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  1. Article ; Online: The relevance of the supramolecular arrangements of the respiratory chain complexes in human diseases and aging.

    Ramírez-Camacho, Ixchel / Flores-Herrera, Oscar / Zazueta, Cecilia

    Mitochondrion

    2019  Volume 47, Page(s) 266–272

    Abstract: Mitochondrial dysfunction, a common factor in several diseases is accompanied with reactive oxygen species (ROS) production. These molecules react with proteins and lipids at their site of generation, establishing a vicious cycle which might result in ... ...

    Abstract Mitochondrial dysfunction, a common factor in several diseases is accompanied with reactive oxygen species (ROS) production. These molecules react with proteins and lipids at their site of generation, establishing a vicious cycle which might result in further mitochondrial injury. It is well established that mitochondrial respiratory complexes can be organized into supramolecular structures called supercomplexes (SCs) or respirasomes; yet, the physiological/pathological relevance of these structures remains unresolved. Changes in their stabilization and content have been documented in Barth's syndrome, degenerative diseases such as Parkinson's and Alzheimer, cardiovascular diseases including heart failure and ischemia-reperfusion damage, as well as in aging. Under pathological conditions, SCs stability could have relevant biomedical implications or might be used as a reliable marker of mitochondrial damage. The purpose of this review is to recapitulate the current state of the significance on mitochondrial bioenergetics of these structures and their possible role in pathophysiologies related with ROS increase.
    MeSH term(s) Aging/metabolism ; Aging/pathology ; Alzheimer Disease/enzymology ; Alzheimer Disease/pathology ; Animals ; Barth Syndrome/enzymology ; Barth Syndrome/pathology ; Electron Transport Chain Complex Proteins/metabolism ; Energy Metabolism ; Humans ; Mitochondria/enzymology ; Mitochondrial Membranes/metabolism ; Mitochondrial Membranes/pathology ; Parkinson Disease/enzymology ; Parkinson Disease/pathology ; Reactive Oxygen Species/metabolism
    Chemical Substances Electron Transport Chain Complex Proteins ; Reactive Oxygen Species
    Language English
    Publishing date 2019-01-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2056923-3
    ISSN 1872-8278 ; 1567-7249
    ISSN (online) 1872-8278
    ISSN 1567-7249
    DOI 10.1016/j.mito.2019.01.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Altered proximal tubule fatty acid utilization, mitophagy, fission and supercomplexes arrangement in experimental Fanconi syndrome are ameliorated by sulforaphane-induced mitochondrial biogenesis.

    Briones-Herrera, Alfredo / Ramírez-Camacho, Ixchel / Zazueta, Cecilia / Tapia, Edilia / Pedraza-Chaverri, José

    Free radical biology & medicine

    2020  Volume 153, Page(s) 54–70

    Abstract: The kidney proximal tubule function relies on oxidative phosphorylation (OXPHOS), thus mitochondrial dysfunction is characteristic of acute kidney injury (AKI). Maleic acid (MA) can induce an experimental model of Fanconi syndrome that is associated to ... ...

    Abstract The kidney proximal tubule function relies on oxidative phosphorylation (OXPHOS), thus mitochondrial dysfunction is characteristic of acute kidney injury (AKI). Maleic acid (MA) can induce an experimental model of Fanconi syndrome that is associated to oxidative stress and decreased oxygen consumption. Sulforaphane (SF) is an antioxidant known to protect against MA-induced AKI. The molecular basis by which SF maintains the bioenergetics in MA-induced AKI is not fully understood. To achieve it, rats were submitted to a protective scheme: SF (1 mg/kg/day i.p.) for four days and, at the fourth day, they received a single dose of MA (400 mg/kg i.p.), getting four main experimental groups: (1) control (CT), (2) MA-nephropathy (MA), (3) SF-protected and (4) SF-control (SF). Additionally, a similar protective schema was tested in cultured NRK-52E cells with different concentrations of SF and MA. In the animal model, SF prevented the MA-induced alterations: decrease in fatty acid-related oxygen consumption rate, OXPHOS capacity, mitochondrial membrane potential (Ψ
    MeSH term(s) Animals ; Fanconi Syndrome/chemically induced ; Fanconi Syndrome/drug therapy ; Fanconi Syndrome/genetics ; Fatty Acids ; Isothiocyanates ; Mitophagy ; Organelle Biogenesis ; Rats ; Sulfoxides
    Chemical Substances Fatty Acids ; Isothiocyanates ; Sulfoxides ; sulforaphane (GA49J4310U)
    Language English
    Publishing date 2020-04-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2020.04.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Effects of calcitriol upon TGF-βs and their receptors in trophoblast cells.

    Noyola-Martínez, Nancy / Chirinos, Mayel / Ramírez-Camacho, Ixchel / Escamilla-Bucio, Joselin Estefania / García-Olivares, Mitzi / Aragón-Hernández, Juan Pablo / Segovia-Mendoza, Mariana / Halhali, Ali / Barrera, David

    Journal of reproductive immunology

    2023  Volume 161, Page(s) 104181

    Abstract: Calcitriol levels increase during pregnancy, contributing to the hormonal and immunological balance, but its deficiency has been associated with problems during this period. Meanwhile, transforming growth factors-β (TGF-βs) play an important role in the ... ...

    Abstract Calcitriol levels increase during pregnancy, contributing to the hormonal and immunological balance, but its deficiency has been associated with problems during this period. Meanwhile, transforming growth factors-β (TGF-βs) play an important role in the maintenance of fetal-maternal immune tolerance; however, exacerbated concentrations of this growth factor are associated with complicated pregnancies. Therefore, we studied the effects of calcitriol on TGF-βs and their receptors in trophoblast cells. Term placentas from uncomplicated pregnancies after cesarean sections were used for cell cultures. Basal gene expression and the effect of calcitriol upon TGF-β1, TGF-β2, TGF-β3, and their receptors TGF-βR1 and TGF-βR2 were assessed using real-time PCR from trophoblast cells. The presence of TGF-β1, 2, 3, and TGF-βR1 were evaluated by immunofluorescence, and the protein abundance and secretion of TGF-β1 were assessed by Western blot and ELISA, respectively. Basal gene expression of TGF-β1 in trophoblast from term placentas was higher than TGF-β2 and TGF-β3, while TGF-βR2 was higher than TGF-βR1. The presence and cellular localization of TGF-β1, 2, 3, and TGF-βR1 were detected in the cytoplasm of syncytiotrophoblast, with TGF-β1 showing the highest intensity. Calcitriol significantly inhibited gene expression of TGF-β1, TGF-β2, and TGF-βR1. Likewise, calcitriol decreased the secretion and abundance of TGF-β1. In conclusion, results indicate that calcitriol is a regulator of TGF-βs in cultured trophoblast cells from term placentas and therefore may be an important player in the development of healthy pregnancies.
    MeSH term(s) Humans ; Pregnancy ; Female ; Transforming Growth Factor beta1 ; Transforming Growth Factor beta2 ; Calcitriol/pharmacology ; Transforming Growth Factor beta3 ; Trophoblasts
    Chemical Substances Transforming Growth Factor beta1 ; Transforming Growth Factor beta2 ; Calcitriol (FXC9231JVH) ; Transforming Growth Factor beta3
    Language English
    Publishing date 2023-12-10
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 424421-7
    ISSN 1872-7603 ; 0165-0378
    ISSN (online) 1872-7603
    ISSN 0165-0378
    DOI 10.1016/j.jri.2023.104181
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Transcriptional landscape of human trophoblast cells treated with calcitriol and TGF-β1.

    Romero-Córdoba, Sandra / Chirinos, Mayel / Noyola-Martínez, Nancy / Torres-Ramírez, Nayeli / García-Olivares, Mitzi / Aragón-Hernández, Juan Pablo / Ramírez-Camacho, Ixchel / Zúñiga, Rosa / Larrea, Fernando / Halhali, Ali / Barrera, David

    Molecular and cellular endocrinology

    2023  Volume 579, Page(s) 112088

    Abstract: Calcitriol and transforming growth factor beta 1 (TGF-β1) are unrelated molecules that regulate biological processes according to the genetic target, cell type, and context. Several studies have shown independent effects of calcitriol and TGF-βs on the ... ...

    Abstract Calcitriol and transforming growth factor beta 1 (TGF-β1) are unrelated molecules that regulate biological processes according to the genetic target, cell type, and context. Several studies have shown independent effects of calcitriol and TGF-βs on the placenta, but there is no information regarding the impact of their combination on these cells. Therefore, this study analyzed the effects of calcitriol, TGF-β1, and their combination in primary cultures of human trophoblast cells using a whole genome expression microarray. Data analysis revealed a set of differentially expressed genes induced by each treatment. Enrichment pathway analysis identified modulatory effects of calcitriol on genes related to metabolic processes such as vitamin D, steroid, and fat-soluble vitamins as well as antimicrobial and immune responses. In relation to TGF-β1, the analysis showed a few differentially expressed genes that were mainly associated with the neutrophil immune response. Lastly, the analysis revealed that the combination of calcitriol and TGF-β1 up-regulated genes involving both immunologic processes and the biosynthesis of unsaturated fatty acids, eicosanoids, and lipoxins, among others. In contrast, pathways down-regulated by the combination were mostly associated with the catabolic process of acylglycerols and peptides, PPAR signaling pathway, cellular response to low-density lipoprotein stimulus, renin angiotensin system and digestion, mobilization and transport of lipids. Consistent with these results, the combined treatment on human trophoblast cells induced the accumulation of intracellular neutral lipid droplets and stimulated both gene and protein expression of 15-hydroxyprostaglandin dehydrogenase. In conclusion, the results revealed that differentially expressed genes induced by the combination modified the transcriptional landscape compared to each treatment alone, mainly altering the storage, activity and metabolism of lipids, which might have an impact on placental development.
    MeSH term(s) Humans ; Female ; Pregnancy ; Transforming Growth Factor beta1/pharmacology ; Transforming Growth Factor beta1/metabolism ; Calcitriol/pharmacology ; Calcitriol/metabolism ; Placenta/metabolism ; Transforming Growth Factor beta/metabolism ; Trophoblasts/metabolism
    Chemical Substances Transforming Growth Factor beta1 ; Calcitriol (FXC9231JVH) ; Transforming Growth Factor beta
    Language English
    Publishing date 2023-10-11
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2023.112088
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Citicoline Modifies the Expression of Specific miRNAs Related to Cardioprotection in Patients with ST-Segment Elevation Myocardial Infarction Subjected to Coronary Angioplasty.

    Silva-Palacios, Alejandro / Arroyo-Campuzano, Miguel / Flores-García, Mirthala / Patlán, Mariana / Hernández-Díazcouder, Adrián / Alcántara, Diego / Ramírez-Camacho, Ixchel / Arana-Hidalgo, Dana / Soria-Castro, Elizabeth / Sánchez, Fausto / González-Pacheco, Héctor / Zazueta, Cecilia

    Pharmaceuticals (Basel, Switzerland)

    2022  Volume 15, Issue 8

    Abstract: Extracellular vesicles are recognized as signaling mediators between cells both in physiological and pathological communication. In this work, we explored the potential effect of citicoline to modify relevant proteins or miRNAs for cardioprotection in ... ...

    Abstract Extracellular vesicles are recognized as signaling mediators between cells both in physiological and pathological communication. In this work, we explored the potential effect of citicoline to modify relevant proteins or miRNAs for cardioprotection in the smallest population of such microvesicles; i.e., in exosomes from patients diagnosed with ST-segment elevation myocardial infarction (STEMI) undergoing coronary angioplasty. The plasma-exosome-enriched fraction from these patients was characterized. Their cellular origin was assessed by flow cytometry and Western blot, whereas miRNA expression was evaluated by real-time polymerase chain reaction (qRT-PCR). The content of caveolin-1, caveolin-3, and hnRNPA2B1, which play a relevant role in selective transport of miRNAs into microvesicles, along with the effect on cell viability of the exosomes obtained from citicoline-treated and untreated groups were also analyzed. Our results showed that hypoxic stress increases exosome release into the circulation. Moreover, we found that CD146+ increased in exosomes from citicoline-treated patients, while CD142+ decreased in these patients compared to the placebo group. No changes were detected in the protein levels of caveolin-1, caveolin-3, and hnRNPA2B1. Citicoline administration modified the expression of miR233-3p, miR92, and miR21-5p in exosomes. Cell viability decreased in the presence of exosomes from infarcted patients, while incubation of H9c2 cells with exosomes from patients reperfused with citicoline did not affect cell viability. In conclusion, citicoline administration modifies the expression of specific miRNAs related to cardioprotection in exosomes.
    Language English
    Publishing date 2022-07-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph15080925
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Cardioprotection by curcumin post-treatment in rats with established chronic kidney disease.

    Hernández-Reséndiz, Sauri / Correa, Francisco / García-Niño, Wylly R / Buelna-Chontal, Mabel / Roldán, Francisco J / Ramírez-Camacho, Ixchel / Delgado-Toral, Carolina / Carbó, Roxana / Pedraza-Chaverrí, José / Tapia, Edilia / Zazueta, Cecilia

    Cardiovascular drugs and therapy

    2015  Volume 29, Issue 2, Page(s) 111–120

    Abstract: Purpose: The pathogenic mechanisms leading to cardiovascular disorders in patients with chronic kidney disease have not been clearly established, although increased oxidative stress has been pointed out as a potential cause. Therefore, as cardiovascular ...

    Abstract Purpose: The pathogenic mechanisms leading to cardiovascular disorders in patients with chronic kidney disease have not been clearly established, although increased oxidative stress has been pointed out as a potential cause. Therefore, as cardiovascular events are still the first cause of death in patients with chronic kidney disease and traditional drugs or therapies rarely have effects on cardiac complications, we sought to determine the effect of curcumin in treating cardiac dysfunction in rats with established chronic renal disease.
    Methods and results: Treatment consisted in daily administration of curcumin (120 mg/kg/day) dissolved in 0.05% carboxymethylcellulose via oral gavages during 30 days, beginning from day 30 after 5/6 nephrectomy (5/6Nx). Cardiac function, markers of oxidative stress, activation of PI3K/Akt/GSK3β and MEK1/2-ERK1/2 pathway, metalloproteinase-II (MMP-2) content, overall gelatinolytic activity, ROS production and mitochondrial integrity were evaluated after 1-month treatment. Curcumin restored systolic blood pressure, diminished interventricular and rear wall thickening, decreased left ventricle dimension at end-systole (LVSd) and restored ejection fraction in nephrectomized rats. Also, it diminished metalloproteinase-II levels and overall gelatinase activity, decreased oxidative stress and inhibited the mitochondrial permeability transition pore opening.
    Conclusion: Our findings suggest that curcumin might have therapeutic potential in treatment of heart disease in patients with established CKD by attenuating oxidative stress-related events as cardiac remodeling, mitochondrial dysfunction and cell death.
    MeSH term(s) Animals ; Blood Pressure/drug effects ; Cardiotonic Agents/pharmacology ; Cardiotonic Agents/therapeutic use ; Curcumin/pharmacology ; Curcumin/therapeutic use ; Gelatinases/metabolism ; Heart/drug effects ; Male ; Matrix Metalloproteinase 2/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/antagonists & inhibitors ; Myocardium/metabolism ; Nephrectomy ; Oxidative Stress/drug effects ; Rats ; Reactive Oxygen Species/metabolism ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction/drug effects ; Stroke Volume/drug effects ; Ventricular Remodeling/drug effects
    Chemical Substances Cardiotonic Agents ; Mitochondrial Membrane Transport Proteins ; Reactive Oxygen Species ; mitochondrial permeability transition pore ; Gelatinases (EC 3.4.24.-) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Curcumin (IT942ZTH98)
    Language English
    Publishing date 2015-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639068-7
    ISSN 1573-7241 ; 0920-3206
    ISSN (online) 1573-7241
    ISSN 0920-3206
    DOI 10.1007/s10557-015-6581-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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