of neurodegeneration, molecular overlap of related pathologies with hypoxic adaptations and sensitivity to brain hypoxia. The aim of this review is to discuss several molecular pathways in relation to hypoxic adaptations that have potential as drug targets in neurodegenerative diseases. We will extract the relevance for Huntington’s disease from this knowledge base.
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Sheehan, Jason, Christopher P. Cifarelli, Kasandra Dassoulas, Claire Olson, Jessica Rainey, and Shaojie Han. "Trans-sodium crocetinate enhancing survival and glioma response on magnetic resonance imaging to radiation and temozolomide." Journal of Neurosurgery 113, no. 2 (August 2010): 234–39. http://dx.doi.org/10.3171/2009.11.jns091314.
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Object Glioblastoma (GB) tumors typically exhibit regions of hypoxia. Hypoxic areas within the tumor can make tumor cells less sensitive to chemotherapy and radiation therapy. Trans-sodium crocetinate (TSC) has been shown to transiently increase oxygen to hypoxic brain tumors. The authors examined whether this improvement in intratumor oxygenation translates to a therapeutic advantage when delivering standard adjuvant treatment to GBs. Methods The authors used C6 glioma cells to create a hypoxic GB model. The C6 glioma cells were stereotactically injected into the rat brain to create a tumor. Fifteen days later, MR imaging was used to confirm the presence of a glioma. The animals were randomly assigned to 1 of 3 groups: 1) temozolomide alone (350 mg/m2/day for 5 days); 2) temozolomide and radiation therapy (8 Gy); or 3) TSC (100 μg/kg for 5 days), temozolomide, and radiation therapy. Animals were followed through survival studies, and tumor response was assessed on serial MR images obtained at 15-day intervals during a 2-month period. Results Mean survival (± SEM) of the temozolomide-alone and the temozolomide/radiotherapy groups was 23.2 ± 0.9 and 29.4 ± 4.4 days, respectively. Mean survival in the TSC/temozolomide/radiotherapy group was 39.8 ± 6 days, a statistically significant improvement compared with either of the other groups (p < 0.05). Although tumor size was statistically equivalent in all groups at the time of treatment initiation, the addition of TSC to temozolomide and radiotherapy resulted in a statistically significant reduction in the MR imaging–documented mean tumor size at 30 days after tumor implantation. The mean tumor size in the TSC/temozolomide/radiotherapy group was 18.9 ± 6.6 mm2 compared with 42.1 ± 2.7 mm2 in the temozolomide-alone group (p = 0.047) and 35.8 ± 5.1 mm2 in the temozolomide/radiation group (p = 0.004). Conclusions In a hypoxic GB model, TSC improves the radiological and clinical effectiveness of temozolomide and radiation therapy. Further investigation of this oxygen diffusion enhancer as a radiosensitizer for hypoxic brain tumors seems warranted.
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Yu, Jicheng, Yuqi Zhang, Yanqi Ye, Rocco DiSanto, Wujin Sun, Davis Ranson, Frances S. Ligler, John B. Buse, and Zhen Gu. "Microneedle-array patches loaded with hypoxia-sensitive vesicles provide fast glucose-responsive insulin delivery." Proceedings of the National Academy of Sciences 112, no. 27 (June 22, 2015): 8260–65. http://dx.doi.org/10.1073/pnas.1505405112.
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A glucose-responsive “closed-loop” insulin delivery system mimicking the function of pancreatic cells has tremendous potential to improve quality of life and health in diabetics. Here, we report a novel glucose-responsive insulin delivery device using a painless microneedle-array patch (“smart insulin patch”) containing glucose-responsive vesicles (GRVs; with an average diameter of 118 nm), which are loaded with insulin and glucose oxidase (GOx) enzyme. The GRVs are self-assembled from hypoxia-sensitive hyaluronic acid (HS-HA) conjugated with 2-nitroimidazole (NI), a hydrophobic component that can be converted to hydrophilic 2-aminoimidazoles through bioreduction under hypoxic conditions. The local hypoxic microenvironment caused by the enzymatic oxidation of glucose in the hyperglycemic state promotes the reduction of HS-HA, which rapidly triggers the dissociation of vesicles and subsequent release of insulin. The smart insulin patch effectively regulated the blood glucose in a mouse model of chemically induced type 1 diabetes. The described work is the first demonstration, to our knowledge, of a synthetic glucose-responsive device using a hypoxia trigger for regulation of insulin release. The faster responsiveness of this approach holds promise in avoiding hyperglycemia and hypoglycemia if translated for human therapy.
Dissertations / Theses on the topic "Hypoxická translace"
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Lettrich, Patrik. "Translační iniciační faktory proteinové rodiny 4E a jejich vliv na regulaci genové exprese." Master's thesis, 2021. http://www.nusl.cz/ntk/nusl-446448.
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The translation represents one of the most crucial processes in the cell. That is why it is often targeted by various regulations. Its initiation phase has a particularly important role in regulatory processes. Initiation of translation usually starts by recognition and binding of canonical eukaryotic initiation factor 4E1 (eIF4E1) to the methylguanosine cap present on the 5' end of the majority of eukaryotic mRNA. The family of 4E translation initiation factors contains two more members - eIF4E2 and eIF4E3. Those two proteins can bind cap structure as well which predetermines it to function in the regulation of translation. Protein eIF4E2 is well known for being a translational repressor in development processes and it takes part in specific miRNA-dependent silencing. It was proven to be able to initiate translation in hypoxia which is consistent with its proposed role in hypoxic tumor cells. The biological roles of the protein eIF4E3 are much less understood. This thesis propounds the picture of the overall functions of all discussed translation initiation factors using cell lines with their overexpression or deletion. Experimental data confirmed the role of the eIF4E2 in the regulation of developmental processes. Cell lines with deleted eIF4E2 and eIF4E3 were characterized based on the influence...
Book chapters on the topic "Hypoxická translace"
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Storz, Jay F. "Biochemical adaptation to environmental hypoxia." In Hemoglobin, 176–200. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198810681.003.0008.
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Chapter 8 explores mechanisms of hemoglobin adaptation to environmental hypoxia. Vertebrates living in hypoxic environments face the physiological challenge of optimizing the trade-off between oxygen loading at the respiratory surfaces and oxygen unloading in the tissue capillaries. In air-breathing and water-breathing vertebrates alike, fine-tuned adjustments in hemoglobin-oxygen affinity provide an energetically efficient means of compensating for a reduced oxygen tension of arterial blood. The adaptive significance of such changes is indicated by evolved changes in hemoglobin function in high-altitude mammals and birds, and erythrocytic acclimatization responses to environmental hypoxia in teleost fishes. An important goal for future research is to elucidate the specific physiological mechanisms by which changes in the oxygenation properties of hemoglobin translate into enhancements of whole-animal aerobic performance.
Conference papers on the topic "Hypoxická translace"
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Sakaruassen, K. S., J. S. Powell, E. W. Raines, and R. Ross. "SELECTIVE EXPRESSION OF PLATELET-DERIVED GROWTH FACTOR B-CHAIN mRNA BY HUMAN ENDOTHELIAL CELLS AND BY HUMAN PERIPHERAL BLOOD MONOCYTES, BUT NOT BY HUMAN SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643752.
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Vascular injury may occur by a variety of mechanisms. Episodes of local hypoxia or conditions leading to local generation of thrombin may influence local cells to release growthregulatory molecules such as platelet-derivedgrowth factor (PDGF) in the surrounding connective tissue. The roles of the cells and of PDGF in these processes are not entirely understood, and this prompted us to investigate effects of hypoxia (5% O2) on cultured human saphenous vein endothelial cells andhuman thoracic aorta smooth muscle cells. Freshly isolated human peripheral blood monocytes were exposed to 3.0 U/ml a-thrombin. PDGF-A and PDGF-B mRNAs were analyzed by Northern blots, and their levels were assessed by dot blots utilizing 32P nick-translated cDNA probes. Selective expressionof PDGF-B mRNA occurred in endothelial cells during hypoxia and in monocytes exposed to thrombin. Genes coding for PDGF-A and PDGF-B are expressed cons tit utively, in endothelium, and after 48 hr of hypoxia a nine-fold increase of PDGF-B mRNA is detected (9 pg mRNA/ug total RNA). No detectable levels of mRNA encoding PDGF-A and PDGF-B were observed in freshly isolated monocytes; however, a 4-hr exposure to a-thrombin resulted in a selective and transitory increase in PDGF-B mRNA, amountingto 1 pg mRNA/ug toted RNA. No PDGF-B mRNA wasdetected after 20 hr. Hypoxic conditions did not trigger any selective expression of PDGF-B mRNA in smooth muscle, including arterialsmooth muscle derived from 1-day- and 3-month-old individuals, or from adult venous smoot muscle. However, constitutive expression of PDGF-A mRNA was observed in each of these, amounting to 0.4 pg mRNA/ug total RNA in the 1-day- and 3-month-old cells, and 0.2 pg mRNA/ugtotal RNA in the venous smooth muscle. Our datashow that endothelium and monocytes selectively express PDGF-B mRNA in vitro in response to conditions mimicking those encountered during vascular injury in some in-vivo situation.The data imply that both endothelial cells and monocyte/macrophages may be sources for mitogens that induce intimal hyperplasia and eventually plaque formation.