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Journal articles on the topic 'Cel Hypoxia'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 July 2025

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1

Guo, Zihan, Yunlan Ding, Mengmeng Wang, Qing Zhai, Jiyong Liu, and Qiong Du. "Comparing the Differences in Adverse Events among Chimeric Antigen Receptor T-Cell Therapies: A Real-World Pharmacovigilance Study." Pharmaceuticals 17, no. 8 (2024): 1025. http://dx.doi.org/10.3390/ph17081025.

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In this study, we compared the similarities and differences in adverse events (AEs) among CAR T-cell products through signal mining via the FDA Adverse Event Reporting System (FAERS) and identified unknown AEs to provide a reference for safe clinical medication. Data from the FAERS database spanning from the fourth quarter of 2017 to the first quarter of 2024 were extracted. Signals were identified using the reporting odds ratio (ROR) method and the Medicines and Healthcare Products Regulatory Agency (MHRA) method. A total of 11,386 AE reports related to six CAR T-cell products were selected.

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Locke, Frederick L., Justin Chou, Saran Vardhanabhuti, et al. "Association of pretreatment (preTx) tumor characteristics and clinical outcomes following second-line (2L) axicabtagene ciloleucel (axi-cel) versus standard of care (SOC) in patients (pts) with relapsed/refractory (R/R) large B-cell lymphoma (LBCL)." Journal of Clinical Oncology 40, no. 16_suppl (2022): 7565. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.7565.

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7565 Background: The Phase 3 randomized ZUMA-7 trial in 2L R/R LBCL showed axi-cel superiority to SOC (salvage chemotherapy and HDT-ASCT) in event-free survival (EFS; hazard ratio [HR], 0.398; P<.0001; Locke et al. N Eng J Med. 2021). We report results of exploratory analyses of tumor characteristics, including preTx tumor burden (TB), tissue hypoxia-related lactate dehydrogenase (LDH) level, and tumor microenvironment (TME). Methods: TB was calculated as the sum of product diameters of ≤6 reference lesions (Locke et al. Blood Adv. 2020). Serum LDH was assessed. PreTx tumor samples were ass

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Locke, Frederick L., Justin Chou, Saran Vardhanabhuti, et al. "Association of pretreatment (preTx) tumor characteristics and clinical outcomes following second-line (2L) axicabtagene ciloleucel (axi-cel) versus standard of care (SOC) in patients (pts) with relapsed/refractory (R/R) large B-cell lymphoma (LBCL)." Journal of Clinical Oncology 40, no. 16_suppl (2022): 7565. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.7565.

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7565 Background: The Phase 3 randomized ZUMA-7 trial in 2L R/R LBCL showed axi-cel superiority to SOC (salvage chemotherapy and HDT-ASCT) in event-free survival (EFS; hazard ratio [HR], 0.398; P<.0001; Locke et al. N Eng J Med. 2021). We report results of exploratory analyses of tumor characteristics, including preTx tumor burden (TB), tissue hypoxia-related lactate dehydrogenase (LDH) level, and tumor microenvironment (TME). Methods: TB was calculated as the sum of product diameters of ≤6 reference lesions (Locke et al. Blood Adv. 2020). Serum LDH was assessed. PreTx tumor samples were ass

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Ho, A. S., X. Huang, H. Cao, A. C. Koong, and Q. T. Le. "Detection of circulating hypoxia-regulated miR-210 in pancreatic adenocarcinoma patients." Journal of Clinical Oncology 27, no. 15_suppl (2009): 4624. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4624.

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4624 Background: MicroRNAs (miRs) are small non-coding transcripts involved in many cellular mechanisms, including tumorigenesis. miR-210, in particular, has been shown to be induced by hypoxia, over-expressed in several different cancers, and correlated with adverse outcomes in breast cancer. Moreover, since pancreatic adenocarcinomas have been previously shown to be extremely hypoxic, we hypothesized that miR-210 may be elevated in the plasma of these patients compared to non-cancer controls. Here, we compared the circulating plasma levels of miR-210 in pancreatic cancer patients and control

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Douiev, Liza, Chaya Miller, Shmuel Ruppo, Hadar Benyamini, Bassam Abu-Libdeh та Ann Saada. "Upregulation of COX4-2 via HIF-1α in Mitochondrial COX4-1 Deficiency". Cells 10, № 2 (2021): 452. http://dx.doi.org/10.3390/cells10020452.

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Cytochrome-c-oxidase (COX) subunit 4 (COX4) plays important roles in the function, assembly and regulation of COX (mitochondrial respiratory complex 4), the terminal electron acceptor of the oxidative phosphorylation (OXPHOS) system. The principal COX4 isoform, COX4-1, is expressed in all tissues, whereas COX4-2 is mainly expressed in the lungs, or under hypoxia and other stress conditions. We have previously described a patient with a COX4-1 defect with a relatively mild presentation compared to other primary COX deficiencies, and hypothesized that this could be the result of a compensatory u

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Storti, Paola, Irma Airoldi, Marina Bolzoni та ін. "Hypoxia-Inducible Factor (HIF)-1α Is a Therapeutic Target in Myeloma-Induced Angiogenesis". Blood 118, № 21 (2011): 3927. http://dx.doi.org/10.1182/blood.v118.21.3927.3927.

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Abstract Abstract 3927 Hypoxia-inducible factor (HIF)-1α is a critical trigger and regulator of tumor associated angiogenesis. It has been previously reported that bone marrow (BM) microenvironment is hypoxic in multiple myeloma (MM) patients and that HIF-1α is overexpressed by CD138+ MM cells and modulates the transcriptional and pro-angiogenic profiles of MM cells. The potential role of HIF-1α as a therapeutic target in MM is under investigation. To deepen this issue, in this study we explored the effect of a stable HIF-1α inhibition in MM cells on cell proliferation, survival and on MM-indu

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Lee, Sohyeon, Yoonyoung Kim, and Eun Seong Lee. "Hypoxia-Responsive Azobenzene-Linked Hyaluronate Dot Particles for Photodynamic Tumor Therapy." Pharmaceutics 14, no. 5 (2022): 928. http://dx.doi.org/10.3390/pharmaceutics14050928.

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In this study, we developed ultra-small hyaluronate dot particles that selectively release phototoxic drugs into a hypoxic tumor microenvironment. Here, the water-soluble hyaluronate dot (dHA) was covalently conjugated with 4,4′-azodianiline (Azo, as a hypoxia-sensitive linker) and Ce6 (as a photodynamic antitumor agent), producing dHA particles with cleavable Azo bond and Ce6 (dHA-Azo-Ce6). Importantly, the inactive Ce6 (self-quenched state) in the dHA-Azo-Ce6 particles was switched to the active Ce6 (dequenched state) via the Azo linker (–N=N–) cleavage in a hypoxic environment. In vitro stu

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Upadhyay, Laxmi, Muhammad Shan Ul Abedin, Stephen Yu, et al. "Managing CAR T-Cell Toxicity: Impact of Steroid Prophylaxis on Toxicity and Outcomes." Blood 144, Supplement 1 (2024): 7246. https://doi.org/10.1182/blood-2024-210573.

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Introduction: Chimeric antigen receptor (CAR) T-cell therapy has shown promising effects in treating relapsed/refractory hematological malignancies, significantly improving outcomes. However, CAR T-cell therapy is associated with side effects like cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). The incidence of CRS ranges from 41% to 94%, and ICANS from 21% to 64%, with grade 3 or higher CRS ranging from 1% to 24%. Prophylactic use of steroids has shown promising results in decreasing the incidence of CRS and ICANS in the ZUMA-1 cohort 6, inc

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Gurevich Shapiro, Anna, Eitan Winter, Pascale Zwicky, et al. "Single Cell Analysis of Pre-Treatment Peripheral Immune Composition Can Predict CAR-T Outcomes in Patients with Diffuse Large B-Cell Lymphoma." Blood 144, Supplement 1 (2024): 4788. https://doi.org/10.1182/blood-2024-203893.

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Background: Chimeric Antigen Receptor (CAR)-T cell therapy has revolutionized the treatment landscape for relapsed/refractory Diffuse Large B-cell Lymphoma (DLBCL). However, CAR-T failure remains a challenge, and an effective pre-treatment prognostic score is yet to be established. Aim: To gain a deeper understanding of the cellular and molecular determinants of response to CAR-T treatment by applying single cell multiomics, which will facilitate early response prediction, address resistance mechanisms, and refine patient selection criteria. This is particularly crucial with the introduction o

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Wei, Guijie, Jianhua Chen, Ziqi Jing, et al. "Glucose transporter 1 (GLUT1)-targeting and hypoxia-activated mitochondria-specific chemo-thermal therapy via a glycosylated poly(amido amine)/celastrol (PAMAM/Cel) complex." Journal of Colloid and Interface Science 608 (February 2022): 1355–65. http://dx.doi.org/10.1016/j.jcis.2021.10.129.

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Shahzad, Moazzam, Muhammad Salman Faisal, Ernie Shippey, et al. "Evolution in Resource Utilization for Unique Toxicities Related to Chimeric Antigen Receptor T Cell Therapy from 2017 to 2020: A Database Review." Blood 138, Supplement 1 (2021): 4844. http://dx.doi.org/10.1182/blood-2021-154341.

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Abstract Introduction: Chimeric antigen receptor T cell therapy (CAR-T) is a novel treatment that utilizes T cells by augmenting them using vector viruses to add antigens to target cancer cells. In 2017, FDA approved CD-19 CAR-T for relapsed/refractory diffuse large B-cell lymphoma and acute lymphoblastic leukemia patients ≤ 26yr old. Unique toxicities associated with CAR-T therapy include cytokine release syndrome (CRS) and immune effector cell-related neurotoxicity (ICANS). Lower-grade CRS and ICANS are managed with tocilizumab, an interleukin-6 antagonist, and steroids. Management of higher

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12

Yang, B. C., and J. L. Mehta. "Alterations in pulmonary artery tone during repeated episodes of hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (1995): L293—L298. http://dx.doi.org/10.1152/ajplung.1995.269.3.l293.

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To examine the basis of pulmonary constriction during chronic hypoxia, rat pulmonary artery rings were precontracted and exposed to multiple episodes of hypoxia. The first hypoxic episode resulted in a transient contraction, followed by potent relaxation, and then a slow sustained contraction. Repeated hypoxic exposure resulted in stronger initial contraction and attenuated relaxation. Prolongation of the normoxic interval between hypoxic episodes reversed the attenuation of hypoxic relaxation. Pulmonary artery rings that were deendothelialized or treated with the nitric oxide synthesis inhibi

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13

Gong, Yanqing, та Faton H. Agani. "Oligomycin inhibits HIF-1α expression in hypoxic tumor cells". American Journal of Physiology-Cell Physiology 288, № 5 (2005): C1023—C1029. http://dx.doi.org/10.1152/ajpcell.00443.2004.

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Hypoxia-inducible factor-1 (HIF-1) is a key regulator of cellular responses to reduced oxygen availability. The contribution of mitochondria in regulation of HIF-1α in hypoxic cells has received recent attention. We demonstrate that inhibition of electron transport complexes I, III, and IV diminished hypoxic HIF-1α accumulation in different tumor cell lines. Hypoxia-induced HIF-1α accumulation was not prevented by the antioxidants Trolox and N-acetyl-cysteine. Oligomycin, inhibitor of F0F1-ATPase, prevented hypoxia-induced HIF-1α protein accumulation and had no effect on HIF-1α induction by hy

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Thompson, Alexis A., Janet L. Kwiatkowski, John B. Porter та ін. "Favorable Outcomes in Pediatric Patients in the Phase 3 Hgb-207 (Northstar-2) and Hgb-212 (Northstar-3) Studies of Betibeglogene Autotemcel Gene Therapy for the Treatment of Transfusion-Dependent β-Thalassemia". Blood 136, Supplement 1 (2020): 52–54. http://dx.doi.org/10.1182/blood-2020-135857.

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Introduction Betibeglogene autotemcel (beti-cel; LentiGlobin for β-thalassemia) gene therapy is being evaluated for the treatment of transfusion-dependent β-thalassemia (TDT). Initial positive results of beti-cel in the phase 3 studies, HGB-207 (NCT02906202; non-β0/β0 genotypes) and HGB-212 (NCT03207009; β0/β0, β0/β+ IVS-I-110 and β+ IVS-I-110/β+ IVS-I-110 genotypes), showed 10/12 adult patients achieved transfusion independence. The studies expanded enrollment to include adolescents and children. We present interim results from pediatric patients &lt;18 yrs who received beti-cel in HGB-20

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Zhang, Hanying, Miyako Okamoto, Evgeniy Panzhinskiy, W. Michael Zawada та Mita Das. "PKCδ/midkine pathway drives hypoxia-induced proliferation and differentiation of human lung epithelial cells". American Journal of Physiology-Cell Physiology 306, № 7 (2014): C648—C658. http://dx.doi.org/10.1152/ajpcell.00351.2013.

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Epithelial cells are key players in the pathobiology of numerous hypoxia-induced lung diseases. The mechanisms mediating such hypoxic responses of epithelial cells are not well characterized. Earlier studies reported that hypoxia stimulates protein kinase C (PKC)δ activation in renal cancer cells and an increase in expression of a heparin-binding growth factor, midkine (MK), in lung alveolar epithelial cells. We reasoned that hypoxia might regulate MK levels via a PKCδ-dependent pathway and hypothesized that PKCδ-driven MK expression is required for hypoxia-induced lung epithelial cell prolife

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Guo, Ying, Jin Tan, Yuyang Miao, Zuoming Sun, and Qiang Zhang. "Effects of Microvesicles on Cell Apoptosis under Hypoxia." Oxidative Medicine and Cellular Longevity 2019 (April 17, 2019): 1–11. http://dx.doi.org/10.1155/2019/5972152.

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Hypoxia, as one of the severe cellular stresses, can cause cellular injury and even cell death. Apoptosis is the main mechanism of regulating cell death and is closely related to the cell death caused by hypoxia. However, hypoxia-induced apoptosis is not entirely the result of direct hypoxic stimulus of cells. In recent years, it has been found that cells injured by hypoxia can shed a kind of membranous vesicles, which are called microvesicles (MVs). MVs can carry bioactive molecules from injured mother cells and appear in blood, cerebrospinal fluid, and other body fluids. MVs can induce norma

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Wodopia, Ralf, Hyun Soo Ko, Javiera Billian, Rudolf Wiesner, Peter Bärtsch, and Heimo Mairbäurl. "Hypoxia decreases proteins involved in epithelial electrolyte transport in A549 cells and rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 6 (2000): L1110—L1119. http://dx.doi.org/10.1152/ajplung.2000.279.6.l1110.

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Fluid reabsorption from alveolar space is driven by active Na reabsorption via epithelial Na channels (ENaCs) and Na-K-ATPase. Both are inhibited by hypoxia. Here we tested whether hypoxia decreases Na transport by decreasing the number of copies of transporters in alveolar epithelial cells and in lungs of hypoxic rats. Membrane fractions were prepared from A549 cells exposed to hypoxia (3% O2) as well as from whole lung tissue and alveolar type II cells from rats exposed to hypoxia. Transport proteins were measured by Western blot analysis. In A549 cells, α1- and β1-Na-K-ATPase, Na/K/2Cl cotr

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Zhou, Shiyu, Yu Lan, Yuqun Li, Zhenxing Li, Jinding Pu, and Liping Wei. "Hypoxic Tumor-Derived Exosomes Induce M2 Macrophage Polarization via PKM2/AMPK to Promote Lung Cancer Progression." Cell Transplantation 31 (January 2022): 096368972211069. http://dx.doi.org/10.1177/09636897221106998.

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Hypoxia is a major regulator of tumor aggressiveness and metastasis in cancer progression. Exosomes (exos) play an important role in the communication between lung cancer and hypoxic microenvironment. However, the underlying mechanisms are largely undefined. Exos were isolated from A549 cells under hypoxia conditions. Transmission electron microscopy and nanoparticle tracking analysis were carried out to characterize exos. CCK-8 assay, flow cytometry, Western blot, wound healing, and transwell assays were performed to assess the proliferation, apoptosis, migration, and invasion of A549 cells,

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Schmaltz, Cornelius, Patricia Harrigan Hardenbergh, Audrey Wells, and David E. Fisher. "Regulation of Proliferation-Survival Decisions during Tumor Cell Hypoxia." Molecular and Cellular Biology 18, no. 5 (1998): 2845–54. http://dx.doi.org/10.1128/mcb.18.5.2845.

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ABSTRACT Hypoxia may influence tumor biology in paradoxically opposing ways: it is lethal as a direct stress trigger, yet hypoxic zones in solid tumors harbor viable cells which are particularly resistant to treatment and contribute importantly to disease relapse. To examine mechanisms underlying growth-survival decisions during hypoxia, we have compared genetically related transformed and untransformed fibroblast cells in vitro for proliferation, survival, clonogenicity, cell cycle, and p53 expression. Hypoxia induces G0/G1 arrest in primary fibroblasts but triggers apoptosis in oncogene-tran

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Gallego-Martin, Teresa, Jesus Prieto-Lloret, Philip Aaronson, Asuncion Rocher, and Ana Obeso. "Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells." Antioxidants 8, no. 3 (2019): 62. http://dx.doi.org/10.3390/antiox8030062.

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Carotid body (CB) chemoreceptor cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bo

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O’Leary, Andrew J., Sarah E. Drummond, Deirdre Edge, and Ken D. O’Halloran. "Diaphragm Muscle Weakness Following Acute Sustained Hypoxic Stress in the Mouse Is Prevented by Pretreatment with N-Acetyl Cysteine." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–19. http://dx.doi.org/10.1155/2018/4805493.

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Oxygen deficit (hypoxia) is a major feature of cardiorespiratory diseases characterized by diaphragm dysfunction, yet the putative role of hypoxic stress as a driver of diaphragm dysfunction is understudied. We explored the cellular and functional consequences of sustained hypoxic stress in a mouse model. Adult male mice were exposed to 8 hours of normoxia, or hypoxia (FiO2 = 0.10) with or without antioxidant pretreatment (N-acetyl cysteine, 200 mg/kg i.p.). Ventilation and metabolism were measured. Diaphragm muscle contractile function, myofibre size and distribution, gene expression, protein

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Itoh, Mai, Yusuke Takahashi, Yuki Okuhashi та Shuji Tohda. "Effects of Hypoxia on HIF, Notch, Akt, and NF-κB Signaling in Leukemia Cell Lines". Blood 122, № 21 (2013): 3874. http://dx.doi.org/10.1182/blood.v122.21.3874.3874.

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Abstract Background Leukemia stem cells reside in the bone marrow niche under hypoxic conditions. The activity of various signaling pathways in the hypoxic environment should be known to understand the pathophysiology of leukemia stem cells. Hypoxia is known to stabilize HIF1α, which transactivates various genes allowing the cell to adapt to hypoxic conditions. Two theories have been reported regarding crosstalk between HIF and Notch signaling; one suggests that HIF1α binds to cleaved Notch1, which results in stabilization of Notch signaling, and the second suggests that HIF1α represses a nega

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Sikarwar, A. S., M. Hinton, K. T. Santhosh, et al. "Hypoxia inhibits adenylyl cyclase catalytic activity in a porcine model of persistent pulmonary hypertension of the newborn." American Journal of Physiology-Lung Cellular and Molecular Physiology 315, no. 6 (2018): L933—L944. http://dx.doi.org/10.1152/ajplung.00130.2018.

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Persistent pulmonary hypertension of the newborn (PPHN) features hypoxemia, pulmonary vasoconstriction, and impaired cardiac inotropy. We previously reported low basal and stimulated cAMP in hypoxic pulmonary artery smooth muscle cells (PASMCs). We now examine pulmonary arterial adenylyl cyclase (AC) activity and regulation in hypoxic PPHN. PPHN was induced in newborn swine by normobaric hypoxia (fraction of inspired oxygen 0.10) for 72 h and compared with age-matched normoxic controls. We studied relaxation of pulmonary arterial (PA) rings to AC activator forskolin and cGMP activator sodium n

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Agani, Faton H., Michelle Puchowicz, Juan Carlos Chavez, Paola Pichiule та Joseph LaManna. "Role of nitric oxide in the regulation of HIF-1α expression during hypoxia". American Journal of Physiology-Cell Physiology 283, № 1 (2002): C178—C186. http://dx.doi.org/10.1152/ajpcell.00381.2001.

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Hypoxia-inducible factor-1 (HIF-1), a heterodimeric transcription factor consisting of HIF-1α and HIF-1β subunits, controls the expression of a large number of genes involved in the regulation of cellular responses to reduced oxygen availability. The oxygen-regulated subunit, HIF-1α, is stabilized in cells exposed to hypoxia. The regulation of hypoxic responses by nitric oxide (NO) is believed to have wide pathophysiological relevance, thus we investigated whether NO affects HIF-1 activation in hypoxic cells. Here we show that NO generated from NO donors prevented HIF-1α hypoxic accumulation i

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Collard, Charles D., Cuneyt Bukusoglu, Azin Agah, et al. "Hypoxia-induced expression of complement receptor type 1 (CR1, CD35) in human vascular endothelial cells." American Journal of Physiology-Cell Physiology 276, no. 2 (1999): C450—C458. http://dx.doi.org/10.1152/ajpcell.1999.276.2.c450.

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Reoxygenation of hypoxic human umbilical vein endothelial cells (HUVECs) increases protein expression of the complement regulators CD46 and CD55. As the receptor for C3b is known to be present on injured bovine endothelial cells, we investigated whether hypoxia or inflammatory mediators induce complement receptor type 1 (CR1; CD35) expression on HUVECs. CR1 protein expression increased 3.7 ± 0.6-fold as measured by ELISA on HUVECs following hypoxia (48 h, 1% O2). Colocalization of CD35 and von Willebrand factor by confocal microscopy confirmed that CD35 was predominantly intracellular. Lipopol

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Muz, Barbara, Feda Azab, Pilar De La Puente, Ravi Vij, and Abdel Kareem Azab. "Tumor Hypoxia Promotes Dissemination and Tumor Colonization In Waldenström Macroglobulinemia." Blood 122, no. 21 (2013): 3011. http://dx.doi.org/10.1182/blood.v122.21.3011.3011.

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Abstract Introduction Waldenström Macroglobulinemia (WM) is a rare, low-grade B-cell lymphoma characterized by lymphoplasmacytic cells spread widely in the bone marrow (BM) and overproduction of monoclonal immunoglobulins M (IgM). Previous studies showed that tumor hypoxia develops in the BM of other hematologic malignancies and promotes dissemination. In this study, we tested the effect of hypoxia on cell proliferation, cell cycle and apoptosis; on egress and homing of WM cells from and into the BM; and on recovery and tumor colonization in the new BM niche. Methods We characterized the effec

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Liu, Xin Hua, Alexander Kirschenbaum, Min Lu та ін. "Prostaglandin E2Induces Hypoxia-inducible Factor-1α Stabilization and Nuclear Localization in a Human Prostate Cancer Cell Line". Journal of Biological Chemistry 277, № 51 (2002): 50081–86. http://dx.doi.org/10.1074/jbc.m201095200.

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Hypoxia-induced up-regulation of vascular endothelial growth factor (VEGF) expression is a critical event leading to tumor neovascularization. Hypoxia stimulates hypoxia-inducible factor-1α (HIF-1α), a transcriptional activator of VEGF. Cyclooxygenase (COX)-2, an inducible enzyme that catalyzes the formation of prostaglandins (PGs) from arachidonic acid, is also induced by hypoxia. We reported previously that COX-2 inhibition prevents hypoxic up-regulation of VEGF in human prostate cancer cells and that prostaglandin E2(PGE2) restores hypoxic effects on VEGF. We hypothesized that PGE2mediates

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Rico, A. J., J. Prieto-Lloret, C. Gonzalez, and R. Rigual. "Hypoxia and acidosis increase the secretion of catecholamines in the neonatal rat adrenal medulla: an in vitro study." American Journal of Physiology-Cell Physiology 289, no. 6 (2005): C1417—C1425. http://dx.doi.org/10.1152/ajpcell.00023.2005.

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Hypoxia elicits catecholamine (CA) secretion from the adrenal medulla (AM) in perinatal animals by acting directly on chromaffin cells. However, whether innervation of the AM, which in the rat occurs in the second postnatal week, suppresses this direct hypoxic response is the subject of debate. Opioid peptides have been proposed as mediators of this suppression. To resolve these controversies, we have compared CA-secretory responses with high external concentrations of K+ ([K+]e) and hypoxia in the AM of neonatal (1- to 2-day-old) and juvenile (14- or 15- and 30-day-old) rats subjected to supe

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Eliasson, Pernilla M., and Jan-Ingvar Jönsson. "A Hypoxic Niche in the Mouse Bone Marrow Diminishes Proliferation and Differentiation of Hematopoietic Stem Cells." Blood 112, no. 11 (2008): 4777. http://dx.doi.org/10.1182/blood.v112.11.4777.4777.

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Abstract In the bone marrow hematopoietic stem cells (HSCs) reside in specialized niches in close contact with stromal cells and endosteal osteoblasts. It is thought that this environment is hypoxic in nature, where HSCs are maintained in a quiescent state to prevent their depletion. Hypoxia stabilizes the transcription factor HIF-1α which triggers angiogenesis as well as genes slowering the cell cycle, promoting cell survival, and leading to a decrease in cellular metabolism. In this study, hypoxic effects of the maintenance of Lin−Sca1+c-kit+* (LSK) cells derived from mouse bone marrow and t

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Kugeratski, Fernanda G., Samuel J. Atkinson, Lisa J. Neilson, et al. "Hypoxic cancer–associated fibroblasts increase NCBP2-AS2/HIAR to promote endothelial sprouting through enhanced VEGF signaling." Science Signaling 12, no. 567 (2019): eaan8247. http://dx.doi.org/10.1126/scisignal.aan8247.

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Intratumoral hypoxia causes the formation of dysfunctional blood vessels, which contribute to tumor metastasis and reduce the efficacy of therapeutic treatments. Blood vessels are embedded in the tumor stroma of which cancer-associated fibroblasts (CAFs) constitute a prominent cellular component. We found that hypoxic human mammary CAFs promoted angiogenesis in CAF-endothelial cell cocultures in vitro. Mass spectrometry–based proteomic analysis of the CAF secretome unraveled that hypoxic CAFs contributed to blood vessel abnormalities by altering their secretion of various pro- and anti-angioge

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Sedivy, Vojtech, Shreena Joshi, Youssef Ghaly, et al. "Role of Kv7 channels in responses of the pulmonary circulation to hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 1 (2015): L48—L57. http://dx.doi.org/10.1152/ajplung.00362.2013.

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Hypoxic pulmonary vasoconstriction (HPV) is a beneficial mechanism that diverts blood from hypoxic alveoli to better ventilated areas of the lung, but breathing hypoxic air causes the pulmonary circulation to become hypertensive. Responses to airway hypoxia are associated with depolarization of smooth muscle cells in the pulmonary arteries and reduced activity of K+channels. As Kv7 channels have been proposed to play a key role in regulating the smooth muscle membrane potential, we investigated their involvement in the development of HPV and hypoxia-induced pulmonary hypertension. Vascular eff

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Kroon, Marielle E., Pieter Koolwijk, Bea van der Vecht, and Victor W. M. van Hinsbergh. "Urokinase receptor expression on human microvascular endothelial cells is increased by hypoxia: implications for capillary-like tube formation in a fibrin matrix." Blood 96, no. 8 (2000): 2775–83. http://dx.doi.org/10.1182/blood.v96.8.2775.

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Abstract Hypoxia stimulates angiogenesis, the formation of new blood vessels. This study evaluates the direct effect of hypoxia (1% oxygen) on the angiogenic response of human microvascular endothelial cells (hMVECs) seeded on top of a 3-dimensional fibrin matrix. hMVECs stimulated with fibroblast growth factor–2 (FGF-2) or vascular endothelial growth factor (VEGF) together with tumor necrosis factor–α (TNF-α) formed 2- to 3-fold more tubular structures under hypoxic conditions than in normoxic (20% oxygen) conditions. In both conditions the in-growth of capillary-like tubular structures into

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Kroon, Marielle E., Pieter Koolwijk, Bea van der Vecht, and Victor W. M. van Hinsbergh. "Urokinase receptor expression on human microvascular endothelial cells is increased by hypoxia: implications for capillary-like tube formation in a fibrin matrix." Blood 96, no. 8 (2000): 2775–83. http://dx.doi.org/10.1182/blood.v96.8.2775.h8002775_2775_2783.

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Hypoxia stimulates angiogenesis, the formation of new blood vessels. This study evaluates the direct effect of hypoxia (1% oxygen) on the angiogenic response of human microvascular endothelial cells (hMVECs) seeded on top of a 3-dimensional fibrin matrix. hMVECs stimulated with fibroblast growth factor–2 (FGF-2) or vascular endothelial growth factor (VEGF) together with tumor necrosis factor–α (TNF-α) formed 2- to 3-fold more tubular structures under hypoxic conditions than in normoxic (20% oxygen) conditions. In both conditions the in-growth of capillary-like tubular structures into fibrin re

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Hong, Sang-Eun, Jong Hun An, Seong-Lan Yu, et al. "Ceria-Zirconia Antioxidant Nanoparticles Attenuate Hypoxia-Induced Acute Kidney Injury by Restoring Autophagy Flux and Alleviating Mitochondrial Damage." Journal of Biomedical Nanotechnology 16, no. 7 (2020): 1144–59. http://dx.doi.org/10.1166/jbn.2020.2948.

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Oxidative stress is one of the principal causes of hypoxia-induced kidney injury. The ceria nanoparticle (CNP) is known to exhibit free radical scavenger and catalytic activities. When zirconia is attached to CNPs (CZNPs), the ceria atom tends to remain in a Ce3+ form and its efficacy as a free radical scavenger thus increases. We determined the effectiveness of CNP and CZNP antioxidant activities against hypoxia-induced acute kidney injury (AKI) and observed that these nanoparticles suppress the apoptosis of hypoxic HK-2 cells by restoring autophagy flux and alleviating mitochondrial damage.

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Rehn, Matilda, André Olsson, Kristian Reckzeh, et al. "Hypoxic induction of vascular endothelial growth factor regulates murine hematopoietic stem cell function in the low-oxygenic niche." Blood 118, no. 6 (2011): 1534–43. http://dx.doi.org/10.1182/blood-2011-01-332890.

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Abstract Hypoxia is emerging as an important characteristic of the hematopoietic stem cell (HSC) niche, but the molecular mechanisms contributing to quiescence, self-renewal, and survival remain elusive. Vascular endothelial growth factor A (VEGFA) is a key regulator of angiogenesis and hematopoiesis. Its expression is commonly regulated by hypoxia-inducible factors (HIF) that are functionally induced in low-oxygen conditions and that activate transcription by binding to hypoxia-response elements (HRE). Vegfa is indispensable for HSC survival, mediated by a cell-intrinsic, autocrine mechanism.

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Sheares, Karen K. K., Trina K. Jeffery, Lu Long, Xudong Yang та Nicholas W. Morrell. "Differential effects of TGF-β1 and BMP-4 on the hypoxic induction of cyclooxygenase-2 in human pulmonary artery smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 287, № 5 (2004): L919—L927. http://dx.doi.org/10.1152/ajplung.00012.2004.

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Chronic hypoxia-induced pulmonary hypertension results partly from proliferation of smooth muscle cells in small peripheral pulmonary arteries. Previously, we demonstrated that hypoxia modulates the proliferation of human peripheral pulmonary artery smooth muscle cells (PASMCs) by induction of cyclooxygenase-2 (COX-2) and production of antiproliferative prostaglandins ( 55 ). The transforming growth factor (TGF)-β superfamily plays a critical role in the regulation of pulmonary vascular remodeling, although to date an interaction with hypoxia has not been examined. We therefore investigated th

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Emerling, Brooke M., Leonidas C. Platanias, Emma Black, Angel R. Nebreda, Roger J. Davis, and Navdeep S. Chandel. "Mitochondrial Reactive Oxygen Species Activation of p38 Mitogen-Activated Protein Kinase Is Required for Hypoxia Signaling." Molecular and Cellular Biology 25, no. 12 (2005): 4853–62. http://dx.doi.org/10.1128/mcb.25.12.4853-4862.2005.

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ABSTRACT Mammalian cells have the ability to sense low oxygen levels (hypoxia). An adaptive response to hypoxia involves the induction of the transcription factor hypoxia-inducible factor 1 (HIF-1). The intracellular signaling pathways that regulate HIF-1 activation during hypoxia remain unknown. Here, we demonstrate that p38α − / − cells fail to activate HIF-1 under hypoxic conditions. Cells deficient in Mkk3 and Mkk6, the upstream regulators of p38α, also fail to activate HIF-1 under hypoxic conditions. The p38α − / − cells are able to activate HIF-1 in response to anoxia or iron chelators d

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Kenneth, Niall Steven, and Sonia Rocha. "Regulation of gene expression by hypoxia." Biochemical Journal 414, no. 1 (2008): 19–29. http://dx.doi.org/10.1042/bj20081055.

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Hypoxia induces profound changes in the cellular gene expression profile. The discovery of a major transcription factor family activated by hypoxia, HIF (hypoxia-inducible factor), and the factors that contribute to HIF regulation have greatly enhanced our knowledge of the molecular aspects of the hypoxic response. However, in addition to HIF, other transcription factors and cellular pathways are activated by exposure to reduced oxygen. In the present review, we summarize the current knowledge of how additional hypoxia-responsive transcription factors integrate with HIF and how other cellular

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O’Reilly, Susan M., Martin O. Leonard, Niamh Kieran, et al. "Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner." American Journal of Physiology-Cell Physiology 290, no. 2 (2006): C592—C600. http://dx.doi.org/10.1152/ajpcell.00278.2005.

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Hypoxia occurs during a number of conditions in which altered epithelial proliferation is critical, including tumor development. Microarray analysis of colon-derived epithelial cells revealed a hypoxia-dependent increase in the expression of amphiregulin, an EGF receptor (EGFR) ligand that activates epithelial proliferation and has been associated with the development of colonic tumors. Amphiregulin expression was also induced in tissues from mice exposed to whole animal hypoxia. The hypoxic upregulation of amphiregulin was independent of the classic transcriptional response mediated via hypox

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Gleadle, Jonathan M., and Peter J. Ratcliffe. "Induction of Hypoxia-Inducible Factor-1, Erythropoietin, Vascular Endothelial Growth Factor, and Glucose Transporter-1 by Hypoxia: Evidence Against a Regulatory Role for Src Kinase." Blood 89, no. 2 (1997): 503–9. http://dx.doi.org/10.1182/blood.v89.2.503.

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Abstract The induction by hypoxia of genes such as erythropoietin, vascular endothelial growth factor (VEGF ), and glucose transporter-1 (Glut-1) is mediated in part by a transcriptional complex termed hypoxia-inducible factor-1 (HIF-1). Several lines of evidence have implicated protein phosphorylation in the mechanism of activation of HIF-1 by hypoxia. Recent reports have described the activation of the tyrosine kinase src by severe hypoxia, and a role in the induction of VEGF by severe hypoxia has been proposed. This led us to examine whether src and related kinases operated more widely in t

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Zhang, Junhui, Geoffrey Thomas Gibney, Peng Zhao та Ying Xia. "Neuroprotective role of δ-opioid receptors in cortical neurons". American Journal of Physiology-Cell Physiology 282, № 6 (2002): C1225—C1234. http://dx.doi.org/10.1152/ajpcell.00226.2001.

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We recently demonstrated that δ-opioid receptor (DOR) activation protects cortical neurons against glutamate-induced injury. Because glutamate is a mediator of hypoxic injury in neurons, we hypothesized that DOR is involved in neuroprotection during O2 deprivation and that its activation/inhibition may alter neuronal susceptibility to hypoxic stress. In this work, we tested the effect of opioid receptor activation and inhibition on cultured cortical neurons in hypoxia (1% O2). Cell injury was assessed by lactate dehydrogenase release, morphology-based quantification, and live/dead staining. Ou

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Chen, Lingjuan, Gaoli Chen, Lixuan Guo, Yaping Wang, and Chengjin Ai. "Hypoxia-Induced GST1 Exerts Protective Effects on Trophoblasts via Inhibiting Reactive Oxygen Species (ROS) Accumulation." Analytical Cellular Pathology 2023 (January 25, 2023): 1–12. http://dx.doi.org/10.1155/2023/9391252.

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Hypoxic conditions are a typical extrinsic factor for the modification of trophoblast biological functions, including cell proliferation, migration, and invasion. Hypoxia-induced reactive oxygen species (ROS) accumulation causes chronic trophoblast injury and contributes to preeclampsia (PE). Glutathione-S-transferase P (GSTP1) is a main regulator of ROS. However, it is still unknown whether GSTP1 is involved in ROS regulation under hypoxic conditions. Here, we investigated the expression level of GSTP1 in first-trimester villi placentas compared with full-term placentas and the effect of hypo

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Shahzad, Moazzam, Muhammad Salman Faisal, Ernie Shippey, et al. "Safety and Cost Effectiveness of Chimeric Antigen Receptor T Cell Therapy in the Outpatient Setting." Blood 138, Supplement 1 (2021): 2823. http://dx.doi.org/10.1182/blood-2021-151872.

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Abstract Introduction Since the commercial approval of chimeric antigen receptor T cell (CAR-T) therapies, administration and toxicity monitoring have largely been in an inpatient setting due to the risk of significant toxicities such as cytokine release syndrome (CRS) and neurotoxicity in the first 30 days. Administration in the outpatient setting can be safe and cost-effective. Here we report the cost savings and adverse events of CAR-T in an outpatient setting as compared to the inpatient setting. Methods Cost differences of the commercial CD19 CAR-T axicabtagene ciloleucel (axi-cel) and ti

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Minamino, T., S. A. Mitsialis, and S. Kourembanas. "Hypoxia Extends the Life Span of Vascular Smooth Muscle Cells through Telomerase Activation." Molecular and Cellular Biology 21, no. 10 (2001): 3336–42. http://dx.doi.org/10.1128/mcb.21.10.3336-3342.2001.

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ABSTRACT Chronic hypoxia induces smooth muscle cell proliferation and vessel wall remodeling in the vasculature of the lung. One well-characterized component of the hypoxic response is transcriptional activation of genes encoding vascular smooth muscle cell (VSMC) mitogens. We report here that chronic hypoxia can also prolong the growth of human VSMC by inducing telomerase activity and telomere stabilization. We demonstrate that hypoxia induced phosphorylation of the telomerase catalytic component (TERT) and sustained high levels of TERT protein expression in VSMC compared to normoxia. Further

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Asosingh, Kewal, Hendrik De Raeve, Mark de Ridder, et al. "Role of the Hypoxic Bone Marrow Microenvironment in Multiple Myeloma Tumor Progression." Blood 104, no. 11 (2004): 2348. http://dx.doi.org/10.1182/blood.v104.11.2348.2348.

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Abstract Recently we reported that pre-clinical myeloma disease progression in the 5T2MM mouse model is characterized by predominant CD45+ MM-cells in the early, pre-angiogenic stage stage of slow tumor progression, followed by expansion of CD45− MM-cells during the subsequent angiogenic stage of progressive tumor growth. Unlike other cancer cells, multiple myeloma (MM) cells have to survive and to grow in a microenvironment which is already hypoxic by nature. This hypoxic bone marrow (BM) microenvironment is essential for normal hematopoiesis. However, the role of BM hypoxia in myeloma tumor

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Tao, Yifan, Jixiang Hua, Siqi Lu, et al. "Ultrastructural, Antioxidant, and Metabolic Responses of Male Genetically Improved Farmed Tilapia (GIFT, Oreochromis niloticus) to Acute Hypoxia Stress." Antioxidants 13, no. 1 (2024): 89. http://dx.doi.org/10.3390/antiox13010089.

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Tilapia tolerate hypoxia; thus, they are an excellent model for the study of hypoxic adaptation. In this study, we determined the effect of acute hypoxia stress on the antioxidant capacity, metabolism, and gill/liver ultrastructure of male genetically improved farmed tilapia (GIFT, Oreochromis niloticus). Fish were kept under control (dissolved oxygen (DO): 6.5 mg/L) or hypoxic (DO: 1.0 mg/L) conditions for 72 h. After 2 h of hypoxia stress, antioxidant enzyme activities in the heart and gills decreased, while the malondialdehyde (MDA) content increased. In contrast, in the liver, antioxidant

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Watt, Suzanne M., Sarah Hale, Dilair Baban, et al. "The Centromeric Protein, CEN(P)-F, a Marker of Cell Proliferation Is Regulated by Hypoxia in Human Mesenchymal Stem Cells and Their Bone Marrow Stromal Progeny." Blood 106, no. 11 (2005): 1385. http://dx.doi.org/10.1182/blood.v106.11.1385.1385.

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Abstract Human bone marrow mesenchymal stem cells (MSC) are multipotent progenitors that generate osteoblasts, chondrocytes, adipocytes, myoblasts and the bone marrow stromal cells that support hematopoiesis. Although the bone marrow microenvironment is hypoxic, little is known about the maintenance and response of MSC and their bone marrow stromal progeny to hypoxia. Using cDNA microarray hybridization technologies, we show, for the first time, that a total of 231 mRNAs in cultured MSCs are regulated by short exposures (4–48hrs) to hypoxia. These include known hypoxia-responsive genes, such a

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Lei, Yan, Xiaoyong Peng, Yi Hu, et al. "The Calcilytic Drug Calhex-231 Ameliorates Vascular Hyporesponsiveness in Traumatic Hemorrhagic Shock by Inhibiting Oxidative Stress and miR-208a-Mediated Mitochondrial Fission." Oxidative Medicine and Cellular Longevity 2020 (December 3, 2020): 1–13. http://dx.doi.org/10.1155/2020/4132785.

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Background. The calcium-sensing receptor (CaSR) plays a fundamental role in extracellular calcium homeostasis in humans. Surprisingly, CaSR is also expressed in nonhomeostatic tissues and is involved in regulating diverse cellular functions. The objective of this study was to determine if Calhex-231 (Cal), a negative modulator of CaSR, may be beneficial in the treatment of traumatic hemorrhagic shock (THS) by improving cardiovascular function and investigated the mechanisms. Methods. Rats that had been subjected to THS and hypoxia-treated vascular smooth muscle cells (VSMCs) were used in this

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Fuhrmann, Dominik C., Michaela Tausendschön, Ilka Wittig, et al. "Inactivation of Tristetraprolin in Chronic Hypoxia Provokes the Expression of Cathepsin B." Molecular and Cellular Biology 35, no. 3 (2014): 619–30. http://dx.doi.org/10.1128/mcb.01034-14.

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Macrophages play important roles in many diseases and are frequently found in hypoxic areas. A chronic hypoxic microenvironment alters global cellular protein expression, but molecular details remain poorly understood. Although hypoxia-inducible factor (HIF) is an established transcription factor allowing adaption to acute hypoxia, responses to chronic hypoxia are more complex. Based on a two-dimensional differential gel electrophoresis (2D-DIGE) approach, we aimed to identify proteins that are exclusively expressed under chronic but not acute hypoxia (1% O2). One of the identified proteins wa

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Azab, Abdel Kareem A., Phong Quang, Feda Azab, et al. "Dynamic Regulation of the Level of Hypoxia In the Bone Marrow Regulates Cell Dissemination In Multiple Myeloma." Blood 116, no. 21 (2010): 4035. http://dx.doi.org/10.1182/blood.v116.21.4035.4035.

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Abstract Abstract 4035 INTRODUCTION: The interaction of multiple myeloma (MM) cells with the bone marrow (BM) microenvironment plays a crucial role in MM pathogenesis, implying that progression of MM occurs through continuous interaction between the BM and MM cells, which controls the ability of MM cells to egress out of the BM and home into new BM niches. We have previously shown that the CXCR4/SDF1 axis as well as Rho GTPases downstream of the receptor was important for chemotaxis, adhesion, homing and egress of MM cells. However, the driving force for MM cells to leave the BM and metastasiz

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