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Your search keyword '"Peroxisome proliferator-activated receptor-gamma coactivator"' showing total 4 results
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4 results on '"Peroxisome proliferator-activated receptor-gamma coactivator"'

1. Deletion of the Transcription Factor PGC-1α in Mice Negatively Regulates Bone Mass.

Author

Colaianni, Graziana, Lippo, Luciana, Sanesi, Lorenzo, Brunetti, Giacomina, Celi, Monica, Cirulli, Nunzio, Passeri, Giovanni, Reseland, Janne, Schipani, Ernestina, Faienza, Maria Felicia, Tarantino, Umberto, Colucci, Silvia, and Grano, Maria

Subjects
*TRANSCRIPTION factors, *PGC-1 protein, *BONES, *HOMEOSTASIS, *OSTEOCALCIN, *OSTEOCLASTS, *MITOCHONDRIA
Abstract

Peroxisome proliferator-activated receptor-gamma coactivator (PGC1α) is a transcription coactivator that interacts with a broad range of transcription factors involved in several biological responses. Here, we show that PGC1α plays a role in skeletal homeostasis since aged PGC1α-deficient mice (PGC1α-/-) display impaired bone structure. Micro-CT of the tibial mid-shaft showed a marked decrease of cortical thickness in PGC1α-/- (- 11.9%, p < 0.05) mice compared to wild-type littermate. Trabecular bone was also impaired in knock out mice which displayed lower trabecular thickness (Tb.Th) (- 5.9% vs PGC1α+/+, p < 0.05), whereas trabecular number (Tb.N) was higher than wild-type mice (+ 72% vs PGC1α+/+, p < 0.05), thus resulting in increased (+ 31.7% vs PGC1α+/+, p < 0.05) degree of anisotropy (DA), despite unchanged bone volume fraction (BV/TV). Notably, these impairments of cortical and trabecular bone led to a dramatic ~ 48.4% decrease in bending strength (p < 0.01). These changes in PGC1α-/- mice were paralleled by a significant increase in osteoclast number at the cortical bone surface and in serum level of the bone resorption marker, namely, C-terminal cross-linked telopeptides of type I collagen (CTX-I). We also found that in cortical bone, there was lower expression of mRNA codifying for the key bone-building protein Osteocalcin (Ocn). Interestingly, Collagen I mRNA expression was reduced in mesenchymal stem cells from bone marrow of PGC1α-/-, thus indicating that differentiation of osteoblast lineage is downregulated. Overall, results presented herein suggest that PGC1α may play a key role in bone metabolism. [ABSTRACT FROM AUTHOR]

Published
2018
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2. Deletion of the Transcription Factor PGC-1α in Mice Negatively Regulates Bone Mass

Author

Giacomina Brunetti, N Cirulli, Graziana Colaianni, Monica Celi, Giovanni Passeri, Lorenzo Sanesi, Silvia Colucci, Ernestina Schipani, Maria Felicia Faienza, Umberto Tarantino, Janne E. Reseland, Luciana Lippo, and Maria Grano

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Osteocalcin, 030209 endocrinology & metabolism, Bone and Bones, Bone resorption, Bone remodeling, Mice, 03 medical and health sciences, Peroxisome proliferator-activated receptor-gamma coactivator, 0302 clinical medicine, Endocrinology, Bone Density, Osteoclast, Internal medicine, Coactivator, Settore MED/33 - Malattie Apparato Locomotore, medicine, Animals, Orthopedics and Sports Medicine, Bone, Mice, Knockout, biology, Chemistry, Osteoblast, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Mitochondria, 030104 developmental biology, medicine.anatomical_structure, biology.protein, Female, Cortical bone, Bone marrow, Type I collagen
Abstract

Peroxisome proliferator-activated receptor-gamma coactivator (PGC1α) is a transcription coactivator that interacts with a broad range of transcription factors involved in several biological responses. Here, we show that PGC1α plays a role in skeletal homeostasis since aged PGC1α-deficient mice (PGC1α−/−) display impaired bone structure. Micro-CT of the tibial mid-shaft showed a marked decrease of cortical thickness in PGC1α−/− (− 11.9%, p

Published
2018

3. Activation of alternative NF-κB signaling during recovery of disuse-induced loss of muscle oxidative phenotype

Author

Nicholas A.M. Pansters, Annemie M. W. J. Schols, Harry R. Gosker, Ramon C. J. Langen, A.H.V. Remels, Pulmonologie, and RS: NUTRIM - R3 - Chronic inflammatory disease and wasting

Subjects
Physiology, Endocrinology, Diabetes and Metabolism, Oxidative Phosphorylation, Weight-Bearing, Mice, Random Allocation, Gene expression, GENE-EXPRESSION, SOLEUS MUSCLE, High Mobility Group Proteins, NF-kappa B, MITOCHONDRIAL BIOGENESIS, Phenotype, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Muscular Disorders, Atrophic, DNA-Binding Proteins, medicine.anatomical_structure, DIFFERENTIATION, Hindlimb Suspension, Receptors, Estrogen, SKELETAL-MUSCLE, Signal Transduction, medicine.medical_specialty, EXERCISE, Oxidative phosphorylation, Biology, ERR-ALPHA, ATROPHY, Mitochondrial Proteins, Immobilization, Atrophy, reloading, Physiology (medical), Internal medicine, medicine, Animals, skeletal muscle, Muscle, Skeletal, Soleus muscle, Myosin Heavy Chains, Skeletal muscle, medicine.disease, Nf κb signaling, Mice, Inbred C57BL, alternative nuclear factor-kappa B, Disease Models, Animal, Endocrinology, Mitochondrial biogenesis, Gene Expression Regulation, ADAPTATIONS, TIBIALIS ANTERIOR, peroxisome proliferator-activated receptor-gamma coactivator, Biomarkers, Transcription Factors
Abstract

Physical inactivity-induced loss of skeletal muscle oxidative phenotype (OXPHEN), often observed in chronic disease, adversely affects physical functioning and quality of life. Potential therapeutic targets remain to be identified, since the molecular mechanisms involved in reloading-induced recovery of muscle OXPHEN remain incompletely understood. We hypothesized a role for alternative NF-κB, as a recently identified positive regulator of muscle OXPHEN, in reloading-induced alterations in muscle OXPHEN. Markers and regulators (including alternative NF-κB signaling) of muscle OXPHEN were investigated in gastrocnemius muscle of mice subjected to a hindlimb suspension/reloading (HLS/RL) protocol. Expression levels of oxidative phosphorylation subunits and slow myosin heavy chain isoforms I and IIA increased rapidly upon RL. After an initial decrease upon HLS, mRNA levels of peroxisome proliferator-activated receptor (PPAR)-γ coactivator (PGC) molecules PGC-1α and PGC-1β and mRNA levels of mitochondrial transcription factor A (Tfam) and estrogen-related receptor α increased upon RL. PPAR-δ, nuclear respiratory factor 1 (NRF-1), NRF-2α, and sirtuin 1 mRNA levels increased during RL although expression levels were unaltered upon HLS. In addition, both Tfam and NRF-1 protein levels increased significantly during the RL period. Moreover, upon RL, IKK-α mRNA and protein levels increased, and phosphorylation of P100 and subsequent processing to P52 were elevated, reflecting alternative NF-κB activation. We conclude that RL-induced recovery of muscle OXPHEN is associated with activation of alternative NF-κB signaling.

Published
2014

4. Activation of alternative NF-κB signaling during recovery of disuse-induced loss of muscle oxidative phenotype.

Author

Remels, A.H. and Remels, A.H.

Abstract

BACKGROUND: Physical inactivity-induced loss of skeletal muscle phenotype (OXPHEN), often observed in chronic disease, adversely affects functioning and quality of life. Potential therapeutic targets remain to identified as the molecular mechanisms involved in reloading-induced muscle OXPHEN remain incompletely understood. We hypothesized a role for alternative NF-kappaB, as a recently identified positive regulator of OXPHEN, in reloading-induced alterations in muscle OXPHEN. METHODS: regulators (including alternative NF-kappaB signaling) of muscle OXPHEN investigated in gastrocnemius muscle of mice subjected to a hind limb suspension/reloading (HLS/RL) protocol. RESULTS: Expression levels of phosphorylation (OXPHOS) sub-units and slow myosin heavy chain (MyHC) and IIA increased rapidly upon RL. After an initial decrease upon HLS, levels of peroxisome proliferator-activated receptor (PPAR) gamma co- (PGC) molecules PGC-1alpha and PGC-1beta and mRNA levels of transcription factor A (Tfam) and estrogen-related receptor alpha (ERR- increased upon RL. PPAR-delta, nuclear respiratory factor 1 (NRF-1), and sirtuin 1 mRNA levels increased during RL although expression levels unaltered upon HLS. In addition, both Tfam and NRF-1 protein levels significantly during the RL period. Moreover, upon RL, IKK-alpha mRNA levels increased and phosphorylation of P100 and subsequent processing elevated, reflecting alternative NF-kappaB activation. CONCLUSION: RL- recovery of muscle OXPHEN is associated with activation of alternative

Published
2014

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