Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/14835
Title: Glutamate carboxypeptidase II (<i style="mso-bidi-font-style:normal">GCPII</i>) genetic variants as determinants of hyperhomocysteinemia: Implications in stroke susceptibility
Authors: Divyya, Shree
Naushad, Shaik Mohammad
Kaul, Subhash
Anusha, Vuppala
Subbarao, Sreedhar Amere
Kutala, Vijay Kumar
Keywords: Glutamate Carboxypeptidase II
NAALADase
Homocysteine
Folate
Haplotype
Stroke
Issue Date: Oct-2012
Publisher: NISCAIR-CSIR, India
Abstract: <span style="mso-bidi-font-size:9.0pt;letter-spacing: -.1pt" lang="EN-GB">The rationale of this case-control study is to ascertain whether glutamate carboxypeptidase II (<i>GCPII</i>) variants serve as determinants of hyperhomocysteinemia and contribute to the etiology of stroke. Hyperhomocysteinemia was observed in stroke cases compared to controls (14.09 ± 7.62 <span style="mso-bidi-font-size:9.0pt;font-family:Symbol; mso-ascii-font-family:" times="" new="" roman";mso-hansi-font-family:"times="" roman";="" letter-spacing:-.1pt;mso-char-type:symbol;mso-symbol-font-family:symbol"="" lang="EN-GB">m<span style="mso-bidi-font-size:9.0pt;letter-spacing:-.1pt" lang="EN-GB">mol/L vs. 8.71 ± 4.35, <i style="mso-bidi-font-style:normal">P</i><0.0001).<i style="mso-bidi-font-style:normal"> GCPII</i> sequencing revealed two known variants (R190W and H475Y) and six novel variants (V108A, P160S, Y176H, G206R, G245S and D520E). Among the haplotypes of <i style="mso-bidi-font-style:normal">GCPII</i>, all wild-haplotype H0 showed independent association with stroke risk (OR: 9.89, 95% CI: 4.13-23.68), while H2 representing P160S variant showed reduced risk (OR: 0.17, 95% CI: 0.06-0.50). When compared to subjects with H2 haplotype, H0 haplotype showed elevated homocysteine levels (18.26 ± 4.31 <span style="mso-bidi-font-size:9.0pt;font-family:Symbol;mso-ascii-font-family: " times="" new="" roman";mso-hansi-font-family:"times="" roman";letter-spacing:-.1pt;="" mso-char-type:symbol;mso-symbol-font-family:symbol"="" lang="EN-GB">m<span style="mso-bidi-font-size:9.0pt;letter-spacing:-.1pt" lang="EN-GB">mol/L vs. 13.66 ± 3.72 <span style="mso-bidi-font-size:9.0pt;font-family:Symbol;mso-ascii-font-family: " times="" new="" roman";mso-hansi-font-family:"times="" roman";letter-spacing:-.1pt;="" mso-char-type:symbol;mso-symbol-font-family:symbol"="" lang="EN-GB">m<span style="mso-bidi-font-size:9.0pt;letter-spacing:-.1pt" lang="EN-GB">mol/L, <i style="mso-bidi-font-style:normal">P</i> = 0.002) and reduced plasma folate levels (<span style="mso-bidi-font-size:9.0pt;letter-spacing: -.1pt;mso-ansi-language:EN-US" lang="EN-US">7.09 ± 1.19 ng/ml vs. 8.21 ± 1.14 ng/ml, <i style="mso-bidi-font-style:normal">P</i> = 0.007<span style="mso-bidi-font-size:9.0pt;letter-spacing:-.1pt" lang="EN-GB">). Using <i style="mso-bidi-font-style:normal">GCPII</i> genetic variants, dietary folate and gender as predictor variables and homocysteine as outcome variable, a multiple linear regression model was developed. This model explained 36% variability in plasma homocysteine levels. To conclude, <i>GCPII </i>haplotypes influenced susceptibility to stroke by influencing homocysteine levels. </span></span></span></span></span></span></span></span></span>
Description: 356-362
URI: http://hdl.handle.net/123456789/14835
ISSN: 0975-0959 (Online); 0301-1208 (Print)
Appears in Collections:IJBB Vol.49(5) [October 2012]

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