4.6 Article

SERCA2b and 3 play a regulatory role in store-operated calcium entry in human platelets

期刊

CELLULAR SIGNALLING
卷 20, 期 2, 页码 337-346

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2007.10.019

关键词

SERCAs; SOCE; human platelet; 2,5-di-(tert-butyl)-1,4-hydroquinone; thapsigargin

向作者/读者索取更多资源

Two agonist-releasable Ca(2+)stores have been identified in human platelets differentiated by the distinct sensitivity of their SERCA isoforms to thapsigargin (TG) and 2,5-di-(tert-butyl)-1,4-hydroquinone (TBHQ). Here we have examined whether the SERCA isotypes might be involved in store-operated Ca(2+)entry (SOCE) activated by the physiological agonist thrombin in human platelets. Ca2+-influx evoked by thrombin (0.01 U/mL) reached a maximum after 3 min, which was consistent with the decrease in the Ca(2+)content in the stores; afterwards, the extent of SOLE decreased with no correlation with the accumulation of Ca(2+)in the stores. Inhibition of SERCA2b, by 10 nM TG, and SERCA3, with 20 mu M TBHQ, individually or simultaneously, accelerated Ca2+ store discharge and subsequently enhanced the extent of SOCE stimulated by thrombin. In addition, TG and TBHQ modified the time course of thrombin-evoked SOCE from a transient to a sustained increase in Ca2+ influx, which reveals a negative role for SERCAs in the regulation of SOLE. This effect was consistent under conditions that inhibit Ca2+ extrusion by PMCA or the Na+/Ca2+ exchanger. Coimmunoprecipitation experiments revealed that thrombin stimulates direct interaction between SERCA2b and 3 with the hTRPC1 channel, an effect that was found to be independent of SERCA activity. In summary, our results suggest that SERCA2b and 3 modulate thrombin-stimulated SOCE probably by direct interaction with the hTRPCI channel in human platelets. (C) 2007 Elsevier Inc. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

Review Cell Biology

Store-Operated Calcium Entry and Its Implications in Cancer Stem Cells

Isaac Jardin, Jose J. Lopez, Jose Sanchez-Collado, Luis J. Gomez, Gines M. Salido, Juan A. Rosado

Summary: Cancer stem cells exhibit stemness features and their behavior is influenced by Ca2+ homeostasis and store-operated Ca2+ entry. Understanding the key components of store-operated Ca2+ entry is important for the understanding of cancer stem cell biology and tumorigenesis.
Article Biochemistry & Molecular Biology

Melatonin controls cell proliferation and modulates mitochondrial physiology in pancreatic stellate cells

Matias Estaras, Candido Ortiz-Placin, Alba Castillejo-Rufo, Miguel Fernandez-Bermejo, Gerardo Blanco, Jose M. Mateos, Daniel Vara, Pedro L. Gonzalez-Cordero, Sandra Chamizo, Diego Lopez, Adela Rojas, Isabel Jaen, Noelia de Armas, Gines M. Salido, Juan L. Iovanna, Patricia Santofimia-Castano, Antonio Gonzalez

Summary: The effects of melatonin on cellular proliferation and energetic metabolism in pancreatic stellate cells were investigated. Melatonin was found to affect the phosphorylation levels of key kinases and proteins involved in cell proliferation and energy metabolism. It also induced mitochondrial oxidative stress and affected mitochondrial function, leading to changes in cell respiration and ATP production. These findings suggest that melatonin can modulate pancreatic stellate cell physiology and energy metabolism.

JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY (2023)

Article Oncology

Store-Operated Calcium Entry in Breast Cancer Cells Is Insensitive to Orai1 and STIM1 N-Linked Glycosylation

Jose Sanchez-Collado, Joel Nieto-Felipe, Isaac Jardin, Rajesh Bhardwaj, Alejandro Berna-Erro, Gines M. Salido, Tarik Smani, Matthias A. Hediger, Jose J. Lopez, Juan A. Rosado

Summary: Breast cancer cells exhibit altered expression and post-translational modification of STIM proteins and Orai channels, resulting in differences in store-operated Ca2+ entry (SOCE) compared to non-tumoral breast epithelial cells. This study showed that N-linked glycosylation of Orai1 and STIM1 is not essential for SOCE in breast cancer cells and may contribute to apoptosis resistance. Additionally, impairment of STIM1 N-linked glycosylation attenuated caspase-3 activation in non-tumoral cells, while breast cancer cells displayed smaller caspase-3 activity and were unaffected by the non-glycosylable STIM1 mutant. Abnormal SOCE and alterations in glycosylation are associated with cancer development and invasion.

CANCERS (2023)

Article Hematology

CAPN1 (Calpain1)-Dependent Cleavage of STIM1 (Stromal Interaction Molecule 1) Results in an Enhanced SOCE (Store-Operated Calcium Entry) in Human Neonatal Platelets

Alejandro Berna-Erro, Girish Ramesh, Elena Delgado, Antonio J. Corbacho, Francisca Ferrer-Marin, Raul Teruel, Maria P. Granados, Juan A. Rosado, Pedro C. Redondo

Summary: This study investigated the changes in Ca2+ entry through the store-operated calcium entry (SOCE) mechanism in neonatal platelets. The results showed altered TG-evoked SOCE, different molecular weight forms of STIM1, and overexpression of SARAF in neonatal platelets compared to maternal and control women platelets. It was also found that CAPN1 may cleave STIM1 in neonatal platelets, impairing SARAF coupling after SOCE activation.

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY (2023)

Review Cell Biology

Role of Orai-family channels in the activation and regulation of transcriptional activity

Joel Nieto-Felipe, Alvaro Macias-Diaz, Jose Sanchez-Collado, Alejandro Berna-Erro, Isaac Jardin, Gines M. Salido, Jose J. Lopez, Juan A. Rosado

Summary: Store operated Ca2+ entry (SOCE) is essential for maintaining intracellular Ca2+ homeostasis and regulating cellular functions. STIM and Orai proteins mediate SOCE, which is initiated by activation of inositol 1,4,5-trisphosphate receptors. STIM proteins sense the decrease in endoplasmic reticulum Ca2+ concentration and activate plasma membrane Ca2+ channels formed by Orai proteins. STIM1/Orai-mediated Ca2+ signals finely regulate the activity of various transcription factors and influence multiple signaling events and cellular functions.

JOURNAL OF CELLULAR PHYSIOLOGY (2023)

Correction Oncology

Orai2 Modulates Store-Operated Ca2+ Entry and Cell Cycle Progression in Breast Cancer Cells (vol 14, 114, 2021)

Jose Sanchez-Collado, Jose J. Lopez, Carlos Cantonero, Isaac Jardin, Sergio Regodon, Pedro C. Redondo, Juan Gordillo, Tarik Smani, Gines M. Salido, Juan A. Rosado

CANCERS (2023)

Article Pharmacology & Pharmacy

Cytotoxic Effects of New Palladium(II) Complexes with Thiazine or Thiazoline Derivative Ligands in Tumor Cell Lines

Elena Fernandez-Delgado, Samuel Estirado, Ana B. Rodriguez, Francisco Luna-Giles, Emilio Vinuelas-Zahinos, Javier Espino, Jose Antonio Pariente

Summary: Six squared-planar Pd(II) complexes with thiazine and thiazoline ligands were synthesized and characterized. Cytotoxicity assay showed that complexes with phenyl substitutions had the lowest IC50 values and induced apoptosis. The presence of bulky substitutions on the ligands, such as phenyl groups, may influence the cytotoxicity of the synthesized chemotherapeutic agents.

PHARMACEUTICS (2023)

Review Biochemistry & Molecular Biology

New Insights into the Reparative Angiogenesis after Myocardial Infarction

Marta Martin-Bornez, Debora Falcon, Rosario Morrugares, Geraldine Siegfried, Abdel-Majid Khatib, Juan A. A. Rosado, Isabel Galeano-Otero, Tarik Smani

Summary: Myocardial infarction (MI) leads to the loss of cardiac myocytes and damage to the coronary microcirculation, which exceeds the regenerative capacity of the heart. The repair process after MI involves angiogenesis, fibroblast proliferation, and scar formation. Various signaling pathways, including Notch, Wnt, PI3K, and modulation of intracellular Ca2+ concentration, regulate angiogenesis in the infarcted heart. Additionally, cell-to-cell communication through extracellular vesicles containing pro-angiogenic proteins and miRNAs plays a role in cardiac repair after MI.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2023)

Review Biochemistry & Molecular Biology

Thrombotic Alterations under Perinatal Hypoxic Conditions: HIF and Other Hypoxic Markers

Alejandro Berna-Erro, Maria Purificacion Granados, Juan Antonio Rosado, Pedro Cosme Redondo

Summary: Hypoxia is a stressful physiological condition that may occur during labor and pregnancy. Newborns adapt to temporary hypoxic conditions through changes in organ functions and intracellular molecular pathways. This review analyzes the main platelet modifications at the protein level during hypoxia and provides updates on research related to platelet markers and regulation of platelet function in response to hypoxia.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2023)

Article Biology

Secretion of Interleukin 6 in Human Skeletal Muscle Cultures Depends on Ca2+ Signalling

Blanca Calle-Ciborro, Teresa Espin-Jaime, Francisco J. Santos, Ana Gomez-Martin, Isaac Jardin, Maria J. Pozo, Juan A. Rosado, Pedro J. Camello, Cristina Camello-Almaraz

Summary: Skeletal muscle releases hormones called myokines, which interact with other organs and mediate the effects of physical activity. The release of interleukin 6 (IL-6), a myokine involved in inflammation, immunity, and metabolism, from muscle cells is not well understood. This study investigated the role of calcium ions in the release of IL-6 from human muscle cells and found that proteins responsible for calcium increase during stimulation induce IL-6 release. These findings could provide insights into the release of IL-6 and other myokines in pathological conditions.

BIOLOGY-BASEL (2023)

Article Cell Biology

DHX38 enhances proliferation, metastasis, and EMT progression in NSCLC through the G3BP1-mediated MAPK pathway

Ke Mi, Lizhong Zeng, Yang Chen, Jingya Ning, Siyuan Zhang, Peilin Zhao, Shuanying Yang

Summary: In this study, the researchers explored the role of DHX38 in NSCLC and its underlying molecular mechanism. They found that DHX38 was overexpressed in NSCLC and patients with high DHX38 expression had poor prognosis. DHX38 promoted cell proliferation, migration, and invasion in NSCLC and activated the MAPK pathway. The researchers also identified G3BP1 as a target protein that interacted with DHX38 and showed that DHX38 regulated the expression of G3BP1. Silencing G3BP1 reversed the effects of DHX38 overexpression on tumor cell proliferation, migration, and invasion and inhibited the MAPK pathway activation.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Functional delineation of the luminal epithelial microenvironment in breast using cell-based screening in combinatorial microenvironments

Tiina A. Jokela, Mark A. Dane, Rebecca L. Smith, Kaylyn L. Devlin, Sundus Shalabi, Jennifer C. Lopez, Masaru Miyano, Martha R. Stampfer, James E. Korkola, Joe W. Gray, Laura M. Heiser, Mark A. Labarge

Summary: Microenvironment signals have a significant impact on cell fate and tissue homeostasis. Understanding how different microenvironment factors regulate cellular phenotype has been challenging. In this study, a high-throughput microenvironment microarray was used to identify factors that support the proliferation and maintenance of primary human mammary luminal epithelial cells. Multiple factors that modulate luminal cell number were identified and their effects were confirmed using RNA sequencing and cell-based functional studies. Hepatocyte growth factor (HGF) was found to be robust to individual variation and played a role in expanding luminal cells. Our approach demonstrates the power of high-dimensional cell-based approaches in dissecting microenvironmental signals.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Stem cell landscape aids in tumor microenvironment identification and selection of therapeutic agents in gastric cancer

Chao He, Yongfeng Ding, Yan Yang, Gang Che, Fei Teng, Haohao Wang, Jing Zhang, Donghui Zhou, Yanyan Chen, Zhan Zhou, Haiyong Wang, Lisong Teng

Summary: This study categorized gastric cancer patients into three stemness subtypes, each demonstrating distinct prognoses, components of tumor microenvironment (TME) infiltration, and varying sensitivity or resistance to treatment. A stemness risk model was constructed to predict treatment response and prognosis.

CELLULAR SIGNALLING (2024)

Article Cell Biology

miR-29c-3p acts as a tumor promoter by regulating β-catenin signaling through suppressing DNMT3A, TET1 and HBP1 in ovarian carcinoma

Haile Zhao, Lijuan Feng, Rui Cheng, Man Wu, Xiaozhou Bai, Lifei Fan, Yaping Liu

Summary: miR-29c-3p is overexpressed in benign and malignant ovarian carcinoma and is associated with poor prognosis. Its overexpression modulates tumorigenesis in ovarian cancer cells, including epithelial-mesenchymal transition, proliferation, migration, and invasion, through the regulation of DNMT3A, TET1, and HBP1. miR-29c-3p may serve as a potential biomarker for clinical diagnosis or co-diagnosis of ovarian carcinoma.

CELLULAR SIGNALLING (2024)

Article Cell Biology

E3 ubiquitin ligase RNF180 impairs IPO4/SOX2 complex stability and inhibits SOX2-mediated malignancy in ovarian cancer

Haiyan Zhao, Fangfang Bi, Mengyuan Li, Yuhan Diao, Chen Zhang

Summary: This study confirmed the tumor suppressor effect of RNF180 on ovarian cancer, elucidated the mechanism of the molecule network related to RNF180 and IPO4 in ovarian cancer, and identified a new therapeutic target for ovarian cancer.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Decreased FoxO1 expression contributes to facet joint osteoarthritis pathogenesis by impairing chondrocyte migration and extracellular matrix synthesis

Chu Chen, Guanhua Xu, Jiajia Chen, Chunshuai Wu, Jinlong Zhang, Jiawei Jiang, Hongxiang Hong, Zhiming Cui

Summary: This study investigated the role of transcription factor FoxO1 in facet joint osteoarthritis (FJOA) and found that FoxO1 deletion led to severe osteoarthritic changes. Transcriptome sequencing and bioinformatics analysis identified differentially expressed genes (DEGs) and potential key contributors to FJOA. Additionally, over-expression of certain genes and inhibition of others were shown to counteract the impairments caused by FoxO1 deletion in chondrocyte migration and extracellular matrix synthesis. These findings help unravel the molecular mechanisms underlying FJOA and open up promising therapeutic avenues for its treatment.

CELLULAR SIGNALLING (2024)

Article Cell Biology

CircFSCN1 induces tumor progression and triggers epithelial-mesenchymal transition in bladder cancer through augmentation of MDM2-mediated p53 silencing

Wen Deng, Ru Chen, Situ Xiong, Jianqiang Nie, Hailang Yang, Ming Jiang, Bing Hu, Xiaoqiang Liu, Bin Fu

Summary: This study demonstrates that circFSCN1 is upregulated in bladder cancer and associated with cancer-specific survival. CircFSCN1 promotes tumor progression and epithelial-mesenchymal transition in bladder cancer through enhancing MDM2-mediated silencing of p53 by sponging miR-145-5p.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Knockdown of SQLE promotes CD8+T cell infiltration in the tumor microenvironment

Jun Wu, Weibin Hu, Wenhui Yang, Yihao Long, Kaizhao Chen, Fugui Li, Xiaodong Ma, Xun Li

Summary: Cholesterol biosynthesis and metabolism play critical roles in tumor development and microenvironmental conditions. Squalene Epoxidase (SQLE), the second rate-limiting enzyme in cholesterol synthesis, is found to be uniquely expressed in various cancers, and its expression level is closely associated with tumor mutation burden and microsatellite instability. SQLE expression is negatively correlated with immune cell infiltration. Inhibition of SQLE alters the immune response in the tumor microenvironment. Furthermore, protein metabolism and translation are identified as main binding factors with SQLE.

CELLULAR SIGNALLING (2024)

Article Cell Biology

ZNF70 regulates IL-1β secretion of macrophages to promote the proliferation of HCT116 cells via activation of NLRP3 inflammasome and STAT3 pathway in colitis-associated colorectal cancer

Zhihong Zhang, Mingyue Li, Yi Tai, Yue Xing, Hongxiang Zuo, Xuejun Jin, Juan Ma

Summary: ZNF70 plays an important role in colitis-associated colorectal cancer (CAC) by regulating macrophages IL-1 beta secretion to promote HCT116 proliferation. It may serve as a promising target for treating CAC.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Immune checkpoints signature-based risk stratification for prognosis of patients with gastric cancer

Zenghong Wu, Gangping Li, Weijun Wang, Kun Zhang, Mengke Fan, Yu Jin, Rong Lin

Summary: This study comprehensively explored the role of immune checkpoints and tumor microenvironment in gastric cancer patients based on genomic data. It constructed an ICIs signature and ICI score to evaluate patient prognosis and heterogeneity.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Inhibition of spinal Rac1 attenuates chronic inflammatory pain by regulating the activation of astrocytes

Yantong Wan, Jieshu Zhou, Panpan Zhang, Xuemei Lin, Hao Li

Summary: This study found that Rac1 plays a role in astrocyte activation and attenuates chronic inflammatory pain by blocking the phosphorylation of NLRP3 inflammasome and NF-kappa B.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Circular RNA CircSATB2 facilitates osteosarcoma progression through regulating the miR-661/FUS-mediated mRNA of ZNFX1

Zhen Wang, Diankun She, Lei Liu, Xianming Hua, Hao Zhu, Lingfeng Yu, Han Wang, Yan Zhu, Gentao Fan, Yicun Wang, Meng Xu, Guangxin Zhou

Summary: Circular RNAs (circRNAs) are non-coding RNAs that play a role in the regulation of various cancers, including osteosarcoma (OS). This study identified circSATB2 as a highly expressed circRNA in OS tissues and cell lines, and demonstrated its involvement in promoting OS proliferation and migration. Mechanistically, circSATB2 was found to regulate the progression of OS by sponging miR-661 and FUS to regulate ZNFX1 mRNA. These findings suggest that circSATB2 could serve as a prognostic marker and therapeutic target for osteosarcoma.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Extracellular vesicles of iPS cells highly capable of producing HGF and TGF-β1 can attenuate Sjogren's syndrome via innate immunity regulation

Kenichi Ogata, Masafumi Moriyama, Tatsuya Kawado, Hiroki Yoshioka, Aiko Yano, Mayu Matsumura-Kawashima, Seiji Nakamura, Shintaro Kawano

Summary: This study found that extracellular vesicles released by induced pluripotent stem cells can reduce inflammatory cell infiltration, increase saliva volume, and decrease the production of antibodies associated with Sjogren's syndrome in a mouse model. The let-7 family in these vesicles may suppress the expression of TLR4 and NF-kappa B, which leads to the inhibition of pro-inflammatory cytokine production through the MAPK pathway.

CELLULAR SIGNALLING (2024)

Article Cell Biology

Phosphodiesterase 4 activity uniquely regulates ciliary cAMP-dependent 3T3-L1 adipogenesis

Mikayla R. Erdelsky, Sarah A. Groves, Charmi Shah, Samantha B. Delios, M. Bibiana Umana, Donald H. Maurice

Summary: Recent evidence suggests that cAMP signaling within the primary cilium plays a crucial role in promoting adipogenic differentiation of 3T3-L1 preadipocytes. In this study, the researchers identified the specific cAMP phosphodiesterases expressed by these cells and found that inhibition of PDE4 promotes FFAR4-mediated adipogenesis. This work could potentially lead to the discovery of more targeted therapeutic approaches for controlling adipogenesis and differentiation of other stem cells.

CELLULAR SIGNALLING (2024)

Article Cell Biology

METTL3 regulates the proliferation, metastasis and EMT progression of bladder cancer through P3H4

Chun-Hui Liu, Jun-Jie Zhang, Qian-Jin Zhang, Yang Dong, Zhen-Duo Shi, Si-Hao Hong, Hou-Guang He, Wei Wu, Cong-Hui Han, Lin Hao

Summary: Bladder cancer, the most common malignant tumor in the urinary system, is associated with significantly up-regulated expression of P3H4, which is regulated by METTL3 and plays a crucial role in the proliferation, metastasis, and EMT progression of bladder cancer. Targeting this METTL3-P3H4 pathway may serve as a potential therapeutic strategy for bladder cancer.

CELLULAR SIGNALLING (2024)