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Articles 1 - 7 of 7
Full-Text Articles in Life Sciences
Maternal Choline Supplementation Modulates Placental Markers Of Inflammation, Angiogenesis, And Apoptosis In A Mouse Model Of Placental Insufficiency, Julia H. King, Sze Ting (Cecilia) Kwan, Jian Yan, Xinyin Jiang, Vladislav G. Fomin, Samantha P. Levine, Emily Wei, Mark S. Roberson, Marie A. Caudill
Maternal Choline Supplementation Modulates Placental Markers Of Inflammation, Angiogenesis, And Apoptosis In A Mouse Model Of Placental Insufficiency, Julia H. King, Sze Ting (Cecilia) Kwan, Jian Yan, Xinyin Jiang, Vladislav G. Fomin, Samantha P. Levine, Emily Wei, Mark S. Roberson, Marie A. Caudill
Publications and Research
Dlx3 (distal-less homeobox 3) haploinsufficiency in mice has been shown to result in restricted fetal growth and placental defects. We previously showed that maternal choline supplementation (4X versus 1X choline) in the Dlx3+/�� mouse increased fetal and placental growth in mid-gestation. The current study sought to test the hypothesis that prenatal choline would modulate indicators of placenta function and development. Pregnant Dlx3+/�� mice consuming 1X (control), 2X, or 4X choline from conception were sacrificed at embryonic (E) days E10.5, E12.5, E15.5, and E18.5, and placentas and embryos were harvested. Data were analyzed separately for each gestational day controlling for litter …
Il-24 Promotes Apoptosis Through Camp-Dependent Pka Pathways In Human Breast Cancer Cells, Leah Persaud, Jason Mighty, Xuelin Zhong, Ashleigh Francis, Marifer Mendez, Hilal Muharam, Stephen M. Redenti, Dibash Das, Bertal Huseyin Aktas, Moira Sauane
Il-24 Promotes Apoptosis Through Camp-Dependent Pka Pathways In Human Breast Cancer Cells, Leah Persaud, Jason Mighty, Xuelin Zhong, Ashleigh Francis, Marifer Mendez, Hilal Muharam, Stephen M. Redenti, Dibash Das, Bertal Huseyin Aktas, Moira Sauane
Publications and Research
Interleukin 24 (IL-24) is a tumor-suppressing protein, which inhibits angiogenesis and induces cancer cell-specific apoptosis. We have shown that IL-24 regulates apoptosis through phosphorylated eukaryotic initiation factor 2 alpha (eIF2α) during endoplasmic reticulum (ER) stress in cancer. Although multiple stresses converge on eIF2α phosphorylation, the cellular outcome is not always the same. In particular, ER stress-induced apoptosis is primarily regulated through the extent of eIF2α phosphorylation and activating transcription factor 4 (ATF4) action. Our studies show for the first time that cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) activation is required for IL-24-induced cell death in a variety of …
Pyronaridine Exerts Potent Cytotoxicity On Human Breast And Hematological Cancer Cells Through Induction Of Apoptosis, Paulina J. Villanueva, Alberto Martinez, Sarah T. Baca, Rebecca E. Dejesus, Manuel Larragoity, Lisett Contreras, Denisse A. Gutierrez, Armando Varela-Ramirez, Renato J. Aguilera
Pyronaridine Exerts Potent Cytotoxicity On Human Breast And Hematological Cancer Cells Through Induction Of Apoptosis, Paulina J. Villanueva, Alberto Martinez, Sarah T. Baca, Rebecca E. Dejesus, Manuel Larragoity, Lisett Contreras, Denisse A. Gutierrez, Armando Varela-Ramirez, Renato J. Aguilera
Publications and Research
The potent antimalarial drug pyronaridine (PND) was tested for its potential as an anticancer drug. After exposing cancerous (17) and non-cancerous (2) cells to PND for 72 hr, PND was found to exhibit consistent and potent cytotoxic activity at low micromolar (μM) concentrations that ranged from 1.6 μM to 9.4 μM. Moreover, PND exerted a significant selective cytotoxicity index (SCI) on five out of seven breast cancer cell lines tested, with favorable values of 2.5 to 4.4, as compared with the non-cancerous breast MCF-10A cell line. By using the same comparison, PND exhibited a significant SCI on three out of …
Eukaryotic Translation Initiation Factor 4a Down-Regulation Mediates Interleukin-24-Induced Apoptosis Through Inhibition Of Translation, Xuelin Zhong, Leah Persaud, Hilal Muharam, Ashleigh Francis, Dibash Das, Bertal Huseyin Atkas, Moire Sauane
Eukaryotic Translation Initiation Factor 4a Down-Regulation Mediates Interleukin-24-Induced Apoptosis Through Inhibition Of Translation, Xuelin Zhong, Leah Persaud, Hilal Muharam, Ashleigh Francis, Dibash Das, Bertal Huseyin Atkas, Moire Sauane
Publications and Research
Dysregulated activity of helicase eIF4A drives transformation to and maintenance of cancer cell phenotype by reprogramming cellular translation. Interleukin 24 (IL-24) is a tumor-suppressing protein, which has the ability to inhibit angiogenesis, sensitize cancer cells to chemotherapy, and induce cancer cell-specific apoptosis. In this study, we found that eIF4A is inhibited by IL-24. Consequently, selective reduction of translation was observed for mRNAs harboring strong secondary structures in their 50 -untranslated regions (50UTRs). These mRNAs encode proteins, which function in cell survival and proliferation. Consistently, overexpression of eIF4A conferred cancer cells with resistance to IL-24-induced cell death. It has been established …
Inhibition Of Apoptosis Exacerbates Fatigue-Damage Tendon Injuries In An In Vivo Rat Model, R. Bell, M. A. Robles-Harris, M. Anderson, D. Laudier, M. B. Schaffler, E. L. Flatow, N. Andarawis-Puri
Inhibition Of Apoptosis Exacerbates Fatigue-Damage Tendon Injuries In An In Vivo Rat Model, R. Bell, M. A. Robles-Harris, M. Anderson, D. Laudier, M. B. Schaffler, E. L. Flatow, N. Andarawis-Puri
Publications and Research
Tendinopathy is a common and progressive musculoskeletal disease. Increased apoptosis is an end-stage tendinopathy manifestation, but its contribution to the pathology of the disease is unknown. A previously established in vivo model of fatigue-damage accumulation shows that increased apoptosis is correlated with the severity of induced tendon damage, even in early onset of the disease, supporting its implication in the pathogenesis of the disease. Consequently, this study aimed to determine: (1) whether apoptosis could be inhibited after fatigue damage and (2) whether its inhibition could lead to remodeling of the extracellular matrix (ECM) and pericellular matrix (PCM), to ultimately improve …
Bone Morphogenetic Protein Inhibition Promotes Neurological Recovery After Intraventricular Hemorrhage, Krishna Dummula, Govindaiah Vinukonda, Philip Chu, Yiping Xing, Furong Hu, Sabrina Mailk, Anna Csiszar, Caroline Chua, Peter Mouton, Robert J. Kayton, Joshua C. Brumberg, Rashmi Bansal, Praveen Ballabh
Bone Morphogenetic Protein Inhibition Promotes Neurological Recovery After Intraventricular Hemorrhage, Krishna Dummula, Govindaiah Vinukonda, Philip Chu, Yiping Xing, Furong Hu, Sabrina Mailk, Anna Csiszar, Caroline Chua, Peter Mouton, Robert J. Kayton, Joshua C. Brumberg, Rashmi Bansal, Praveen Ballabh
Publications and Research
Intraventricular hemorrhage (IVH) results in neural cell death and white matter injury in premature infants. No therapeutic strategy is currently available against this disorder. Bone morphogenetic protein (BMP) signaling suppresses oligodendrocyte development through basic-helix-loop-helix (bHLH) transcription factors and promotes astrocytosis. Therefore, we hypothesized that IVH in premature newborns initiates degeneration and maturation arrest of oligodendrocyte lineage and that BMP inhibition alleviates hypomyelination, gliosis, and motor impairment in the survivors of IVH. To test the hypotheses, a rabbit model of IVH was used in which premature rabbit pups (E29) are treated with intraperitoneal glycerol at 2 hours of age to induce …
Cell Death In Health And Disease, Richard A. Lockshin, Zahra Zakeri
Cell Death In Health And Disease, Richard A. Lockshin, Zahra Zakeri
Publications and Research
Cell death is clearly an important factor in development, homeostasis, pathology and in aging, but medical efforts based on controlling cell death have not become major aspects of medicine. There are several reasons why hopes have been slow to be fulfilled, and they present indications for new directions in research. Most effort has focused on the machinery of cell death, or the proximate effectors of apoptosis and their closely associated and interacting proteins. But cells have many options other than apoptosis. These include autophagy, necrosis, atrophy and stepwise or other alternate means of self-disassembly. The response of a cell to …