IGF-I mediated survival pathways in normal and malignant cells

Kurmasheva, Raushan T.; Houghton, Peter J.

doi:10.1016/j.bbcan.2006.05.003

Cited by 124 publications

(142 citation statements)

References 199 publications

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“…Both circulating and locally produced IGF-I have cell-proliferative and anti-apoptotic properties (Kooijman, 2006;Kurmasheva and Houghton, 2006) by acting directly through its receptor, which is present in most organs and tissues (Werner and LeRoith, 2000), or indirectly by inhibiting inflammatory mediators such as TNF-α or nitric oxide (Hijikawa et al, 2008;Hill et al, 1999). Accordingly, it has been recently reported that IGF-I treatment prevents liver injury through the inhibition of TNF-α and iNOS induction in D-galactosamine and LPS-treated rats (Hijikawa et al, 2008) and that GHRP-2 treatment, a ghrelin analogue, prevents LPSinduced liver injury by increasing hepatic IGF-I and decreasing nitric oxide concentrations and TNF-α gene expression (Granado et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Ghrelin treatment protects lactotrophs from apoptosis in the pituitary of diabetic rats

Granado¹,

Chowen²,

García‐Cáceres³

et al. 2009

Molecular and Cellular Endocrinology

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Poorly controlled diabetes is associated with hormonal imbalances, including decreased prolactin production partially due to increased lactotroph apoptosis. In addition to its metabolic actions, ghrelin inhibits apoptosis in several cell types. Thus, we analyzed ghrelin's effects on diabetes-induced pituitary cell death and hormonal changes. Six weeks after onset of diabetes in male Wistar rats (streptozotocin 70 mg/kg), mini-pumps infusing saline or 24 nmol ghrelin/day were implanted (jugular). Rats were killed two weeks later. Ghrelin did not modify body weight or serum glucose, leptin or adiponectin, but increased total ghrelin (p<0.05), IGF-I (p<0.01) and prolactin (p<0.01) levels. Ghrelin decreased cell death, iNOS and active caspase-8 (p<0.05) and increased prolactin (p<0.05), Bcl-2 (p<0.01) and Hsp70 (p<0.05) content in the pituitary. In conclusion, ghrelin prevents diabetes-induced death of lactotrophs, decreasing caspase-8 activation and iNOS content and increasing anti-apoptotic pathways such as pituitary Bcl-2 and Hsp70 and serum IGF-I concentrations.

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Section: Discussionmentioning

confidence: 99%

Ghrelin treatment protects lactotrophs from apoptosis in the pituitary of diabetic rats

Granado¹,

Chowen²,

García‐Cáceres³

et al. 2009

Molecular and Cellular Endocrinology

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“…The antiapoptotic activity of IGF-I has been ascribed to multiple signal transduction pathways. 24,25 The PI3K pathway is considered a major intracellular route that mediates the antiapoptotic activity of IGF-I, but MAPK (ERK1/2, JNK and p38 kinase) pathways are implicated as well. 24 It has been demonstrated previously that protection against ER stress-induced apoptosis is mediated, at least in part, by the PI3K/Akt/glycogen synthase-3b pathway.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor-I protects cells from ER stress-induced apoptosis via enhancement of the adaptive capacity of endoplasmic reticulum

et al. 2008

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“…T he insulin-like growth factor receptor (IGF-1R) 3 pathway plays important and diverse roles in growth and development (1). This tyrosine kinase receptor has been implicated in several metabolic, neoplastic, and immunological diseases (2)(3)(4).…”

mentioning

confidence: 99%

“…This tyrosine kinase receptor has been implicated in several metabolic, neoplastic, and immunological diseases (2)(3)(4). IGF-1R and associated IGF-1-binding proteins constitute a cell surface signaling complex (5).…”

mentioning

confidence: 99%

Aberrant Expression of the Insulin-Like Growth Factor-1 Receptor by T Cells from Patients with Graves’ Disease May Carry Functional Consequences for Disease Pathogenesis

Douglas

Gianoukakis

Kamat

et al. 2007

The Journal of Immunology

131

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Graves’ disease (GD), an autoimmune process involving thyroid and orbital tissue, is associated with lymphocyte abnormalities including expansion of memory T cells. Insulin-like growth factor receptor-1 (IGF-1R)-bearing fibroblasts overpopulate connective tissues in GD. IGF-1R on fibroblasts, when ligated with IgGs from these patients, results in the expression of the T cell chemoattractants, IL-16 and RANTES. We now report that a disproportionately large fraction of peripheral blood T cells express IGF-1R (CD3+IGF-R+). CD3+IGF-1R+ T cells comprise 48 ± 4% (mean ± SE; n = 33) in patients with GD compared with 15 ± 3% (n = 21; p < 10−8) in controls. This increased population of IGF-1R+ T cells results, at least in part, from an expansion of CD45RO+ T cells expressing the receptor. In contrast, the fraction of CD45RA+IGF-1R+ T cells is similar in GD and controls. T cells harvested from affected orbital tissues in GD reflect similar differences in the proportion of IGF-1R+CD3+ and IGF-1R+CD4+CD3+ cells as those found in the peripheral circulation. GD-derived peripheral T cells express durable, constitutive IGF-1R expression in culture and receptor levels are further up-regulated following CD3 complex activation. IGF-1 enhanced GD-derived T cell incorporation of BrdU (p < 0.02) and inhibited Fas-mediated apoptosis (p < 0.02). These findings suggest a potential role for IGF-1R displayed by lymphocytes in supporting the expansion of memory T cells in GD.

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IGF-I mediated survival pathways in normal and malignant cells

Cited by 124 publications

References 199 publications

Ghrelin treatment protects lactotrophs from apoptosis in the pituitary of diabetic rats

Ghrelin treatment protects lactotrophs from apoptosis in the pituitary of diabetic rats

Insulin-like growth factor-I protects cells from ER stress-induced apoptosis via enhancement of the adaptive capacity of endoplasmic reticulum

Aberrant Expression of the Insulin-Like Growth Factor-1 Receptor by T Cells from Patients with Graves’ Disease May Carry Functional Consequences for Disease Pathogenesis

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