Insulin-like growth factor I regulates renal development in rodents

Rogers, Sharon A.; Powell-Braxton, Lyn; Hammerman, Marc R.

doi:10.1002/(sici)1520-6408(1999)24:3/4<293::aid-dvg12>3.0.co;2-s

Cited by 88 publications

(45 citation statements)

References 16 publications

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“…Transgenic mice with global overexpression of GH and/or IGF-I have selective renal enlargement and glomerular hypertrophy, whereas only the mice with global overexpression of GH have mesangial proliferation followed by progressive glomerulosclerosis (Doi et al 1988, 1990, Mathews et al 1988, Cingel-Ristic et al 2004. Mice with global inactivation of the IGF-I gene that survive the postnatal period have reduced body weight, proportionally reduced kidney size, reduced glomerular size, and decreased number of nephrons (Rogers et al 1999, Cingel-Ristic et al 2004. However, these studies cannot evaluate the role of IGF-I in adult or aging animals, as they are confounded by affected IGF-I activity during development.…”

Section: Discussionmentioning

confidence: 99%

Liver-derived IGF-I regulates kidney size, sodium reabsorption, and renal IGF-II expression

Svensson¹,

Tivesten²,

Sjögren³

et al. 2007

Journal of Endocrinology

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Section: Discussionmentioning

confidence: 99%

Liver-derived IGF-I regulates kidney size, sodium reabsorption, and renal IGF-II expression

Svensson¹,

Tivesten²,

Sjögren³

et al. 2007

Journal of Endocrinology

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“…Studies of knockout mice and experiments using metanephron culture systems (Wada et al 1993, Rogers et al 1999 have shown that these genes play an important role in kidney development, indeed mice lacking the IGF-I gene have proportionately smaller kidneys with fewer nephrons and reduced glomerular size. It is possible, therefore, that following NR kidney development in twins may not be as effective as in nutrient restricted singletons.…”

Section: Discussionmentioning

confidence: 99%

“…This same period of NR has also been shown to affect the expression of insulin-like growth factor (IGF) -I and -II in both the liver and skeletal muscle without having any effect on organ weight (Brameld et al 2000). IGFs have an important role in the normal development of the fetal kidney (Rogers et al 1999) and the kidneys of growth retarded fetuses are much more sensitive to the effects of growth hormone (GH) administration (Bauer et al 2003) thus it is likely that maternal NR could compromise kidney development through local disruption of growth factor abundance. An increase in fat mass surrounding the kidney is also likely to have important later consequences as this can influence the local endocrine environment of the kidney and cause a direct physical constraint upon the kidney (Hall 2003).…”

Section: Introductionmentioning

confidence: 99%

Impact of maternal undernutrition and fetal number on glucocorticoid, growth hormone and insulin-like growth factor receptor mRNA abundance in the ovine fetal kidney

Brennan

Gopalakrishnan²,

Kurlak³

et al. 2005

Reproduction

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Epidemiological and animal studies strongly indicate that the environment experienced in utero determines, in part, an individual's likelihood of developing cardiovascular disease in later life. This risk has been further linked to impaired kidney function, as a result of compromised development during fetal life. The present study therefore examined the influence of maternal nutrient restriction (NR), targeted at specific periods of kidney development during early to mid gestation, on the mRNA abundance of receptors for glucocorticoid (GCR), growth hormone (GHR) and insulin-like growth factors-I (IGF-IR) and -II (IGF-IIR), and the IGF-I and -II ligands. This was undertaken in both singleton and twin fetuses. At conception ewes were randomly allocated to either an adequately fed control group or one of four nutrient-restricted groups that were fed half the control amount from 0 to 30, 31 to 65, 66 to110 or 0 to110 days gestation. At 110 days gestation all ewes were humanely euthanased and fetal kidneys and surrounding adipose tissue sampled. There was no effect of NR or fetal number on kidney weight, shape or nephron number, but the surrounding fat mass was increased in singleton fetuses exposed to NR for 110 days. An increase in kidney mRNA abundance with NR only occurred in singleton fetuses where IGF-IR mRNA was enhanced with NR from 66 -110 days gestation. In twin fetuses, NR had no effect on mRNA abundance. However, for all genes examined mRNA expression was lower in the kidneys of twin compared with singleton fetuses following NR, and the magnitude of the effect was dependent on the timing of NR. In conclusion, the abundance of mRNA for receptors which regulate fetal kidney development are lower in twin animals compared with singletons following periods of nutrient deficiency. This may impact on later kidney development and function.

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“…Whatever cell is used, an ability to manipulate these cells genetically also may allow for the regulation of red cell count and bone density. The onward development and neovascularization of transplanted metanephroi can be enhanced via the addition of growth hormone, IGF1, hepatocyte growth factor, and fibroblast growth factor 2 (90,(103)(104)(105). Such research starts to define growth factors that may assist in de novo organ generation.…”

Section: Recapitulating Development To Create a Kidney De Novomentioning

confidence: 99%

Regrow or Repair

Little

2006

Journal of the American Society of Nephrology

153

121

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Regenerative medicine is being heralded in a similar way as gene therapy was some 15 yr ago. It is an area of intense excitement and potential, as well as myth and disinformation. However, with the increasing rate of end-stage renal failure and limited alternatives for its treatment, we must begin to investigate seriously potential regenerative approaches for the kidney. This review defines which regenerative options there might be for renal disease, summarizes the progress that has been made to date, and investigates some of the unique obstacles to such treatments that the kidney presents. The options discussed include in situ organ repair via bone marrow recruitment or dedifferentiation; ex vivo stem cell therapies, including both autologous and nonautologous options; and bioengineering approaches for the creation of a replacement organ.

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Insulin-like growth factor I regulates renal development in rodents

Cited by 88 publications

References 16 publications

Liver-derived IGF-I regulates kidney size, sodium reabsorption, and renal IGF-II expression

Liver-derived IGF-I regulates kidney size, sodium reabsorption, and renal IGF-II expression

Impact of maternal undernutrition and fetal number on glucocorticoid, growth hormone and insulin-like growth factor receptor mRNA abundance in the ovine fetal kidney

Regrow or Repair

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