Pentraxin 3 (PTX3) is an acute phase protein strongly expressed by advanced atherosclerotic lesions. We investigated (a) PTX3 expression and secretion in subcutaneous adipose tissue (SAT) and omental visceral adipose tissue (VAT) obtained from 21 obese (37.4 ± 8.15 yr) and 10 normal weight subjects (43.7 ± 11.07 yr) and (b) the relationships of adipose PTX3 with tumour necrosis factor α (TNFα) and adiponectin expression and with cardiometabolic risk factors. Real-time PCR was used to quantify specific mRNA for PTX3, CD68 (macrophage marker), TNFα and adiponectin. Fresh adipose tissue was cultured and PTX3 measured in the medium. Serum insulin, glucose, HDL and LDL cholesterol, triglycerides, C-reactive protein (CRP), fibrinogen, adiponectin, TNFα and PTX3 were measured. PTX3 expression was similar in the two fat compartments and tended to be higher in obese than in normal weight subjects in VAT only (p = 0.05). CD68 and PTX3 expressions were correlated with each other in SAT but not in VAT. After adjustment for age and sex, VAT-PTX3 expression and release were correlated with VAT-TNFα expression (p < 0.01 for both) and with LDL/HDL ratio (p < 0.01 and p < 0.001). VAT-PTX3 expression was also correlated with BMI, triglycerides, CRP, fibrinogen and adiponectin (p < 0.05 for all). In the multivariate analysis with VAT-PTX3 RNA levels as dependent variable, LDL/HDL ratio and fibrinogen remained independently associated with VAT-PTX3 expression (p < 0.01 for both). These associations were not seen within SAT. Conclusions: Human adipose tissue expresses and releases PTX3 likely under TNFα control. VAT production of PTX3 seems to contribute to the mechanisms underlying the development of atherosclerosis.

Expression of long pentraxin PTX3 in human adipose tissue and its relation with cardiovascular risk factors / L. Alberti, L. Gilardini, A. Zulian, G. Micheletto, G. Peri, A. Doni, A. Mantovani, C. Invitti. - In: ATHEROSCLEROSIS SUPPLEMENTS. - ISSN 1567-5688. - 202:2(2009), pp. 455-460.

Expression of long pentraxin PTX3 in human adipose tissue and its relation with cardiovascular risk factors

G. Micheletto
Writing – Review & Editing
;
2009

Abstract

Pentraxin 3 (PTX3) is an acute phase protein strongly expressed by advanced atherosclerotic lesions. We investigated (a) PTX3 expression and secretion in subcutaneous adipose tissue (SAT) and omental visceral adipose tissue (VAT) obtained from 21 obese (37.4 ± 8.15 yr) and 10 normal weight subjects (43.7 ± 11.07 yr) and (b) the relationships of adipose PTX3 with tumour necrosis factor α (TNFα) and adiponectin expression and with cardiometabolic risk factors. Real-time PCR was used to quantify specific mRNA for PTX3, CD68 (macrophage marker), TNFα and adiponectin. Fresh adipose tissue was cultured and PTX3 measured in the medium. Serum insulin, glucose, HDL and LDL cholesterol, triglycerides, C-reactive protein (CRP), fibrinogen, adiponectin, TNFα and PTX3 were measured. PTX3 expression was similar in the two fat compartments and tended to be higher in obese than in normal weight subjects in VAT only (p = 0.05). CD68 and PTX3 expressions were correlated with each other in SAT but not in VAT. After adjustment for age and sex, VAT-PTX3 expression and release were correlated with VAT-TNFα expression (p < 0.01 for both) and with LDL/HDL ratio (p < 0.01 and p < 0.001). VAT-PTX3 expression was also correlated with BMI, triglycerides, CRP, fibrinogen and adiponectin (p < 0.05 for all). In the multivariate analysis with VAT-PTX3 RNA levels as dependent variable, LDL/HDL ratio and fibrinogen remained independently associated with VAT-PTX3 expression (p < 0.01 for both). These associations were not seen within SAT. Conclusions: Human adipose tissue expresses and releases PTX3 likely under TNFα control. VAT production of PTX3 seems to contribute to the mechanisms underlying the development of atherosclerosis.
Adipose tissue; PTX3; HDL; Fibrinogen; Adiponectin
Settore MED/18 - Chirurgia Generale
Settore MED/09 - Medicina Interna
2009
15-mag-2008
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/60435
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