Patterns of angiotensin converting enzyme insertion/deletion gene polymorphism among an <scp>E</scp>gyptian cohort of patients with rheumatoid arthritis

Ahmed, Afaf Z.; El-Shahaly, Hassan A.; Omar, Aziza Sayed; Ghattas, Maivel H.

doi:10.1111/j.1756-185x.2012.01820.x

Cited by 10 publications

(11 citation statements)

References 19 publications

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“…Therefore, we speculated that there may be an alternative inflammatory pathway through bradykinin activation in patients with AS. This speculation is also consistent with the results of various studies which suggested ACE inhibition for therapeutic effects in human inflammatory arthritis [12] and also a role for this enzyme in the pathophysiology of RA [35]. I allele of the ACE I/D polymorphism was found to be related to radiographically severe form of osteoarthritis and poor function.…”

Section: Discussionsupporting

confidence: 80%

“…This relationship suggests a link between disease severity of osteoarthritis and I allele; however, there were no significant relationships between the distribution of genotypes and alleles of the ACE I/D polymorphism and susceptibility of knee osteoarthritis [14]. No relationships between disease severity and ACE ID genotypes' and alleles' distribution and RA patients were also reported [35]. Conversely, we found significant relationships between I allele of the ACE I/D polymorphism and susceptibility of AS.…”

Section: Discussionmentioning

confidence: 61%

“…No significant relationships between ACE I/D polymorphism and the patients with RA [23] and psoriatic arthritis [33] were reported. Inconsistent with these results, the ACE gene D allele and DD genotype were found to be related to increased risk of RA [10,34,35]. The DD genotype was found to increase RA development for approximately threefold and sixfold, respectively [34,35].…”

Section: Discussionmentioning

confidence: 76%

“…Inconsistent with these results, the ACE gene D allele and DD genotype were found to be related to increased risk of RA [10,34,35]. The DD genotype was found to increase RA development for approximately threefold and sixfold, respectively [34,35]. Similarly, DD genotype of ACE I/D polymorphism was linked to increased susceptibility to osteoarthritis [16] and AS [9].…”

Section: Discussionmentioning

confidence: 79%

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Association of GSTM1, GSTT1, GSTP1-ILE105VAL and ACE I/D polymorphisms with ankylosing spondylitis

et al. 2015

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Ankylosing spondylitis (AS) is a chronic inflammatory disease of unknown origin. The aim of this study is to clarify the relationships between susceptibility and severity of AS and GST-mu1 (GSTM1), GST-theta1 (GSTT1), GST-pi1 (GSTP1)-Ile105Val and angiotensin-converting enzyme (ACE) I/D polymorphisms in AS patients. One hundred thirty-eight AS patients and seventy-one healthy controls were enrolled in this study. Erythrocyte sedimentation rate and C-reactive protein (CRP) levels of the AS patients were recorded. The scores of the numeric rating scale (NRS) pain, the Bath Ankylosing Spondylitis Activity Index, the Bath Ankylosing Spondylitis Metrology Index and the Bath Ankylosing Spondylitis Functional Index were calculated. The genotypes distributions and allele frequencies of GSTM1, GSTT1, GSTP1-Ile105Val and ACE I/D polymorphisms were compared between patients and healthy controls. The Multiplex polymerase chain reaction (PCR) and the PCR-restriction fragment length polymorphism methods were used to detect the polymorphisms of ACE I/D, the GSTT1 and GSTM1 genes and the GSTP1-Ile105Val polymorphism, respectively. There were significantly higher levels of the GSTT1 null and the ACE II genotypes in AS patients compared to those in healthy controls (p = 0.002 and 0.005, respectively). We found significantly higher levels of CRP and the NRS pain scores in the patients with ACE ID or DD genotypes compared to those in the patients with ACE II genotypes (p = 0.005 and 0.035, respectively). The present results showed that genes involved in protection from oxidative stress and ACE gene may influence disease development and course in AS.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 79%

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Association of GSTM1, GSTT1, GSTP1-ILE105VAL and ACE I/D polymorphisms with ankylosing spondylitis

et al. 2015

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“…However, stimulation of AT2R has physiological effects opposite to stimulation of AT1R, such as vasodilation, inhibition of infl ammatory response, anti-fi brosis, and promotion of neuronal repair and regeneration (8)(9)(10)(11). Study showed that Ang II, AT1R, AT2R iNOS and TGM2 were signifi cantly increased in rheumatoid arthritis (RA), but AT1R was more signifi cantly increased than AT2R (12). The ratio of AT1R to AT2R was signifi cantly increased which has broken the original balance of AT1R/AT2R.…”

Section: Introductionmentioning

confidence: 99%

AT1/2R affects the proliferation and apoptosis of chondrocytes induced by oxygen-glucose deprivation

Cai¹,

Miao²,

Zhang³

2020

BLL

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AIM: Investigate how AT1/2R affected the proliferation and apoptosis of chondrocytes induced by oxygenglucose deprivation. METHODS: The proliferation and apoptosis of ATDC5 cells was detected by CCK-8 assay and fl ow cytometry analysis. The expression of Bax, Bcl-2, caspase-3, cleaved-caspase-3, AT1R, AT2R and HIF-1 was determined by Western blot analysis. The collagen II expression was detected by ELISA assay. RESULTS: Increased ratio of AT1R to AT2R induced by Ang II suppressed the proliferation of oxygen-glucose deprivation ATDC5 cells. Telmisartan, as AT1R inhibitor, promoted the proliferation and inhibited the apoptosis of ATDC5 cells and oxygen-glucose deprivation ATDC5 cells. The collagen II expression either intracellular or cellular supernatant was decreased after Ang II treatment, which was reversed by telmisartan. And, telmisartan reduced the AT1R expression while increased the AT2R expression in ATDC5 cells and oxygenglucose deprivation ATDC5 cells. CONCLUSIONS: Ang II caused an increased ratio of AT1R to AT2R, which suppressed the proliferation of oxygen-glucose deprivation ATDC5 cells. Furthermore, telmisartan caused a decrease of AT1R and increase of AT2R, which promoted the proliferation and inhibited the apoptosis of oxygen-glucose deprivation ATDC5 cells. This new fi nding could provide a new insight into the treatment of osteoarthritis (Fig. 4, Ref. 19).

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Insertion-deletion polymorphism of angiotensin converting enzyme and susceptibility to rheumatoid arthritis in South Gujarat population

Dwivedi

Patel

Pathak³

et al. 2018

Gene Reports

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Patterns of angiotensin converting enzyme insertion/deletion gene polymorphism among an Egyptian cohort of patients with rheumatoid arthritis

Abstract: Our study suggests that high frequency of the ACE D allele contributes to the heritability of RA susceptibility compared to other ACE alleles. On the other hand, no association was detected between ACE I/D polymorphism and the severity of RA.

Cited by 10 publications

References 19 publications

Association of GSTM1, GSTT1, GSTP1-ILE105VAL and ACE I/D polymorphisms with ankylosing spondylitis

Association of GSTM1, GSTT1, GSTP1-ILE105VAL and ACE I/D polymorphisms with ankylosing spondylitis

AT1/2R affects the proliferation and apoptosis of chondrocytes induced by oxygen-glucose deprivation

Insertion-deletion polymorphism of angiotensin converting enzyme and susceptibility to rheumatoid arthritis in South Gujarat population

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