Genetic control of chemokines in severe human internal carotid artery stenosis

Ghilardi, G; Biondi, Maria Luisa; Turri, Olivia; Pateri, F.; d’Eril, Gianvico Melzi; Scorza, Roberto

doi:10.1016/j.cyto.2007.10.007

Cited by 23 publications

(15 citation statements)

References 43 publications

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“…Recent studies have illustrated the clinical importance of gene polymorphisms 86 or serum levels of circulating chemokines to predict clinically significant atherosclerosis 85 or even acute cardiovascular events 22. These findings emphasize the importance of a good understanding of chemokine function in atherosclerosis.…”

Section: Discussionmentioning

confidence: 97%

Platelet Chemokines in Vascular Disease

Gleissner

Hundelshausen

Ley

2008

ATVB

268

202

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Abstract-Platelets are a rich source of different chemokines and express chemokine receptors. CXCL4 is highly abundant in platelets and involved in promoting monocyte arrest from rolling and monocyte differentiation to macrophages. CXCL4 can also associate with CCL5 and amplify its effect on monocytes. The megakaryocyte CXCL7 gene product is proteolytically cleaved into the strong neutrophil chemoattractant, NAP-2, which has also been implicated in repair cell homing to vascular lesions. Platelet adhesion can induce release of CCL2 and CXCL8 from endothelial cells. Conversely, the chemokines CCL17, CCL22, and CXCL12 made by other cells amplify platelet activation. Platelet chemokines enhance recruitment of various hematopoietic cells to the vascular wall, fostering processes such as neointima formation, atherosclerosis, and thrombosis, but also vessel repair and regeneration after vascular injury.

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Section: Discussionmentioning

confidence: 97%

Platelet Chemokines in Vascular Disease

Gleissner

Hundelshausen

Ley

2008

ATVB

268

202

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“…Chemokines have been demonstrated as mediators of inflammation that play important roles, including regulation, leukocyte activation, and recruitment, in inflammation areas via their interactions with chemokine receptors (Lazennec and Richmond, 2010). Genetic variations in chemokine receptor genes can affect several chemokine functions, such as the control of leukocyte infiltration into tumors and the initiation of primary tumor growth and survival (Ghilardi et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Effects of genetic variants of CCR5 chemokine receptors on oral squamous cell carcinoma

Tanyel¹,

Çinçin²,

Röhlig³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. We aimed to evaluate the effect of genetic variants of the chemokine C-C motif receptor (CCR5) in the pathogenesis of oral squamous cell carcinoma (OSCC). A total of 127 patients diagnosed with OSCC and 104 healthy individuals were included in the study. The polymorphisms CCR5 59029 and CCR5-delta32 were assessed with the polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP) method from peripheral blood samples of both groups. There was a statistically significant difference between the control and patient groups for CCR5 59029 A/G genotypes (P < 0.01). Individuals carrying the CCR5 59029 G allele (GG +AG genotypes) had a 2.84-fold increased risk for OSCC (P < 0.0001), and the CCR5 59029 AA genotype frequency was higher in the control group than in the patient group (P < 0.0001). The CCR5-delta 32 genotype frequencies did not differ significantly between controls and cases (P > 0.05). CCR5 59029 GG and CCR5- CCR5 gene in oral carcinoma delta32 DD + ID genotype frequencies were significantly increased in Grade II-III OSCC patients compared with Grade I-II OSCC patients. In conclusion, these results suggested that the G allele of the CCR5 59029 polymorphism might be a risk factor due to the loss of receptor function that might cause increased inflammation leading to the development of OSCC.

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“…In addition to its role in T-lymphocyte migration, SDF-1 is also a co-stimulator of CD4 + T cells and plays a role in HIV progression [10,11], microvascular complications among systemic sclerosis patients [21], and progression of carotid artery stenosis [22]. …”

Section: Discussionmentioning

confidence: 99%

Stromal Cell-Derived Factor 1 Gene Polymorphism Is Associated with Susceptibility to Adverse Long-Term Allograft Outcomes in Non-Diabetic Kidney Transplant Recipients

Wang

Tsai

Yang

et al. 2014

IJMS

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Although the genetic polymorphism of Stromal Cell-Derived Factor 1 (SDF-1) is associated with higher mortality of liver allograft recipients, the role of SDF-1 in the modulation of renal allograft outcomes is unclear. Between March 2000 and January 2008, we recruited 252 non-diabetic renal transplant recipients (RTRs). Baseline characteristics and blood chemistry were recorded. Genomic DNA extraction with polymerase chain reaction-restriction fragment length polymorphism was utilized to analyze the genetic polymorphisms of SDF-1 (rs1801157). The influence of SDF-1 on an adverse renal allograft outcome, defined as either a doubling of serum creatinine, graft failure, or patient death was evaluated. Sixteen patients with the SDF-1 AA/AG genotype and nine with the SDF-1 GG genotype reached an adverse outcome. According to Kaplan-Meier analysis, patients carrying the SDF-1 AA/AG genotype or A allele showed a significantly higher risk of reaching an adverse outcome than those carrying the SDF-1 GG genotype or G allele (p = 0.041; p = 0.0051, respectively; log rank test). Stepwise multivariate Cox proportional regression analysis revealed that patients carrying the SDF-1 AA/AG genotype and A allele had a 2.742-fold (95% CI. 1.106–6.799, p = 0.03) and 2.306-fold (95% CI. 1.254–4.24, p = 0.008) risk of experiencing an adverse outcome. The SDF-1 AA/AG genotype and A allele have a detrimental impact on the long-term outcome of RTRs.

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Genetic control of chemokines in severe human internal carotid artery stenosis

Cited by 23 publications

References 43 publications

Platelet Chemokines in Vascular Disease

Platelet Chemokines in Vascular Disease

Effects of genetic variants of CCR5 chemokine receptors on oral squamous cell carcinoma

Stromal Cell-Derived Factor 1 Gene Polymorphism Is Associated with Susceptibility to Adverse Long-Term Allograft Outcomes in Non-Diabetic Kidney Transplant Recipients

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