Insulin-like growth factor II gene Apa I polymorphism is not associated with endometriosis susceptibility

Hsieh, Yao Yuan; Chang, Chi Chen; Tsai, Fuu Jen; Peng, Ching Tien; Yeh, Lian Shun; Lin, Cheng Chieh

doi:10.1590/s1415-47572004000200006

Cited by 4 publications

(2 citation statements)

References 11 publications

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“…In our previous reports, we observed a positive correlation of endometriosis with IL-1 (IL-1β-511 promoter, IL-1β exon 5) and p53 polymorphisms (Hsieh et al, 2001a,b;Chang et al, 2002). We also noted the non-correlation of endometriosis with the insulin growth factor (Hsieh et al, 2003), IL-4, TNF, and p21 . In this series, using the DdeI restriction enzyme polymorphism in exon 509 of TGF, we tried to evaluate whether this TGF-B1 polymorphism is a useful marker for predicting susceptibility to endometriosis.…”

Section: Introductionsupporting

confidence: 53%

Polymorphism for Transforming Growth Factor Beta 1-509 (TGF-B1-509): Association with Endometriosis

et al. 2005

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Transforming growth factor beta (TGF-B) family members are multi-functional cytokines that play a key role in cellular growth, proliferation, and differentiation. The aim of the study was to investigate whether the TGF-B1-509 gene polymorphism could be used as a marker of susceptibility in endometriosis. Women were divided into two groups: endometriosis (n = 150) and non-endometriosis (n = 159). Polymorphisms for TGF-B 1-509 genes were amplified by polymerase chain reaction and detected after restriction enzyme digestion. Genotypes and allelic frequencies in both groups were compared. Genotype proportions and allele frequencies of TGF-B1 gene polymorphisms differed significantly in both groups. Proportions of C homozygote, heterozygote, and T homozygote for TGF-B1 gene polymorphisms were 9.3/61.3/29.4% in the endometriosis group and 41.3158.510% in the non-endometriosis group. Alleles C and T for TGF-B1 gene polymorphism were 40/60% (endometriosis) and 70.8/29.2% (non-endometriosis). Association of endometriosis with TGF-B 1-509 gene polymorphism exists. T homozygote and T allele for TGF-B1 are associated with higher susceptibility to endometriosis.

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Section: Introductionsupporting

confidence: 53%

Polymorphism for Transforming Growth Factor Beta 1-509 (TGF-B1-509): Association with Endometriosis

et al. 2005

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“…The insulin-like growth factor II (IGF2) ApaI polymorphism was not found to be associated with endometriosis in Taiwanese women ( Hsieh et al ., 2004c ). Also, a polymorphism in the TGF beta 1 gene (509C/T) was not associated with deep infiltrating endometriosis in Dutch women ( van Kaam et al ., 2007a ).…”

Section: Resultsmentioning

confidence: 99%

Functional genetic polymorphisms and female reproductive disorders: Part II--endometriosis

Tempfer

Simoni

Destenaves

et al. 2008

Human Reproduction Update

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BACKGROUNDEndometriosis has a strong genetic component, and numerous genetic studies have been reported.METHODSWe have systematically reviewed these studies and included 114 in our final selection.RESULTSWe found no consistent evidence linking endometriosis with specific polymorphisms in genes encoding inflammatory mediators, proteins involved in sex steroid metabolism, vascular function and tissue remodelling. Although a number of polymorphisms have been associated with endometriosis in selected populations, the associations have not been independently confirmed, either because only single studies were carried out on these markers/genes or because other studies reported no association. The most solid evidence linking specific polymorphisms to endometriosis came from studies investigating glutathione-S-transferase, a phase II detoxification enzyme. Carriage of the GSTT1 null deletion variant showed consistent association with endometriosis with a 29% increased risk; however, it cannot be excluded that this result was due to publication bias, and this association should be independently confirmed in large-scale, well-designed case–control studies.CONCLUSIONSThe evidence of an association between genetic polymorphisms and endometriosis is weak. Carriage of the GSTT1 null deletion may moderately increase the risk of this disease. We suggest that the methodology of association studies should be improved in order to identify and validate associations in endometriosis.

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Relevance of insulin‐like growth factor 2 in the etiopathophysiology of diabetic nephropathy: Possible roles of phosphatase and tensin homolog on chromosome 10 and secreted protein acidic and rich in cysteine as regulators of repair

Movva

Venkatasubramanian

Kumar³

et al. 2009

Journal of Diabetes

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Background: Diabetic nephropathy (DN) is a devastating complication of diabetes, the exact molecular pathophysiology of which is not well established. Hyperglycemia increases insulin‐like growth factors (IGFs), especially IGF2, which acts via the IGF1 receptor present on renal cells. Elevated glucose levels damage the kidney, which is repaired by modulators such as secreted protein acidic and rich in cysteine (SPARC). Hence, it was hypothesized that IGF2 and SPARC may have an important role in the etiology of DN. Methods: Human renal biopsies, histopathologically categorized as normal, early Type 2 diabetes mellitus (T2DM), or established DN, were analyzed for the localization and expression of IGF2, its negative regulator phosphatase and tensin homolog on chromosome 10 (PTEN), and SPARC. Results: Expression of IGF2, PTEN, and SPARC was increased in renal biopsies from T2DM patients compared with normal samples. Although IGF2 protein was increased in biopsies from DN patients, PTEN and SPARC levels were decreased. Real‐time reverse transcription–polymerase chain reaction indicated that transcript levels of IGF2 and PTEN were greater than those of β‐actin in all human renal biopsy samples. Conclusion: The results suggest the following molecular etiopathophysiology of DN: (i) hyperglycemia upregulates IGF2, which initiates PTEN, a regulator of IGF2 signaling; (ii) loss of this IGF2–PTEN feedback loop causes changes that are characteristic of DN; and (iii) lowered expression of the repair modulator SPARC results in the development and/or progression of DN. Hence, targeting relevant modulators, such as like IGF2, PTEN, and SPARC, may be important in the management of DN.

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Insulin-like growth factor II gene Apa I polymorphism is not associated with endometriosis susceptibility

Cited by 4 publications

References 11 publications

Polymorphism for Transforming Growth Factor Beta 1-509 (TGF-B1-509): Association with Endometriosis

Polymorphism for Transforming Growth Factor Beta 1-509 (TGF-B1-509): Association with Endometriosis

Functional genetic polymorphisms and female reproductive disorders: Part II--endometriosis

Relevance of insulin‐like growth factor 2 in the etiopathophysiology of diabetic nephropathy: Possible roles of phosphatase and tensin homolog on chromosome 10 and secreted protein acidic and rich in cysteine as regulators of repair

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