Low Doses of Insulin-Like Growth Factor-I Induce Mitochondrial Protection in Aging Rats

Puche, Juan Enrique; García-Fernández, María; Muntané, Jordi; Rioja, José; González-Barón, S; Castilla‐Cortázar, Inma

doi:10.1210/en.2007-1563

Cited by 100 publications

(95 citation statements)

References 38 publications

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“…Mitochondria are important cellular targets of IGF-I [5,6], different groups have described that IGF-I decreases mitochondrial superoxide production [37] and low levels of IGF-I have been linked to increase in oxidative stress damage [3,5,[40][41][42]. IGF-I also acts as an anti-apoptosis factor of multiple cell types, and its anti-apoptotic effects occur through engagement with IGF-I receptor (IGF-IR) and thought to activate an intracellular signal transduction pathway that may modulate the mitochondria, cytochrome c and caspase pathway [38,39].…”

Section: Mitochondrial Damagementioning

confidence: 99%

“…IGF-I also acts as an anti-apoptosis factor of multiple cell types, and its anti-apoptotic effects occur through engagement with IGF-I receptor (IGF-IR) and thought to activate an intracellular signal transduction pathway that may modulate the mitochondria, cytochrome c and caspase pathway [38,39]. Recent studies show that treatment of aged rodents with IGF-I confer mitochondrial protection, including an attenuation of mitochondrial ROS generation in the liver [40][41][42]. The available data suggest that treatments that increase circulating IGF-I levels exert citoprotective effects in aging and degenerative diseases [1-3, 5-7, 42].…”

Section: Mitochondrial Damagementioning

confidence: 99%

“…It has been proposed that polymorphisms in these enzymes are associated with DNA damage and subsequently the individual's risk of wide range of diseases susceptibility [42,43].…”

Section: Antioxidant Defensesmentioning

confidence: 99%

“…We propose that IGF-I can exert direct effects on cells and can alter in opposite ways the expression of antioxidant enzymes depending on the ROS levels. This regulation may contribute to the citoprotective effects of treatment with low doses of IGF-I in experimental "IGF-I deficiency" conditions [2,5,6,[40][41][42]. This model is summarized in Fig.…”

Section: Foxo Transcription Factorsmentioning

confidence: 99%

“…Oxidative Stress is one of the most important mechanisms of the cellular damage in aging [42,131] and in others "IGF-I deficiency" conditions such as liver cirrhosis where there are a diminution in IGF-I levels but not in GH levels followed of a decrease in liver biosynthetic capacity. In order to reproduce of "IGF-I deficiency" condition and the possible benefices of treatment with low doses of IGF-I, we used two different experimental models: a.…”

Section: Aging and Others Conditions Of "Igf-i Deficiency" And Oxidatmentioning

confidence: 99%

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Protection Against Oxidative Stress and “IGF-I Deficiency Conditions”

Morón¹,

Castilla‐Cortázar²

2012

Antioxidant Enzyme

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Section: Mitochondrial Damagementioning

confidence: 99%

Section: Mitochondrial Damagementioning

confidence: 99%

“…It has been proposed that polymorphisms in these enzymes are associated with DNA damage and subsequently the individual's risk of wide range of diseases susceptibility [42,43].…”

Section: Antioxidant Defensesmentioning

confidence: 99%

Section: Foxo Transcription Factorsmentioning

confidence: 99%

Section: Aging and Others Conditions Of "Igf-i Deficiency" And Oxidatmentioning

confidence: 99%

See 3 more Smart Citations

Protection Against Oxidative Stress and “IGF-I Deficiency Conditions”

Morón¹,

Castilla‐Cortázar²

2012

Antioxidant Enzyme

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Clinical and molecular diagnosis of a cartilage‐hair hypoplasia with IGF‐1 deficiency

Castilla‐Cortázar

Ita

Martín-Estal

et al. 2016

American J of Med Genetics Pt A

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Cartilage-hair hypoplasia syndrome (CHH) is a rare autosomal recessive condition characterized by metaphyseal chondrodysplasia and characteristic hair, together with a myriad of other symptoms, being most common immunodeficiency and gastrointestinal complications. A 15-year-old Mexican male initially diagnosed with Hirschsprung disease and posterior immunodeficiency, presents to our department for genetic and complementary evaluation for suspected CHH. Physical, biochemical, and genetic studies confirmed CHH together with IGF-1 deficiency. For this reason, we propose IGF-1 replacement therapy for its well-known actions on hematopoiesis, immune function and maturation, and metabolism. Ó 2016 Wiley Periodicals, Inc.Key words: cartilage-hair hypoplasia; IGF-1; RMRP gene; GHR INTRODUCTIONCartilage-hair hypoplasia syndrome (CHH) is a rare autosomal recessive condition that was originally described by McKusik in 1964 in Amish children. In this population, it accounts for one in 1,300 newborns [McKusick et al., 1965], while in the Finnish population it accounts for one in 23,000 newborns [M€ akitie and Kaitila, 1993]. Outside those populations it is extremely rare, with no incidence data available [M€ akitie and Kaitila, 1993]. The genetic locus for this disease falls within the RNA Component Of Mitochondrial RNA Processing Endoribonuclease (RMRP) gene, localized in chromosome 9p12, which codes for the RMRP, believed to be required for cell cycle, mtDNA replication and rRNA processing [Ridanp€ a€ a et al., 2001;Hermanns et al., 2005;Thiel et al., 2005;Martin and Li, 2007]. The RMRP RNA product associates with at least seven proteins whose interactions and roles remain to be discovered [Welting et al., 2004].The hallmark of this condition is a metaphyseal chondrodysplasia and characteristic hair (fine, sparse with scalp, blond eyelashes-93%), with other several signs and symptoms including short stature and skeletal dysplasia (100%) with varum deformation of lower extremities, hypoplastic anemia during childhood (79%), immunodeficiency (during childhood they may present different recurrent infections secondary to an immunodeficiency that may be humoral, B-cell or T-cell, or combined-56%) [Pierce and Polmar, 1982;M€ akitie et al., 1998, 2000bBaradaran-Heravi et al., 2008] with higher risk of malignancies, skin and nails abnormalities, gastrointestinal diseases (such as Hirschsprung disease [HD], malabsorption, anal stenosis and esophageal atresia-18%) [M€ akitie et al., 2002, 2000a], and failure to thrive [M€ akitie et al., 1992;Glass and Tifft, 1999;Riley et al., 2015]. The growth failure is progressive, owing, partly, to a weak or absent pubertal growth spurt; pubertal maturation is normal; testicular size is abnormal in some patients with normal serum concentrations of testosterone, inhibin B and gonadotropins [M€ akitie et al., 2001].These patients are symptomatic since birth, showing short-limb dwarfism and short puffy hands, with normal head circumference [Giedion, 1998]. The final adult heights range from 100.7 t...

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Partial IGF‐1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy

et al. 2016

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Insulin‐like growth factor 1 (IGF‐1) induces multiple cytoprotective effects on every tissue, including the brain. Since the mechanisms by which IGF‐1 produces neuroprotection are not fully understood, the aim of this work was to delve into the underlying mechanisms. IGF‐1 deficient mice (Hz) were compared with wild type (WT) and Hz mice treated with low doses of IGF‐1 (2 µg/100 g body weight/day) for 10 days (Hz + IGF). Gene expression, quantitative PCR, histology, and magnetic resonance imaging were performed in the three groups. IGF‐1 deficiency induced increased oxidative damage determined by markers of lipid peroxidation and hypoxia, as well as gene expression of heat shock proteins, antioxidant enzymes, and molecules involved in inflammation, apoptosis, and mitochondrial protection. These changes correlated with edema and learning impairment in Hz mice. IGF‐1 therapy improved all these alterations. In conclusion, IGF‐1 deficiency is responsible for increased brain oxidative damage, edema, and impaired learning and memory capabilities which are rescued by IGF‐1 replacement therapy. © 2016 BioFactors, 42(1):60–79, 2016

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Low Doses of Insulin-Like Growth Factor-I Induce Mitochondrial Protection in Aging Rats

Cited by 100 publications

References 38 publications

Protection Against Oxidative Stress and “IGF-I Deficiency Conditions”

Protection Against Oxidative Stress and “IGF-I Deficiency Conditions”

Clinical and molecular diagnosis of a cartilage‐hair hypoplasia with IGF‐1 deficiency

Partial IGF‐1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy

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