FOXC2 and FLT4 Gene Variants in Lymphatic Filariasis.
Identifieur interne : 000E21 ( PubMed/Corpus ); précédent : 000E20; suivant : 000E22FOXC2 and FLT4 Gene Variants in Lymphatic Filariasis.
Auteurs : Yasmeen Sheik ; Sameera Fatima Qureshi ; Basheeruddin Mohhammed ; Pratibha NallariSource :
- Lymphatic research and biology [ 1557-8585 ] ; 2015.
English descriptors
- KwdEn :
- Adult, Alleles, Cohort Studies, Elephantiasis, Filarial (diagnosis), Elephantiasis, Filarial (genetics), Female, Forkhead Transcription Factors (genetics), Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, Genotype, Humans, Male, Middle Aged, Odds Ratio, Polymorphism, Single Nucleotide, Vascular Endothelial Growth Factor Receptor-3 (genetics).
- MESH :
- chemical , genetics : Forkhead Transcription Factors, Vascular Endothelial Growth Factor Receptor-3.
- diagnosis : Elephantiasis, Filarial.
- genetics : Elephantiasis, Filarial.
- Adult, Alleles, Cohort Studies, Female, Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, Genotype, Humans, Male, Middle Aged, Odds Ratio, Polymorphism, Single Nucleotide.
Abstract
Lymphatic filariasis is the leading cause of secondary lymphedema wherein lymph transport is impaired due to lymphatic damage. FLT4 signaling and transcription factors such as FOXC2 play an important role in this type of lymphangiogenesis process induced by filarial parasites. The present study aims to assess the association of FLT4 and FOXC2 genes in lymphatic development/remodeling in lymphatic filariasis. A total of 118 lymphatic filariasis patients and 100 non-endemic and 50 endemic healthy subjects were enrolled for the present study. Allele-specific PCR and PCR-RFLP were adopted for the genotyping, and screening of FLT4 and FOXC2 genes was carried out by PCR-SSCP, followed by in-silico and statistical analysis. A novel variation (G357A SNP) was identified on FOXC2 gene screening that may have an effect on codon usage frequency during translational process. In FLT4, A3123G mutation was found in 3.39% of the case subjects but the functional role of this mutation, along with subject's clinical presentations and patient's age, emphasize its pathogenic role in lymphedema development. Two of the subjects exhibit compound heterozygosity (A3123G FLT4 mutation and G357A SNP of FOXC2 gene). As these two genes share a common pathway, we hypothesise a synergistic interaction of these two SNPs in inhibiting the downstream signaling resulting in lymphedema progression.
DOI: 10.1089/lrb.2014.0025
PubMed: 26091406
Links to Exploration step
pubmed:26091406Le document en format XML
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<author><name sortKey="Sheik, Yasmeen" sort="Sheik, Yasmeen" uniqKey="Sheik Y" first="Yasmeen" last="Sheik">Yasmeen Sheik</name>
<affiliation><nlm:affiliation>1 Department of Genetics, Osmania University , Hyderabad, Telangana, India .</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Qureshi, Sameera Fatima" sort="Qureshi, Sameera Fatima" uniqKey="Qureshi S" first="Sameera Fatima" last="Qureshi">Sameera Fatima Qureshi</name>
<affiliation><nlm:affiliation>1 Department of Genetics, Osmania University , Hyderabad, Telangana, India .</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Mohhammed, Basheeruddin" sort="Mohhammed, Basheeruddin" uniqKey="Mohhammed B" first="Basheeruddin" last="Mohhammed">Basheeruddin Mohhammed</name>
<affiliation><nlm:affiliation>2 NFCP (National Filariasis Control program Centre) , Siddipet, Medak, Telangana, India .</nlm:affiliation>
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<author><name sortKey="Nallari, Pratibha" sort="Nallari, Pratibha" uniqKey="Nallari P" first="Pratibha" last="Nallari">Pratibha Nallari</name>
<affiliation><nlm:affiliation>1 Department of Genetics, Osmania University , Hyderabad, Telangana, India .</nlm:affiliation>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">FOXC2 and FLT4 Gene Variants in Lymphatic Filariasis.</title>
<author><name sortKey="Sheik, Yasmeen" sort="Sheik, Yasmeen" uniqKey="Sheik Y" first="Yasmeen" last="Sheik">Yasmeen Sheik</name>
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<author><name sortKey="Qureshi, Sameera Fatima" sort="Qureshi, Sameera Fatima" uniqKey="Qureshi S" first="Sameera Fatima" last="Qureshi">Sameera Fatima Qureshi</name>
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<author><name sortKey="Mohhammed, Basheeruddin" sort="Mohhammed, Basheeruddin" uniqKey="Mohhammed B" first="Basheeruddin" last="Mohhammed">Basheeruddin Mohhammed</name>
<affiliation><nlm:affiliation>2 NFCP (National Filariasis Control program Centre) , Siddipet, Medak, Telangana, India .</nlm:affiliation>
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<author><name sortKey="Nallari, Pratibha" sort="Nallari, Pratibha" uniqKey="Nallari P" first="Pratibha" last="Nallari">Pratibha Nallari</name>
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<series><title level="j">Lymphatic research and biology</title>
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<term>Elephantiasis, Filarial (diagnosis)</term>
<term>Elephantiasis, Filarial (genetics)</term>
<term>Female</term>
<term>Forkhead Transcription Factors (genetics)</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease</term>
<term>Genetic Variation</term>
<term>Genotype</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Odds Ratio</term>
<term>Polymorphism, Single Nucleotide</term>
<term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Forkhead Transcription Factors</term>
<term>Vascular Endothelial Growth Factor Receptor-3</term>
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<keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Elephantiasis, Filarial</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Elephantiasis, Filarial</term>
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<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Alleles</term>
<term>Cohort Studies</term>
<term>Female</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease</term>
<term>Genetic Variation</term>
<term>Genotype</term>
<term>Humans</term>
<term>Male</term>
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<front><div type="abstract" xml:lang="en">Lymphatic filariasis is the leading cause of secondary lymphedema wherein lymph transport is impaired due to lymphatic damage. FLT4 signaling and transcription factors such as FOXC2 play an important role in this type of lymphangiogenesis process induced by filarial parasites. The present study aims to assess the association of FLT4 and FOXC2 genes in lymphatic development/remodeling in lymphatic filariasis. A total of 118 lymphatic filariasis patients and 100 non-endemic and 50 endemic healthy subjects were enrolled for the present study. Allele-specific PCR and PCR-RFLP were adopted for the genotyping, and screening of FLT4 and FOXC2 genes was carried out by PCR-SSCP, followed by in-silico and statistical analysis. A novel variation (G357A SNP) was identified on FOXC2 gene screening that may have an effect on codon usage frequency during translational process. In FLT4, A3123G mutation was found in 3.39% of the case subjects but the functional role of this mutation, along with subject's clinical presentations and patient's age, emphasize its pathogenic role in lymphedema development. Two of the subjects exhibit compound heterozygosity (A3123G FLT4 mutation and G357A SNP of FOXC2 gene). As these two genes share a common pathway, we hypothesise a synergistic interaction of these two SNPs in inhibiting the downstream signaling resulting in lymphedema progression.</div>
</front>
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<ArticleTitle>FOXC2 and FLT4 Gene Variants in Lymphatic Filariasis.</ArticleTitle>
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<Abstract><AbstractText>Lymphatic filariasis is the leading cause of secondary lymphedema wherein lymph transport is impaired due to lymphatic damage. FLT4 signaling and transcription factors such as FOXC2 play an important role in this type of lymphangiogenesis process induced by filarial parasites. The present study aims to assess the association of FLT4 and FOXC2 genes in lymphatic development/remodeling in lymphatic filariasis. A total of 118 lymphatic filariasis patients and 100 non-endemic and 50 endemic healthy subjects were enrolled for the present study. Allele-specific PCR and PCR-RFLP were adopted for the genotyping, and screening of FLT4 and FOXC2 genes was carried out by PCR-SSCP, followed by in-silico and statistical analysis. A novel variation (G357A SNP) was identified on FOXC2 gene screening that may have an effect on codon usage frequency during translational process. In FLT4, A3123G mutation was found in 3.39% of the case subjects but the functional role of this mutation, along with subject's clinical presentations and patient's age, emphasize its pathogenic role in lymphedema development. Two of the subjects exhibit compound heterozygosity (A3123G FLT4 mutation and G357A SNP of FOXC2 gene). As these two genes share a common pathway, we hypothesise a synergistic interaction of these two SNPs in inhibiting the downstream signaling resulting in lymphedema progression.</AbstractText>
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