Mitochondrial adenine nucleotide transport and cardioprotection

Das, Samarjit; Steenbergen, Charles

doi:10.1016/j.yjmcc.2011.09.007

Cited by 18 publications

(11 citation statements)

References 85 publications

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“…Once released, Cyt c forms a complex with Apaf1 and procaspase-9, leading to caspase-9 activation, which further activates effector molecules such as cleaved-caspases-3, finally resulting in programmed cell death. Bcl-2 is located in the mitochondrial membrane [34] and plays a key role in maintaining its integrity. Bax is usually located in the cytoplasm and migrates to the mitochondrial membrane when it is undergoing destructive stimuli and subsequently increases the permeability of the mitochondrial outer membrane.…”

Section: Discussionmentioning

confidence: 99%

Luteolin Suppresses the Proliferation of Gastric Cancer Cells and Acts in Synergy with Oxaliplatin

Ren

Zhang

2020

BioMed Research International

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Objective. Gastric cancer, one of the most common malignant tumors worldwide, arises from the gastric mucosal epithelium and severely affects patient health and quality of life. Luteolin (LUT) is a flavonoid found in vegetables and fruits with diverse functions. A large number of studies have confirmed that LUT has an antitumor effect. Therefore, this study is aimed at verifying whether LUT can exert antitumor effects in synergy with oxaliplatin (OXA). As such, we examined the effects of LUT, OXA, and their coadministration in a gastric adenocarcinoma cell line (SGC-7901). We used the MTT assay to quantify the proliferation of SGC-7901 cells, flow cytometry to detect the cell cycle and apoptosis, ELISA to detect the expression of cell-cycle-related proteins, and western blot to detect the expression of related apoptotic factors. The results of this study show that the combination of LUT and OXA inhibited SGC-7901 cell proliferation and induced apoptosis by altering cell-cycle proportions. In addition, the combination also activated Cyt c/caspase signaling in SGC-7901 cells. In summary, LUT synergy with OXA inhibited the proliferation of gastric cancer cells in vitro. The present study also elucidated the mechanism by which LUT potentiated the sensitivity of SGC-7901 cells to OXA through the Cyt c/caspase pathway.

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Section: Discussionmentioning

confidence: 99%

Luteolin Suppresses the Proliferation of Gastric Cancer Cells and Acts in Synergy with Oxaliplatin

Ren

Zhang

2020

BioMed Research International

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“…The mPTP has been shown to relate to neuronal cell death and also play a role in reperfusion injury in the heart (Das and Steenbergen, 2012). Bongkrekic acid at 16 microg/kg has been documented to be neuroprotective in ischemic conditions (Muranyi and Li, 2005).…”

Section: Mitochondrial Adp/atp Translocation Inhibitorsmentioning

confidence: 99%

The bizarre pharmacology of the ATP release channel pannexin1

2013

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Pannexins were originally thought to represent a second and redundant family of gap junction proteins in addition to the well characterized coonexins. However, it is now evident that pannexins function as unapposed membrane channels and the major role of Panx1 is that of an ATP release channel. Despite the contrasting functional roles, connexins, innexins and pannexins share pharmacological properties. Most gap junction blockers also attenuate the function of Panx1, including carbenoxolone, mefloquine and flufenamic acid. However, in contrast to connexin based gap junction channels, Panx1 channel activity can be attenuated by several groups of drugs hitherto considered very specific for other proteins. The drugs affecting Panx1 channels include several transport inhibitors, chloride channel blockers, mitochondrial inhibitors, P2X7 receptor ligands, inflammasome inhibitors and malaria drugs. These observations indicate that Panx1 may play an extended role in a wider spectrum of physiological functions. Alternatively, Panx1 may share structural domains with other proteins, not readily revealed by sequence alignments.

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“…Mitochondria, which possess their own DNA, mRNA, tRNA, and ribosomes, are semiautonomous organelles, but they import many critical proteins that are encoded by nuclear genes . Critical to mitochondrial function are 5 respiratory chain complexes in the inner mitochondrial membrane that generate a proton gradient across the membrane, which produces ATP . Most of the respiratory chain complex subunits are encoded by nuclear genes except for some subunits of complexes I, III, and IV, which are encoded by mitochondrial DNA and synthesized on mitochondrial ribosomes .…”

Section: Introductionmentioning

confidence: 99%

Divergent Effects of miR‐181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets

Das¹,

Kohr

Dunkerly‐Eyring³

et al. 2017

JAHA

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BackgroundMicroRNA (miRNA) is a type of noncoding RNA that can repress the expression of target genes through posttranscriptional regulation. In addition to numerous physiologic roles for miRNAs, they play an important role in pathophysiologic processes affecting cardiovascular health. Previously, we reported that nuclear encoded microRNA (miR‐181c) is present in heart mitochondria, and importantly, its overexpression affects mitochondrial function by regulating mitochondrial gene expression.Methods and ResultsTo investigate further how the miR‐181 family affects the heart, we suppressed miR‐181 using a miR‐181‐sponge containing 10 repeated complementary miR‐181 “seed” sequences and generated a set of H9c2 cells, a cell line derived from rat myoblast, by stably expressing either a scrambled or miR‐181‐sponge sequence. Sponge‐H9c2 cells showed a decrease in reactive oxygen species production and reduced basal mitochondrial respiration and protection against doxorubicin‐induced oxidative stress. We also found that miR‐181a/b targets phosphatase and tensin homolog (PTEN), and the sponge‐expressing stable cells had increased PTEN activity and decreased PI3K signaling. In addition, we have used miR‐181a/b−/− and miR‐181c/d−/− knockout mice and subjected them to ischemia‐reperfusion injury. Our results suggest divergent effects of different miR‐181 family members: miR‐181a/b targets PTEN in the cytosol, resulting in an increase in infarct size in miR‐181a/b−/− mice due to increased PTEN signaling, whereas miR‐181c targets mt‐COX1 in the mitochondria, resulting in decreased infarct size in miR‐181c/d−/− mice.ConclusionsThe miR‐181 family alters the myocardial response to oxidative stress, notably with detrimental effects by targeting mt‐COX1 (miR‐181c) or with protection by targeting PTEN (miR‐181a/b).

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Mitochondrial adenine nucleotide transport and cardioprotection

Cited by 18 publications

References 85 publications

Luteolin Suppresses the Proliferation of Gastric Cancer Cells and Acts in Synergy with Oxaliplatin

Luteolin Suppresses the Proliferation of Gastric Cancer Cells and Acts in Synergy with Oxaliplatin

The bizarre pharmacology of the ATP release channel pannexin1

Divergent Effects of miR‐181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets

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