Angiotensin-converting enzyme insertion/deletion (rs106180) and angiotensin type 1 receptor A1166C (rs106165) genotypes and psoriasis: Correlation with cellular immunity, lipid profile, and oxidative stress markers

Maryam Tanhapour, Badieh Falahi, Asad Vaisi-Raygani, Fariborz Bahrehmand, Amir Kiani, Zohreh Rahimi, Ali Akbar Vaisi-Raygani, Ebrahim Shakiba, Tayebeh Pourmotabbed

Research output: Contribution to journalArticle

Abstract

Psoriasis is a chronic inflammatory skin condition and angiotensin-converting enzyme (ACE) is a key circulating enzyme converting angiotensin (Ang) I to the vasoactive peptide Ang II. The exact role of ACE insertion (I)/deletion (D) polymorphism (rs106180) in psoriasis is not clear. We aimed to examine whether the ACE I/D and Ang II type 1 receptor (AT1R) A1166C-polymorphisms (rs106165), lipid profile, and stress oxidative are associated with susceptibility to psoriasis. One hundred patients with psoriasis and 100 sex- and age-matched unrelated healthy controls were recruited for this case-control study. ACE I/D and AT1R A1166C polymorphisms were identified by the polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism, respectively, malondialdehyde (MDA) was detected by the high-performance liquid chromatography, serum arylesterase (ARE) activity of paraoxonase and catalase activities were detected by the spectrophotometry, superoxide dismutase (SOD) activity and vascular adhesion protein (VAP)-1 were measured by ELISA. The presence of C allele of AT1R A1166C and I allele of ACE considerably increased the risk of psoriasis by 6.42-fold (P < 0.001). The distribution of II-genotype of ACE was significantly higher in psoriasis patients than in control group and increased the risk of disease by 3.11-times (P = 0.023). The higher levels of MDA in patients and the higher activity of SOD, ARE, and CAT was observed in healthy controls with I/D+I/I-genotype of ACE I/D. This study for the first time demonstrated that the ACE I/D and AT1R A 1166C genes polymorphisms robustly increases the risk of developing psoriasis in population from west of Iran. In addition, these individuals had significantly higher VAP-1 and MDA concentration and lower enzymatic and nonenzymatic antioxidant-status, suggesting that psoriatic patients carrying C allele of AT1R1166 polymorphism may be more susceptible to cardiovascular disease and myocardial infarction compared with A allele.

Original languageEnglish (US)
Pages (from-to)2627-2633
Number of pages7
JournalJournal of Cellular Biochemistry
Volume120
Issue number2
DOIs
StatePublished - Feb 1 2019

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Angiotensin Type 1 Receptor
Oxidative stress
Peptidyl-Dipeptidase A
Psoriasis
Cellular Immunity
Oxidative Stress
Genotype
Polymorphism
Lipids
Malondialdehyde
Alleles
Polymerase chain reaction
Superoxide Dismutase
Blood Vessels
Adhesion
Aryldialkylphosphatase
Polymerase Chain Reaction
Spectrophotometry
High performance liquid chromatography
Iran

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Angiotensin-converting enzyme insertion/deletion (rs106180) and angiotensin type 1 receptor A1166C (rs106165) genotypes and psoriasis : Correlation with cellular immunity, lipid profile, and oxidative stress markers. / Tanhapour, Maryam; Falahi, Badieh; Vaisi-Raygani, Asad; Bahrehmand, Fariborz; Kiani, Amir; Rahimi, Zohreh; Vaisi-Raygani, Ali Akbar; Shakiba, Ebrahim; Pourmotabbed, Tayebeh.

In: Journal of Cellular Biochemistry, Vol. 120, No. 2, 01.02.2019, p. 2627-2633.

Research output: Contribution to journalArticle

Tanhapour, Maryam ; Falahi, Badieh ; Vaisi-Raygani, Asad ; Bahrehmand, Fariborz ; Kiani, Amir ; Rahimi, Zohreh ; Vaisi-Raygani, Ali Akbar ; Shakiba, Ebrahim ; Pourmotabbed, Tayebeh. / Angiotensin-converting enzyme insertion/deletion (rs106180) and angiotensin type 1 receptor A1166C (rs106165) genotypes and psoriasis : Correlation with cellular immunity, lipid profile, and oxidative stress markers. In: Journal of Cellular Biochemistry. 2019 ; Vol. 120, No. 2. pp. 2627-2633.
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abstract = "Psoriasis is a chronic inflammatory skin condition and angiotensin-converting enzyme (ACE) is a key circulating enzyme converting angiotensin (Ang) I to the vasoactive peptide Ang II. The exact role of ACE insertion (I)/deletion (D) polymorphism (rs106180) in psoriasis is not clear. We aimed to examine whether the ACE I/D and Ang II type 1 receptor (AT1R) A1166C-polymorphisms (rs106165), lipid profile, and stress oxidative are associated with susceptibility to psoriasis. One hundred patients with psoriasis and 100 sex- and age-matched unrelated healthy controls were recruited for this case-control study. ACE I/D and AT1R A1166C polymorphisms were identified by the polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism, respectively, malondialdehyde (MDA) was detected by the high-performance liquid chromatography, serum arylesterase (ARE) activity of paraoxonase and catalase activities were detected by the spectrophotometry, superoxide dismutase (SOD) activity and vascular adhesion protein (VAP)-1 were measured by ELISA. The presence of C allele of AT1R A1166C and I allele of ACE considerably increased the risk of psoriasis by 6.42-fold (P < 0.001). The distribution of II-genotype of ACE was significantly higher in psoriasis patients than in control group and increased the risk of disease by 3.11-times (P = 0.023). The higher levels of MDA in patients and the higher activity of SOD, ARE, and CAT was observed in healthy controls with I/D+I/I-genotype of ACE I/D. This study for the first time demonstrated that the ACE I/D and AT1R A 1166C genes polymorphisms robustly increases the risk of developing psoriasis in population from west of Iran. In addition, these individuals had significantly higher VAP-1 and MDA concentration and lower enzymatic and nonenzymatic antioxidant-status, suggesting that psoriatic patients carrying C allele of AT1R1166 polymorphism may be more susceptible to cardiovascular disease and myocardial infarction compared with A allele.",
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AU - Vaisi-Raygani, Asad

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AU - Kiani, Amir

AU - Rahimi, Zohreh

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