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  1. Article ; Online: Improving therapeutic potential in breast cancer via histone deacetylase inhibitor loaded nanofibrils.

    Senthilkumar, Praveetha / Gogoi, Bhaskar / Dhan, Swati Smita / Subramani, Ramesh / Pushparaj, Charumathi / Mahesh, Ayyavu

    Drug development research

    2024  Volume 85, Issue 2, Page(s) e22172

    Abstract: Epigenetic modifications play a significant role in cancer progression, making them potential targets for therapy. Histone deacetylase inhibitors have shown promise in inhibiting cancer cell growth, including in breast cancer (BC). In this research, we ... ...

    Abstract Epigenetic modifications play a significant role in cancer progression, making them potential targets for therapy. Histone deacetylase inhibitors have shown promise in inhibiting cancer cell growth, including in breast cancer (BC). In this research, we examined the potential of using suberoyl anilide hydroxamic acid (SAHA)-loaded β-lg nanofibrils as a drug delivery system for triple-negative BC cell lines. We assessed their impact on cell cycle progression, apoptosis, levels of reactive oxygen species, and mitochondrial membrane potential in cancer cells. The combination of SAHA and β-lg nanofibrils demonstrated enhanced efficacy in inhibiting cell growth, inducing cell cycle arrest, and promoting apoptosis (43.78%) compared to SAHA alone (40.09%). Moreover, it effectively targeted cancer cells without promoting drug resistance while using a low concentration of the nanofibrils. These findings underscore the promising potential of nanofibril-based drug delivery systems for BC treatment.
    MeSH term(s) Humans ; Female ; Histone Deacetylase Inhibitors/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Hydroxamic Acids/pharmacology ; Vorinostat/pharmacology ; Vorinostat/therapeutic use ; Cell Cycle ; Apoptosis ; Cell Proliferation ; Cell Line, Tumor ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use
    Chemical Substances Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Vorinostat (58IFB293JI) ; Antineoplastic Agents
    Language English
    Publishing date 2024-03-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604587-x
    ISSN 1098-2299 ; 0272-4391
    ISSN (online) 1098-2299
    ISSN 0272-4391
    DOI 10.1002/ddr.22172
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 2542: Show issues Location:
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  2. Article ; Online: Utilizing protein nanofibrils as a scaffold for enhancing nutritional value in toned milk.

    Senthilkumar, Praveetha / Natarajan, Arunadevi / Salmen, Saleh H / Alharbi, Sulaiman Ali / Shavrov, Vladimir / Lega, Petr / Subramani, Ramesh / Pushparaj, Charumathi

    Environmental research

    2023  Volume 239, Issue Pt 2, Page(s) 117420

    Abstract: Toned milk is a lower-fat, healthier alternative to whole milk that still contains all essential nutrients. A number of methods have been developed to improve the functionality of toned milk and make it more appealing to the consumers. However, these ... ...

    Abstract Toned milk is a lower-fat, healthier alternative to whole milk that still contains all essential nutrients. A number of methods have been developed to improve the functionality of toned milk and make it more appealing to the consumers. However, these methods often involve extensive processing techniques and can be expensive. Therefore, alternative methods are needed. Proteins are well known for their ability to form well-defined nanofibril materials that can be used as a scaffold for various applications. In this article, a straightforward self-assembly process was used to load inulin into protein nanofibrils, creating unique composite nanofibrils. Characterization using AFM and SEM revealed well-defined composite nanofibrils with an average diameter of 4-6 nm and lengths ranging from 0.25 μm up to 10 μm. FT-IR and in-vitro release assays show that inulin was successfully attached to prepared protein nanofibrils. The composite nanofibrils were tested on toned milk to enhance the physico/chemical properties and nutritional values. The findings can be applied to the food industry to create a number of novel functional food products cost-effectively.
    MeSH term(s) Animals ; Milk/chemistry ; Inulin/analysis ; Spectroscopy, Fourier Transform Infrared ; Nutritive Value
    Chemical Substances Inulin (9005-80-5)
    Language English
    Publishing date 2023-10-16
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 205699-9
    ISSN 1096-0953 ; 0013-9351
    ISSN (online) 1096-0953
    ISSN 0013-9351
    DOI 10.1016/j.envres.2023.117420
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Inhibition of WNT-CTNNB1 signaling upregulates SQSTM1 and sensitizes glioblastoma cells to autophagy blockers.

    Nàger, Mireia / Sallán, Marta C / Visa, Anna / Pushparaj, Charumathi / Santacana, Maria / Macià, Anna / Yeramian, Andrée / Cantí, Carles / Herreros, Judit

    Autophagy

    2018  Volume 14, Issue 4, Page(s) 619–636

    Abstract: WNT-CTNN1B signaling promotes cancer cell proliferation and stemness. Furthermore, recent evidence indicates that macroautophagy/autophagy regulates WNT signaling. Here we investigated the impact of inhibiting WNT signaling on autophagy in glioblastoma ( ... ...

    Abstract WNT-CTNN1B signaling promotes cancer cell proliferation and stemness. Furthermore, recent evidence indicates that macroautophagy/autophagy regulates WNT signaling. Here we investigated the impact of inhibiting WNT signaling on autophagy in glioblastoma (GBM), a devastating brain tumor. Inhibiting TCF, or silencing TCF4 or CTNNB1/β-catenin upregulated SQSTM1/p62 in GBM at transcriptional and protein levels and, in turn, autophagy. DKK1/Dickkopf1, a canonical WNT receptor antagonist, also induced autophagic flux. Importantly, TCF inhibition regulated autophagy through MTOR inhibition and dephosphorylation, and nuclear translocation of TFEB, a master regulator of lysosomal biogenesis and autophagy. TCF inhibition or silencing additionally affected GBM cell proliferation and migration. Autophagy induction followed by its blockade can promote cancer cell death. In agreement with this notion, halting both TCF-CTNNB1 and autophagy pathways decreased cell viability and induced apoptosis of GBM cells through a SQSTM1-dependent mechanism involving CASP8 (caspase 8). In vivo experiments further underline the therapeutic potential of such dual targeting in GBM.
    MeSH term(s) Autophagy/drug effects ; Autophagy/physiology ; Cell Line, Tumor ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Humans ; Lysosomes/drug effects ; Lysosomes/metabolism ; RNA, Small Interfering/genetics ; Sequestosome-1 Protein/metabolism ; Signal Transduction/drug effects ; Transcription Factor 4/genetics ; beta Catenin/drug effects ; beta Catenin/metabolism
    Chemical Substances CTNNB1 protein, human ; RNA, Small Interfering ; SQSTM1 protein, human ; Sequestosome-1 Protein ; TCF4 protein, human ; Transcription Factor 4 ; beta Catenin
    Language English
    Publishing date 2018-02-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2017.1423439
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6741: Show issues Location:
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  4. Article ; Online: Voltage-gated calcium channel blockers deregulate macroautophagy in cardiomyocytes.

    Pushparaj, Charumathi / Das, Arindam / Purroy, Rosa / Nàger, Mireia / Herreros, Judit / Pamplona, Reinald / Cantí, Carles

    The international journal of biochemistry & cell biology

    2015  Volume 68, Page(s) 166–175

    Abstract: Voltage-gated calcium channel blockers are widely used for the management of cardiovascular diseases, however little is known about their effects on cardiac cells in vitro. We challenged neonatal ventricular cardiomyocytes (CMs) with therapeutic L-type ... ...

    Abstract Voltage-gated calcium channel blockers are widely used for the management of cardiovascular diseases, however little is known about their effects on cardiac cells in vitro. We challenged neonatal ventricular cardiomyocytes (CMs) with therapeutic L-type and T-type Ca(2+) channel blockers (nifedipine and mibefradil, respectively), and measured their effects on cell stress and survival, using fluorescent microscopy, Q-PCR and Western blot. Both nifedipine and mibefradil induced a low-level and partially transient up-regulation of three key mediators of the Unfolded Protein Response (UPR), indicative of endoplasmic (ER) reticulum stress. Furthermore, nifedipine triggered the activation of macroautophagy, as evidenced by increased lipidation of microtubule-associated protein 1 light chain 3 (LC3), decreased levels of polyubiquitin-binding protein p62/SQSTM1 and ubiquitinated protein aggregates, that was followed by cell death. In contrast, mibefradil inhibited CMs constitutive macroautophagy and did not promote cell death. The siRNA-mediated gene silencing approach confirmed the pharmacological findings for T-type channels. We conclude that L-type and T-type Ca(2+) channel blockers induce ER stress, which is divergently transduced into macroautophagy induction and inhibition, respectively, with relevance for cell viability. Our work identifies VGCCs as novel regulators of autophagy in the heart muscle and provides new insights into the effects of VGCC blockers on CMs homeostasis, that may underlie both noxious and cardioprotective effects.
    MeSH term(s) Animals ; Animals, Newborn ; Autophagy/drug effects ; Calcium Channel Blockers/pharmacology ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Calcium Channels, L-Type/genetics ; Calcium Channels, L-Type/metabolism ; Calcium Channels, T-Type/genetics ; Calcium Channels, T-Type/metabolism ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Endoplasmic Reticulum Stress/drug effects ; Gene Expression Regulation ; Heart Ventricles/cytology ; Heart Ventricles/drug effects ; Heart Ventricles/metabolism ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Macrolides/pharmacology ; Mibefradil/pharmacology ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Nifedipine/pharmacology ; Rats ; Sequestosome-1 Protein ; Signal Transduction ; Thapsigargin/pharmacology ; Unfolded Protein Response/drug effects
    Chemical Substances Cacna1g protein, rat ; Cacna1h protein, rat ; Calcium Channel Blockers ; Calcium Channels ; Calcium Channels, L-Type ; Calcium Channels, T-Type ; Heat-Shock Proteins ; L-type calcium channel alpha(1C) ; LC3 protein, rat ; Macrolides ; Microtubule-Associated Proteins ; Sequestosome-1 Protein ; Sqstm1 protein, rat ; Cacna1d protein, rat (166872-16-8) ; Mibefradil (27B90X776A) ; Thapsigargin (67526-95-8) ; bafilomycin A1 (88899-55-2) ; Nifedipine (I9ZF7L6G2L)
    Language English
    Publishing date 2015-11
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2015.09.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 431: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Voltage-gated calcium channel blockers deregulate macroautophagy in cardiomyocytes

    Pushparaj, Charumathi / Arindam Das / Carles Cantí / Judit Herreros / Mireia Nàger / Reinald Pamplona / Rosa Purroy

    International Journal of Biochemistry and Cell Biology. 2015 Nov., v. 68

    2015  

    Abstract: Voltage-gated calcium channel blockers are widely used for the management of cardiovascular diseases, however little is known about their effects on cardiac cells in vitro.We challenged neonatal ventricular cardiomyocytes (CMs) with therapeutic L-type ... ...

    Abstract Voltage-gated calcium channel blockers are widely used for the management of cardiovascular diseases, however little is known about their effects on cardiac cells in vitro.We challenged neonatal ventricular cardiomyocytes (CMs) with therapeutic L-type and T-type Ca2+ channel blockers (nifedipine and mibefradil, respectively), and measured their effects on cell stress and survival, using fluorescent microscopy, Q-PCR and Western blot. Both nifedipine and mibefradil induced a low-level and partially transient up-regulation of three key mediators of the Unfolded Protein Response (UPR), indicative of endoplasmic (ER) reticulum stress. Furthermore, nifedipine triggered the activation of macroautophagy, as evidenced by increased lipidation of microtubule-associated protein 1 light chain 3 (LC3), decreased levels of polyubiquitin-binding protein p62/SQSTM1 and ubiquitinated protein aggregates, that was followed by cell death. In contrast, mibefradil inhibited CMs constitutive macroautophagy and did not promote cell death. The siRNA-mediated gene silencing approach confirmed the pharmacological findings for T-type channels.We conclude that L-type and T-type Ca2+ channel blockers induce ER stress, which is divergently transduced into macroautophagy induction and inhibition, respectively, with relevance for cell viability. Our work identifies VGCCs as novel regulators of autophagy in the heart muscle and provides new insights into the effects of VGCC blockers on CMs homeostasis, that may underlie both noxious and cardioprotective effects.
    Keywords autophagy ; calcium channel blockers ; calcium channels ; cardiomyocytes ; cardioprotective effect ; cardiovascular diseases ; cell viability ; fluorescence microscopy ; gene silencing ; homeostasis ; muscles ; protein aggregates ; reticulum ; unfolded protein response ; Western blotting
    Language English
    Dates of publication 2015-11
    Size p. 166-175.
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2015.09.010
    Database NAL-Catalogue (AGRICOLA)

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    Zs.A 431: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article ; Online: T-type calcium channel blockers inhibit autophagy and promote apoptosis of malignant melanoma cells.

    Das, Arindam / Pushparaj, Charumathi / Herreros, Judit / Nager, Mireia / Vilella, Ramon / Portero, Manuel / Pamplona, Reinald / Matias-Guiu, Xavier / Martí, Rosa M / Cantí, Carles

    Pigment cell & melanoma research

    2013  Volume 26, Issue 6, Page(s) 874–885

    Abstract: We have recently reported that human melanoma cells express a variety of voltage-gated calcium (Ca(2+) ) channel types, including low-voltage-activated T-type channels that play a significant role in melanoma cell cycle progression. Here, we challenged ... ...

    Abstract We have recently reported that human melanoma cells express a variety of voltage-gated calcium (Ca(2+) ) channel types, including low-voltage-activated T-type channels that play a significant role in melanoma cell cycle progression. Here, we challenged melanoma metastatic cells with T-type channel blockers of clinical use and found a dual effect on cell viability: (i) a reduction in the proliferation rate, through a halt in the progression to the G1 -S phase; and (ii) a promotion of cell death that was partially dependent on the activation of caspases. An in-depth analysis of the death process showed that the apoptotic pathway is preceded by endoplasmic reticulum stress and the subsequent inhibition of the basal macroautophagy which is active in these cells. The effects of pharmacological blockers on Ca(2+) homeostasis, autophagy, and cell death were mimicked by T-type channel gene silencing. These results provide the basis for a new pharmacological and/or gene silencing approach toward tackling melanoma metastasis.
    MeSH term(s) Apoptosis/drug effects ; Autophagy/drug effects ; Calcium Channel Blockers/pharmacology ; Calcium Channels, T-Type/metabolism ; Caspases/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Endoplasmic Reticulum Stress/drug effects ; Enzyme Activation/drug effects ; Gene Knockdown Techniques ; Gene Silencing/drug effects ; Humans ; Melanocytes/drug effects ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/enzymology ; Melanoma/pathology ; Mitochondria/drug effects ; Mitochondria/enzymology ; Skin Neoplasms ; Unfolded Protein Response/drug effects ; Melanoma, Cutaneous Malignant
    Chemical Substances Calcium Channel Blockers ; Calcium Channels, T-Type ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2013-09-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.12155
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2444: Show issues Location:
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