The Role of Insulin-Like Growth Factor-I in the Physiopathology of Hearing

Murillo-Cuesta, Silvia; Rosa, Lourdes Rodríguez-de la; Cediel, Rafael; Lassaletta, Luis; Varela-Nieto, Isabel

doi:10.3389/fnmol.2011.00011

Cited by 49 publications

(51 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ACCEPTED MANUSCRIPT [20], metabolic diseases, and cancer [21]. Examples of mechanisms that produce such epigenetic changes are DNA methylation in regions of the IGF-1 promoter that are dense with CpG dinucleotides (CpG islands), and histone modification, each of which alters how the IGF-1 gene is expressed [6,7].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Epigenetic regulation of insulin-like growth factor signaling: A novel insight into the pathophysiology of neonatal pulmonary hypertension

Madonna

Caterina

Geng

2015

Vascular Pharmacology

View full text Add to dashboard Cite

Section: Accepted Manuscriptmentioning

confidence: 99%

Epigenetic regulation of insulin-like growth factor signaling: A novel insight into the pathophysiology of neonatal pulmonary hypertension

Madonna

Caterina

Geng

2015

Vascular Pharmacology

View full text Add to dashboard Cite

“…Human homozygous loss-of-function IGF1 gene mutations cause intrauterine and postnatal growth failure and severe sensorineural deafness (OMIM 608747) [1], [2]. Treatment with recombinant human IGF-I has been shown to improve short stature in patients with severe IGF-I deficiency [3], supporting the key role of IGF-I in skeletal development.…”

Section: Introductionmentioning

confidence: 99%

Treatment with N- and C-Terminal Peptides of Parathyroid Hormone-Related Protein Partly Compensate the Skeletal Abnormalities in IGF-I Deficient Mice

et al. 2014

Self Cite

View full text Add to dashboard Cite

Insulin-like growth factor-I (IGF-I) deficiency causes growth delay, and IGF-I has been shown to partially mediate bone anabolism by parathyroid hormone (PTH). PTH-related protein (PTHrP) is abundant in bone, and has osteogenic features by poorly defined mechanisms. We here examined the capacity of PTHrP (1–36) and PTHrP (107–111) (osteostatin) to reverse the skeletal alterations associated with IGF-I deficiency. Igf1-null mice and their wild type littermates were treated with each PTHrP peptide (80 µg/Kg/every other day/2 weeks; 2 males and 4 females for each genotype) or saline vehicle (3 males and 3 females for each genotype). We found that treatment with either PTHrP peptide ameliorated trabecular structure in the femur in both genotypes. However, these peptides were ineffective in normalizing the altered cortical structure at this bone site in Igf1-null mice. An aberrant gene expression of factors associated with osteoblast differentiation and function, namely runx2, osteoprotegerin/receptor activator of NF-κB ligand ratio, Wnt3a , cyclin D1, connexin 43, catalase and Gadd45, as well as in osteocyte sclerostin, was found in the long bones of Igf1-null mice. These mice also displayed a lower amount of trabecular osteoblasts and osteoclasts in the tibial metaphysis than those in wild type mice. These alterations in Igf1-null mice were only partially corrected by each PTHrP peptide treatment. The skeletal expression of Igf2, Igf1 receptor and Irs2 was increased in Igf1-null mice, and this compensatory profile was further improved by treatment with each PTHrP peptide related to ERK1/2 and FoxM1 activation. In vitro, PTHrP (1–36) and osteostatin were effective in promoting bone marrow stromal cell mineralization in normal mice but not in IGF-I-deficient mice. Collectively, these findings indicate that PTHrP (1–36) and osteostatin can exert several osteogenic actions even in the absence of IGF-I in the mouse bone.

show abstract

“…Two major signal transduction systems activated by binding of IGF1 to the IGF1R are the MAPK pathway, which leads to increases in proliferation, growth, and differentiation, and the PI3K/AKT pathway, which inhibits apoptosis (63). Actions of IGF1 on the preimplantation embryo indicate that both MAPK and PI3K/AKT pathways are activated (Figure 2).…”

Section: Insulin-like Growth Factormentioning

confidence: 99%

Maternal embryokines that regulate development of the bovine preimplantation embryo

Hansen¹,

Denicol²,

Dobbs³

2014

Turk J Vet Anim Sci

View full text Add to dashboard Cite

The zygote contains within its genome and epigenome the program to direct development through the embryonic, fetal, and postnatal periods. The execution of that program is dependent on the embryo's nongenetic inheritance from the oocyte and sperm (1,2) as well as on the environment in which development proceeds. Variation in the maternal environment can affect the ability of the preimplantation embryo to establish pregnancy. In cattle, the focus of this review, competence of the preimplantation embryo for growth and survival can be affected by maternal parity (3), lactational status (4), and circulating concentrations of progesterone (5). Moreover, patterns of gene expression in the endometrium are associated with survival of an embryo transferred to the uterus in the next ovulatory cycle (6,7).Development of the bovine embryo to the blastocyst in the absence of maternal signals (i.e. through in vitro production procedures) results in embryos with aberrant gene expression (8,9), lipid content (10,11), DNA methylation (12), and, as shown in the Table, reduced competence to establish pregnancy after transfer into recipients (13-17). Additionally, an increased proportion of embryos produced in vitro have developmental abnormalities that lead to increased neonatal death losses (18-20). Some of the problems with the in vitro-produced embryo could result from selection of incompetent oocytes or inadequate oocyte maturation. However, the importance of the maternal environment during development is indicated by observations that transfer of in vitro-produced embryos to the oviduct after fertilization limits some of the abnormalities associated with in vitro production (9,21).One function of the reproductive tract is to secrete bioactive molecules that regulate the embryo, oviduct, or endometrium. Genes for 115 ligands expressed in the endometrium had the corresponding receptor gene expressed by the embryo (22). Regulatory molecules produced by the oviduct and endometrium, which include hormones, growth factors, and cytokines, are referred to as embryokines when they function to regulate embryonic growth and development (23).It is likely that some of the variation in the ability of the reproductive tract to support embryonic development represents variation in secretion of embryokines. Indeed, several genes that were overexpressed in the endometrium of cows that subsequently became pregnant after embryo transfer as compared to cows that did not establish pregnancy are potential embryokines. These include NGF,

show abstract

The Role of Insulin-Like Growth Factor-I in the Physiopathology of Hearing

Cited by 49 publications

References 130 publications

Epigenetic regulation of insulin-like growth factor signaling: A novel insight into the pathophysiology of neonatal pulmonary hypertension

Epigenetic regulation of insulin-like growth factor signaling: A novel insight into the pathophysiology of neonatal pulmonary hypertension

Treatment with N- and C-Terminal Peptides of Parathyroid Hormone-Related Protein Partly Compensate the Skeletal Abnormalities in IGF-I Deficient Mice

Maternal embryokines that regulate development of the bovine preimplantation embryo

Contact Info

Product

Resources

About