Emanuel Strehler’s work on calcium pumps and calcium signaling

Strehler, Emanuel E.

doi:10.4331/wjbc.v2.i4.67

Cited by 4 publications

(4 citation statements)

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“…Both abnormal Ca 2+ levels and inappropriate Ca 2+ signaling are related to many clinical disorders such as stroke, obesity, cardiac dysfunction, aging and Alzheimer's disease [22][23][24][25]. It is worth noting that Ca 2+ signaling is a key element of apoptotic signaling pathways.…”

Section: +mentioning

confidence: 99%

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Xiao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Ultraviolet B (UVB) irradiation can easily induce apoptosis in human lens epithelial cells (HLECs) and further lead to various eye diseases including cataract. Here for the first time, we investigated the role of cartilage acidic protein 1 (CRTAC1) gene in UVB irradiation induced-apoptosis in HLECs. Methods: Three groups of HLECs were employed including model group, empty vector group, and CRTAC1 interference group. Results: After UVB irradiation, the percentage of primary apoptotic cells was obviously fewer in CRTAC1 interference group. Meanwhile, inhibition of CRTAC1 also reduced both reactive oxygen species (ROS) production and intracellular Ca²⁺ concentration, but the level of mitochondrial membrane potential (Δψm) was increased in HLECs. Further studies indicated that superoxide dismutase (SOD) activity and total antioxidative (T-AOC) level were significantly increased in CRTAC1-inhibited cells, while the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) were significantly decreased. ELISA analysis of CRTAC1-inhibited cells showed that the concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly decreased, but the concentration of interleukin-10 (IL-10) was significantly increased. Western blot analyses of eight apoptosis-associated proteins including Bax, Bcl-2, p38, phospho-p38 (p-p38), Jun amino-terminal kinases (JNK1/2), phospho-JNK1/2 (p-JNK1/2), calcium-sensing receptor (CasR), and Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) indicated that the inhibition of CRTAC1 alleviated oxidative stress and inflammation response, inactivated calcium-signaling pathway, p38 and JNK1/2 signal pathways, and eventually reduced UVB irradiation induced-apoptosis in HLECs. Conclusion: These results provided new insights into the mechanism of cataract development, and demonstrated that CRTAC1 could be a potentially novel target for cataract treatment.

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Section: +mentioning

confidence: 99%

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Xiao

et al. 2016

Cell Physiol Biochem

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“…The above analysis shows that Ca 2+ can affect AD. Strehler (42) already found that the CALML3 gene is involved in the transport of Ca 2+ . Therefore, the gene CALML3 will affect the onset of AD.…”

Section: Discussionmentioning

confidence: 99%

A Machine Learning Method for Identifying Critical Interactions Between Gene Pairs in Alzheimer's Disease Prediction

Chen

et al. 2019

Front. Neurol.

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Background: Alzheimer's disease (AD) is the most common type of dementia. Scientists have discovered that the causes of AD may include a combination of genetic, lifestyle, and environmental factors, but the exact cause has not yet been elucidated. Effective strategies to prevent and treat AD therefore remain elusive. The identified genetic causes of AD mainly focus on individual genes, but growing evidence has shown that complex diseases are usually affected by the interaction of genes in a network. Few studies have focused on the interactions and correlations between genes and how they are gradually destroyed or disappear during AD progression. A differential network analysis has been recognized as an essential tool for identifying the underlying pathogenic mechanisms and significant genes for prediction analysis. We therefore aim to conduct a differential network analysis to reveal potential networks involved in the neuropathogenesis of AD and identify genes for AD prediction.Methods: In this paper, we selected 365 samples from the Religious Orders Study and the Rush Memory and Aging Project, including 193 clinically and neuropathologically confirmed AD subjects and 172 no cognitive impairment (NCI) controls. Then, we selected 158 genes belonging to the AD pathway (hsa05010) of the Kyoto Encyclopedia of Genes and Genomes. We employed a machine learning method, namely, joint density-based non-parametric differential interaction network analysis and classification (JDINAC), in the analysis of gene expression data (RNA-seq data). We searched for the differential networks in the RNA-seq data with a pathological diagnosis of AD. Finally, an optimal prediction model was built through cross-validation, which showed good discrimination and calibration for AD prediction.Results: We used JDINAC to derive a gene co-expression network and to explore the relationship between the interaction of gene pairs and AD, and the top 10 differential gene pairs were identified. We then compared the prediction performance between JDINAC and individual genes based on prediction methods. JDINAC provides better accuracy of classification than the latest methods, such as random forest and penalized logistic regression.Conclusions: The interaction between gene pairs is related to AD and can provide more insight than the individual genes in AD prediction.

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“…There was no significant difference in the number of apoptotic between the groups treated with 2 W/m 2 and 4 W/m 2 UVB irradiation, thus 2 W/m 2 UVB irradiation was used in subsequent experiments. To further determine the effects of UVB irradiation on apoptosis of HLECs, the cells were also treated with 2 W/m 2 UVB for various durations (5,15,30,60, 90, 120 and 180 min). After 15 min irradiation, the number of apoptotic cells ~4.2%, and the percent of apoptotic cells was increased with the increasing duration of UVB irradiation (Fig.…”

Section: Uvb Induces Apoptosis Of Hlecsmentioning

confidence: 99%

“…Cellular calcium (Ca 2+ ) homeostasis in the lens epithelial cells is essential for maintaining lens clarity. Inappropriate Ca 2+ signaling and abnormal Ca 2+ levels are associated with various clinical disorders, including stroke, cardiac dysfunction, obesity, aging and Alzheimer's diseases (15)(16)(17)(18). Ca 2+ is also involved in cell growth, differentiation and motility during the transformation and progression of cancer.…”

Section: Introductionmentioning

confidence: 99%

UVB induces apoptosis via downregulation of CALML3-dependent JNK1/2 and ERK1/2 pathways in cataract

et al. 2018

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The aim of the current study was to understand the mechanisms of apoptosis occurring in cultured human lens epithelial cells (HLECs) following ultraviolet B (UVB) irradiation. The investigations intended to confirm the presence of apoptosis and to reveal the roles of oxidative stress, calcium (Ca2+), c‑Jun NH2‑terminal kinase (JNK)1/2, and extracellular signal‑regulated kinase (ERK)1/2 signaling pathway in these progresses. Cell apoptosis, ROS generation and intracellular Ca2+ concentration was measured by flow cytometry. The expression of CALML3, caspase-3, Bax, Bcl-2, p-JNK1/2, JNK1/2, p-ERK1/2 and ERK1/2 was measured by RT-qPCR and western blot analysis. Annexin V‑fluorescein isothiocyanate/propidium iodide staining demonstrated that UVB irradiation increased the apoptotic rate, reactive oxygen species (ROS) production and intracellular Ca2+ concentration of HLECs in dose‑ and time‑dependent manners. Overexpression of calmodulin like 3 (CALML3) reversed the effects of UVB irradiation on apoptosis, ROS production and Ca2+ concentration of HLECs, and decreased expressions of caspase‑3 and Bax, with increased expressions of Bcl‑2. Notably, silencing of CALML3 had similar effects to UVB irradiation and inhibited the activation JNK1/2 and ERK1/2 pathways. Nimodipine, a Ca2+‑channel antagonist, significantly attenuated the damages induced by CALML3 downregulation. In conclusion, UVB irradiation induced increase in apoptosis, ROS production and Ca2+ concentration of HLECs, in part, by downregulating the expression of CALML3 and involved oxidative stress, Ca2+, JNK1/2 and ERK1/2 signaling pathways, suggesting that investigating CALML3 may useful for developing cataract treatment.

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Emanuel Strehler’s work on calcium pumps and calcium signaling

Cited by 4 publications

References 38 publications

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

A Machine Learning Method for Identifying Critical Interactions Between Gene Pairs in Alzheimer's Disease Prediction

UVB induces apoptosis via downregulation of CALML3-dependent JNK1/2 and ERK1/2 pathways in cataract

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