Cellular Physiology and Biochemistry

Journal Information
ISSN / EISSN : 10158987 / 14219778
Current Publisher: Cell Physiol Biochem Press GmbH and Co KG (10.33594)
Former Publisher: S. Karger AG (10.1159)
Total articles ≅ 5,994
Google Scholar h5-index: 52
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Latest articles in this journal

Rui Curi, Adriana Cristina Levada-Pires, Eliane Borges Da Silva, Sarah De Oliveira Poma, Raquel Freitas Zambonatto, Paola Domenech, Mariana Mendes De Almeida, Raquel Bragante Gritte, Talita Souza-Siqueira, Renata Gorjão, et al.
Cellular Physiology and Biochemistry, Volume 54, pp 629-647; doi:10.33594/000000245

Tomasz Jędrzejewski, Małgorzata Pawlikowska, Justyna Sobocińska, Sylwia Wrotek
Cellular Physiology and Biochemistry, Volume 54, pp 615-628; doi:10.33594/000000244

Abstract:
The tumour microenvironment is rich in multiple cells that influence cancer development. Among them, macrophages are the most abundant immune cells, which secrete factors involved in carcinogenesis. Since protein-bound polysaccharides (PBP) from the Coriolus versicolor fungus are believed to inhibit the growth of cancers, in the present study, we investigated whether these PBP influence crosstalk between triple-negative 4T1 breast cancer cells and RAW 264.7 macrophages. 4T1 cells were cultured in conditioned media (CM) collected after: stimulation of the macrophages with PBP (CM-PBP) or incubation of non-treated macrophages (CM-NT). A co-cultured model of both cell lines was also employed to investigate the crosstalk between the cells. Cell viability was measured using the MTT assay. The levels of cytokines and chemokines were determined by ELISA methods. Commercial assay kits were used to assess the activity of both arginase 1 and inducible nitric oxide synthase (iNOS) and the level of cell migration. The results revealed that CM-NT promotes proliferation and migration of 4T1 cells, and increases the secretion of pro-angiogenic factors (VEGF, MCP-1) by cancer cells. In contrast, CM-PBP inhibits 4T1 cell growth and migration, decreases the secretion of pro-angiogenic factors (VEGF, MCP-1) and upregulates the production of pro-inflammatory mediators (IL-6, TNF-α) with certain anti-tumoral properties Moreover, PBP-treated CM significantly decreases the level of M2 macrophage markers (arginase 1 activity, IL-10 and TGF-β concentrations), but upregulates iNOS activity and IL-6 and TNF-α production, which are M1 cell markers. The results suggest that PBP suppress the favourable tumour microenvironment by inhibiting the crosstalk between 4T1 cells and macrophages through the regulation of production of angiogenic and inflammatory mediators, and modulating the M1/M2 macrophage subtype.
Ichiro Katahira, Sakurako Neo, Masaki Nagane, Saki Miyagi, Masaharu Hisasue, Abdulla Al Mamum Bhuyan
Cellular Physiology and Biochemistry, Volume 54, pp 605-614; doi:10.33594/000000243

The publisher has not yet granted permission to display this abstract.
Małgorzata Pawlikowska, Tomasz Jędrzejewski, Anna A. Brożyna, Sylwia Wrotek
Cellular Physiology and Biochemistry, Volume 54, pp 591-604; doi:10.33594/000000242

The publisher has not yet granted permission to display this abstract.
Bianca Flores, Eric Delpire
Cellular Physiology and Biochemistry, Volume 54, pp 577-590; doi:10.33594/000000241

Abstract:
Loss-of-Function (LOF) of the potassium chloride cotransporter 3 (KCC3) results in hereditary sensorimotor neuropathy with Agenesis of the Corpus Callosum (HSMN/ACC). Our KCC3 knockout mouse recapitulated axonal swelling and tissue vacuolization observed in autopsies of individuals with HSMN/ACC. We previously documented the first human case of a KCC3 gain-of-function (GOF) in which the patient also exhibited severe peripheral neuropathy. Furthermore, the GOF mouse model exhibited shrunken axons implicating the cotransporter in cell volume homeostasis. It is unclear how both KCC3 LOF and GOF lead to peripheral neuropathy. Thus, we sought to study differences in cell volume regulation of dorsal root ganglion neurons isolated from different mouse lines. Using wide-field microscopy, we measured calcein fluorescence intensity through pinhole measurements at the center of cells and compared cell swelling and cell volume regulation/recovery of wild-type, LOF, and GOF dorsal root ganglia neurons, as well as wild-type neurons treated with a KCC-specific inhibitor. In contrast to control neurons that swell and volume regulate under a hypotonic challenge, neurons lacking KCC3 swell but fail to volume regulate. Similar data were observed in wild-type neurons treated with the KCC inhibitor. We also show that sensory neurons expressing a constitutively active KCC3 exhibited a blunted swelling phase compared to wild-type neurons, questioning the purely osmotic nature of the swelling phase. These findings demonstrate the integral role of KCC3 in cell volume homeostasis and support the idea that cell volume homeostasis is critical to the health of peripheral nerves.
Ricardo Aparecido Baptista Nucci, Laura Beatriz Mesiano Maifrino, Alexandre Leopold Busse, Romeu Rodrigues De Souza, Carlos Augusto Pasqualucci, Carlos Alberto Anaruma, Renata Elaine Paraizo Leite, Roberta Diehl Rodriguez, Claudia Kimie Suemoto, Wilson Jacob-Filho
Cellular Physiology and Biochemistry, Volume 54, pp 567-576; doi:10.33594/000000240

The publisher has not yet granted permission to display this abstract.
Valentina E. Yurinskaya, Nikolay D. Aksenov, Alexey V. Moshkov, Tatyana S. Goryachaya, Alexey A. Vereninov
Cellular Physiology and Biochemistry, Volume 54, pp 556-566; doi:10.33594/000000239

The publisher has not yet granted permission to display this abstract.
Rafiqul Islam, Toshiaki Okada, Petr G. Merzlyak, Abduqodir H. Toychiev, Yuhko Ando-Akatsuka, Ravshan Z. Sabirov, Yasunobu Okada
Cellular Physiology and Biochemistry, Volume 54, pp 538-555; doi:10.33594/000000238

Abstract:
Maxi-anion channel (Maxi-Cl) is ubiquitously expressed and involved in a number of important cell functions especially by serving as an ATP release pathway. We recently identified SLCO2A1 as its essential core component. However, the regulatory component required for the channel activation/inactivation remains unidentified. In the present study, to identify the regulatory component, we made genome-wide analysis combined with siRNA screening and performed patch-clamp studies and ATP release assay after gene silencing and overexpression. Comparative microarray analysis between Maxi-Cl-rich C127 and -deficient C1300 cells revealed highly differential expression not only of SLCO2A1 but also of four annexin family members. Gene silencing study showed that Anxa2 is involved in Maxi-Cl activity. The Maxi-Cl events appeared in C1300 cells by overexpression of Slco2a1 and more efficiently by that of Slco2a1 plus Anxa2. Immunoprecipitation assay supported the interaction between ANXA2 and SLCO2A1. Suppressive effects of overexpression of a phospho-mimicking mutant of Anxa2, Anxa2-Y23E, indicated that protein tyrosine dephosphorylation dependence of Maxi-Cl is conferred by ANXA2. Maxi-Cl activity was suppressed by gene silencing of S100A10, a binding partner of ANXA2, and by applying a synthetic ANXA2 peptide, Ac-(1-14), which interferes with the ANXA2-S100A10 complex formation. Intracellular Ca2+ dependence of Maxi-Cl activity was abolished by S100a10 knockdown. The ANXA2-S100A10 complex represents the regulatory component of Maxi-Cl conferring protein tyrosine dephosphorylation dependence and intracellular Ca2+ sensitivity on this channel.
Hala Guedouari, Marie-Claude Savoie, Stéphanie Jean, Marie-Ange Djeungoue-Petga, Nicolas Pichaud, Etienne Hebert-Chatelain
Cellular Physiology and Biochemistry, Volume 54, pp 517-537; doi:10.33594/000000237

Abstract:
Src kinase family members, including c-Src, are involved in numerous signaling pathways and have been observed inside different cellular compartments. Notably, c-Src modulates carbohydrate and fatty acid metabolism and is involved in the metabolic rewiring of cancer cells. This kinase is found within mitochondria where it targets different proteins to impact on the organelle functions and overall metabolism. Surprisingly, no global metabolic characterization of Src has been performed although c-Src knock-out mice have been available for 30 years. Considering that c-Src is sensitive to various metabolites, c-Src might represent a crucial player in metabolic adjustments induced by nutrient stress. The aim of this work was to characterize the impact of c-Src on mitochondrial activity and overall metabolism using multi-omic characterization. Src+/+ and Src-/- mice were fed ad libitum or fasted during 24h and were then analyzed using multi-omics. We observed that deletion of c-Src is linked to lower phosphorylation of Y412-NDUFA8, inhibition of oxygen consumption and accumulation of metabolites involved in glycolysis, TCA cycle and amino acid metabolism in mice fed ad libitum. Finally, metabolomics and (phosphotyrosine) proteomics are differently impacted by Src according to nutrient availability. The findings presented here highlight that c-Src reduces mitochondrial metabolism and impacts the metabolic adjustment induced by nutrient stress.
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