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1. Magnesium accumulation upon cyclin M4 silencing activates microsomal triglyceride transfer protein improving NASH

Author

Simón, Jorge, primary, Goikoetxea-Usandizaga, Naroa, additional, Serrano-Maciá, Marina, additional, Fernández-Ramos, David, additional, Sáenz de Urturi, Diego, additional, Gruskos, Jessica J., additional, Fernández-Tussy, Pablo, additional, Lachiondo-Ortega, Sofía, additional, González-Recio, Irene, additional, Rodríguez-Agudo, Rubén, additional, Gutiérrez-de-Juan, Virginia, additional, Rodríguez-Iruretagoyena, Begoña, additional, Varela-Rey, Marta, additional, Gimenez-Mascarell, Paula, additional, Mercado-Gomez, María, additional, Gómez-Santos, Beatriz, additional, Fernandez-Rodriguez, Carmen, additional, Lopitz-Otsoa, Fernando, additional, Bizkarguenaga, Maider, additional, Dames, Sibylle, additional, Schaeper, Ute, additional, Martin, Franz, additional, Sabio, Guadalupe, additional, Iruzubieta, Paula, additional, Crespo, Javier, additional, Aspichueta, Patricia, additional, Chu, Kevan H.-Y., additional, Buccella, Daniela, additional, Martín, César, additional, Delgado, Teresa Cardoso, additional, Martínez-Cruz, Luis Alfonso, additional, and Martínez-Chantar, María Luz, additional

Published
2021
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2. Magnesium Accumulation Upon Cyclin M4 Silencing Activates Microsomal Triglyceride Transfer Protein Improving NASH

Author

Bioquímica y biología molecular, Fisiología, Biokimika eta biologia molekularra, Fisiologia, Simón Espinosa, Jorge, Goikoetxea Usandizaga, Naroa, Serrano Maciá, Marina, Fernández Ramos, David, Sáenz de Urturi Indart, Diego, Gruskos, Jessica J., Fernández Tussy, Pablo, Lachiondo Ortega, Sofía, González Recio, Irene, Rodríguez Agudo, Rubén, Gutiérrez de Juan, Virginia, Rodríguez Iruretagoyena, Begoña, Varela Rey, Marta, Giménez Mascarell, Paula, Mercado Gómez, María, Gómez Santos, Beatriz, Fernández Rodríguez, Carmen, Lopitz Otsoa, Fernando, Bizkarguenaga, Maider, Dames, Sibylle, Schaeper, Ute, Martin, Franz, Sabio, Guadalupe, Iruzubieta, Paula, Crespo, Javier, Aspichueta Celaá, Patricia, Chu, Kevan H. Y., Buccella, Daniela, Martín Plágaro, César Augusto, Cardoso Delgado, Teresa de Jesús, Martínez de la Cruz, Alfonso, Martínez Chantar, María Luz, Bioquímica y biología molecular, Fisiología, Biokimika eta biologia molekularra, Fisiologia, Simón Espinosa, Jorge, Goikoetxea Usandizaga, Naroa, Serrano Maciá, Marina, Fernández Ramos, David, Sáenz de Urturi Indart, Diego, Gruskos, Jessica J., Fernández Tussy, Pablo, Lachiondo Ortega, Sofía, González Recio, Irene, Rodríguez Agudo, Rubén, Gutiérrez de Juan, Virginia, Rodríguez Iruretagoyena, Begoña, Varela Rey, Marta, Giménez Mascarell, Paula, Mercado Gómez, María, Gómez Santos, Beatriz, Fernández Rodríguez, Carmen, Lopitz Otsoa, Fernando, Bizkarguenaga, Maider, Dames, Sibylle, Schaeper, Ute, Martin, Franz, Sabio, Guadalupe, Iruzubieta, Paula, Crespo, Javier, Aspichueta Celaá, Patricia, Chu, Kevan H. Y., Buccella, Daniela, Martín Plágaro, César Augusto, Cardoso Delgado, Teresa de Jesús, Martínez de la Cruz, Alfonso, and Martínez Chantar, María Luz

Abstract

Background & Aims: Perturbations of intracellular magnesium (Mg2+) homeostasis have implications for cell physiology. The cyclin M family, CNNM, perform key functions in the transport of Mg2+ across cell membranes. Herein, we aimed to elucidate the role of CNNM4 in the development of non-alcoholic steatohepatitis (NASH). Methods: Serum Mg2+ levels and hepatic CNNM4 expression were characterised in clinical samples. Primary hepatocytes were cultured under methionine and choline deprivation. A 0.1% methionine and choline-deficient diet, or a choline-deficient high-fat diet were used to induce NASH in our in vivo rodent models. Cnnm4 was silenced using siRNA, in vitro with DharmaFECT and in vivo with Invivofectamine (R) or conjugated to N-acetylgalactosamine. Results: Patients with NASH showed hepatic CNNM4 over-expression and dysregulated Mg2+ levels in the serum. Cnnm4 silencing ameliorated hepatic lipid accumulation, inflammation and fibrosis in the rodent NASH models. Mechanistically, CNNM4 knockdown in hepatocytes induced cellular Mg2+ accumulation, reduced endoplasmic reticulum stress, and increased microsomal triglyceride transfer activity, which promoted hepatic lipid clearance by increasing the secretion of VLDLs. Conclusions: CNNM4 is overexpressed in patients with NASH and is responsible for dysregulated Mg2+ transport. Hepatic CNNM4 is a promising therapeutic target for the treatment of NASH. Lay summary: Cyclin M4 (CNNM4) is overexpressed in nonalcoholic steatohepatitis (NASH) and promotes the export of magnesium from the liver. The liver-specific silencing of Cnnm4 ameliorates NASH by reducing endoplasmic reticulum stress and promoting the activity of microsomal triglyceride transfer protein.

Published
2021

3. Magnesium accumulation upon cyclin M4 silencing activates microsomal triglyceride transfer protein improving NASH

Author

Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Eusko Jaurlaritza, European Commission, Fundación Vasca de Innovación e Investigación Sanitarias, Radio Televisión Pública Vasca, Asociación Española Contra el Cáncer, Fundación la Caixa, Fundación BBVA, Ministerio de Economía y Competitividad (España), National Institutes of Health (US), Junta de Andalucía, Simón, Jorge, Goikoetxea-Usandizaga, Naroa, Serrano-Maciá, Marina, Fernández-Ramos, David, Sáenz de Urturi, Diego, Gruskos, Jessica J., Fernández-Tussy, Pablo, Lachiondo-Ortega, Sofía, González-Recio, Irene, Rodríguez-Agudo, Rubén, Gutiérrez de Juan, Virginia, Rodríguez-Iruretagoyena, Begoña, Varela-Rey, Marta, Gimenez-Mascarell, Paula, Mercado-Gomez, María, Gómez-Santos, Beatriz, Fernández-Rodríguez, Carmen, Lopitz-Otsoa, Fernando, Bizkarguenaga, Maider, Dames, Sibylle, Schaeper, Ute, Martín, Franz, Sabio, Guadalupe, Iruzubieta, Paula, Crespo, Javier, Aspichueta, Patricia, Chu, Kevan H.-Y., Buccella, Daniela, Martín, César, Cardoso Delgado, Teresa de Jesús, Martínez-Cruz, Luis Alfonso, Martínez-Chantar, María Luz, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Eusko Jaurlaritza, European Commission, Fundación Vasca de Innovación e Investigación Sanitarias, Radio Televisión Pública Vasca, Asociación Española Contra el Cáncer, Fundación la Caixa, Fundación BBVA, Ministerio de Economía y Competitividad (España), National Institutes of Health (US), Junta de Andalucía, Simón, Jorge, Goikoetxea-Usandizaga, Naroa, Serrano-Maciá, Marina, Fernández-Ramos, David, Sáenz de Urturi, Diego, Gruskos, Jessica J., Fernández-Tussy, Pablo, Lachiondo-Ortega, Sofía, González-Recio, Irene, Rodríguez-Agudo, Rubén, Gutiérrez de Juan, Virginia, Rodríguez-Iruretagoyena, Begoña, Varela-Rey, Marta, Gimenez-Mascarell, Paula, Mercado-Gomez, María, Gómez-Santos, Beatriz, Fernández-Rodríguez, Carmen, Lopitz-Otsoa, Fernando, Bizkarguenaga, Maider, Dames, Sibylle, Schaeper, Ute, Martín, Franz, Sabio, Guadalupe, Iruzubieta, Paula, Crespo, Javier, Aspichueta, Patricia, Chu, Kevan H.-Y., Buccella, Daniela, Martín, César, Cardoso Delgado, Teresa de Jesús, Martínez-Cruz, Luis Alfonso, and Martínez-Chantar, María Luz

Abstract

Background & Aims: Perturbations of intracellular magnesium (Mg) homeostasis have implications for cell physiology. The cyclin M family, CNNM, perform key functions in the transport of Mg across cell membranes. Herein, we aimed to elucidate the role of CNNM4 in the development of non-alcoholic steatohepatitis (NASH). Methods: Serum Mg levels and hepatic CNNM4 expression were characterised in clinical samples. Primary hepatocytes were cultured under methionine and choline deprivation. A 0.1% methionine and choline-deficient diet, or a choline-deficient high-fat diet were used to induce NASH in our in vivo rodent models. Cnnm4 was silenced using siRNA, in vitro with DharmaFECT and in vivo with Invivofectamine® or conjugated to N-acetylgalactosamine. Results: Patients with NASH showed hepatic CNNM4 overexpression and dysregulated Mg levels in the serum. Cnnm4 silencing ameliorated hepatic lipid accumulation, inflammation and fibrosis in the rodent NASH models. Mechanistically, CNNM4 knockdown in hepatocytes induced cellular Mg accumulation, reduced endoplasmic reticulum stress, and increased microsomal triglyceride transfer activity, which promoted hepatic lipid clearance by increasing the secretion of VLDLs. Conclusions: CNNM4 is overexpressed in patients with NASH and is responsible for dysregulated Mg transport. Hepatic CNNM4 is a promising therapeutic target for the treatment of NASH. Lay summary: Cyclin M4 (CNNM4) is overexpressed in non-alcoholic steatohepatitis (NASH) and promotes the export of magnesium from the liver. The liver-specific silencing of Cnnm4 ameliorates NASH by reducing endoplasmic reticulum stress and promoting the activity of microsomal triglyceride transfer protein.

Published
2021

4. Murine double minute 2 regulates Hu antigen R stability in human liver and colon cancer through NEDDylation

Author

Embade, Nieves, Fernández-Ramos, David, Varela-Rey, Marta, Beraza, Naiara, Sini, Marcella, de Juan, Virginia Gutiérrez, Woodhoo, Ashwin, Martínez-López, Nuria, Rodríguez-Iruretagoyena, Begoña, Bustamante, Francisco Javier, de la Hoz, Ana Belén, Carracedo, Arkaitz, Xirodimas, Dimitris P., Rodríguez, Manuel S., Lu, Shelly C., Mato, José M., and Martínez-Chantar, María L.

Published
2012
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5. MCJ: A therapeutic target in hepatic ischemia and reperfusion injury

Author

Goikoetxea-Usandizaga, Naroa, Fernández-Ramos, David, Serrano-Maciá, Marina, Eugenia Cornide, Maria, Jimenez-Castro, Monica, Alfano, Bennedetta, Sáenz de Urturi, Diego, Gonzalez-Romero, Francisco, Gutiérrez de Juan, Virginia, Rodríguez-Iruretagoyena, Begoña, Cardoso Delgado, Teresa, Lopitz-Otsoa, Fernando, Barbier Torres, Lucia, Fernández-Tussy, Pablo, Simón, Jorge, Martín, Paloma, Anguita, Juan, Perez Redondo, Marina, Miñambres, Eduardo, Lu, Shelly C., Mato, José M., Sabio, Guadalupe, Peralta, Carmen, Aspichueta, Patricia, Casado, Marta, Martín, César, Varela-Rey, Marta, and Martínez-Chantar, María Luz

Abstract

Trabajo presentado en The International Liver Congress, celebrado en Viena (Austria) del 10 al 14 de abril de 2019., [Background and aims]: Ischemia/reperfusion (IR) injury, a frequent pathological process during liver resection, is a leading cause of post transplantation organ dysfunction. The extent of the injury can determine the success of the procedure and the survival of the patient. Therefore, attenuation of pathology caused by the injury and improving liver function after the procedure would be critical for clinicians to diminish IR injury prevalence and improve the outcome. Mitochondria play a key role in liver homeostasis; indeed, more functional mitochondria induce hepatic regeneration. MCJ, also known as DNACJ15, is an endogenous negative regulator of complex I, located in the mitochondrial electron transport chain. While under normal conditions MCJ deficiency does not result in an altered phenotype in mice, its absence improves mitochondrial activity without increasing mitochondrial ROS. We present MCJ as a new target to minimize hepatic damage caused by IR injury and enhance the efficiency of liver regeneration during liver resection., [Method]: Partial hepatectomies (PH) and PH combined with IR injuries were performed in MCJ-KO mice and in WT mice after MCJ silencing., [Results]: We observed that the lack of MCJ reduced liver damage and induced hepatic regeneration after IR injury; MCJ-KO mice showed lower levels of Caspase 3 and a significantly higher Cyclin D1 expression. Moreover, we saw an improved metabolic response to hepatic insufficiency and an accelerated cell cycle progression during liver resection, which led to a faster recovery of the hepatic mass. In the initial phase after the PH, glucagon response was amplified in MCJ-KO mice, characterized by increased cAMP and AKT signaling, along with higher Ca+2 release from the endoplasmic reticulum (ER), glycogen synthase kinase (GSK-3beta) inhibition and nuclear factorKbeta (NFKbeta) translocation to the nucleus. In the proliferative phase, ablation of MCJ accelerated the induction of proliferative markers. Indeed, after MCJ silencing, an improved phenotype was detected in an aging mice model that underwent partial hepatectomy. Hepatic insufficiency was ameliorated, PCNA expression increased and steatosis reverted. Importantly, the combined procedure of PH and IR injury that resemble liver transplant procedure resulted in a 100% survival rate for MCJ-KO mice while just the 33% of MCJ-WT mice survived the operation. Increased levels of MCJ were found in liver biopsies from all liver donors at 60 minutes after normothermic regional perfusion (nRP) was started., [Conclusion]: Overall, MCJ silencing during liver resection emerges as a promising therapy for IR injury and restoration of hepatic mass.

Published
2019

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