Plasminogen Activator Inhibitor-1 Regulates LPS Induced Inflammation in Rat Macrophages through Autophagy Activation

Wang, Zhonghui; Ren, Weiying; Zhu, Liangliang; Hu, Lijuan

doi:10.1155/2014/189168

Cited by 34 publications

(34 citation statements)

References 37 publications

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“…Moreover, recent experimental studies indicate that PAI-1 also plays a role in upregulating inflammation after exposure to lipopolysaccharides or avian flu virus in conditions like ARDS (35, 36). However, in the present study, when we compared the ARDS group with non-ARDS patients, we found no significant differences in t-PA levels during the first week after inclusion.…”

Section: Discussionmentioning

confidence: 99%

Activation of Coagulation and Fibrinolysis in Acute Respiratory Distress Syndrome: A Prospective Pilot Study

et al. 2016

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IntroductionCoagulation and fibrinolysis remain sparsely addressed with regards to acute respiratory distress syndrome (ARDS). We hypothesized that ARDS development might be associated with changes in plasma coagulation and fibrinolysis. Our aim was to investigate the relationships between ARDS diagnosis and plasma concentrations of tissue factor (TF), tissue plasminogen activator (t-PA), and plasminogen activator inhibitor-1 (PAI-1) in mechanically ventilated patients at increased risk of developing ARDS.Materials and methodsWe performed an ethically approved prospective observational pilot study. Inclusion criteria were patients with PaO2/FiO2 < 300 mmHg admitted to the intensive care unit (ICU) for mechanical ventilation for 24 h, or more, because of one or more disease conditions associated with increased risk of developing ARDS. Exclusion criteria were age below 18 years; cardiac disease. We sampled plasma prospectively and compared patients who developed ARDS with those who did not using descriptive statistics and chi-square analysis of baseline demographical and clinical data. We also analyzed plasma concentrations of TF, t-PA, and PAI-1 at inclusion (T0) and on third (T3) and seventh day (T7) of the ICU stay with non-parametric statistics inclusive their sensitivity and specificity associated with the development of ARDS using receiver operating characteristic curve analysis. Statistical significance: p < 0.05.ResultsOf 24 patients at risk, 6 developed mild ARDS and 4 of each moderate or severe ARDS, respectively, 3 ± 2 (mean ± SD) days after inclusion. Median plasma concentrations of TF and PAI-1 were significantly higher at T7 in patients with ARDS, as compared to non-ARDS. Simultaneously, we found moderate correlations between plasma concentrations of TF and PAI-1, TF and PaO2/FiO2, and positive end-expiratory pressure and TF. TF plasma concentration was associated with ARDS with 71% sensitivity and 100% specificity, a cut off level of 145 pg/ml and AUC 0.78, p = 0.02. PAI-1 displayed 64% sensitivity and 100% specificity with a cut off concentration of 117.5 pg/ml and AUC 0.77, p = 0.02. t-PA did not change significantly during the observation time.ConclusionThis pilot study showed that increased plasma concentrations of TF and PAI-1 might support ARDS diagnoses in mechanically ventilated patients after 7 days in ICU.

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Section: Discussionmentioning

confidence: 99%

Activation of Coagulation and Fibrinolysis in Acute Respiratory Distress Syndrome: A Prospective Pilot Study

et al. 2016

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“…Quantitative real-time PCR was carried out using FastStart Universal SYBR Green Master (Bioteke Corporation, Beijing, China) on an ABI 7500 SDS RT-PCR system (Applied Biosystems, Foster City, CA, USA). According to the previous study [29], the s y n t h e s i s o f p r i m e r s w a s L C 3 , F o r w a r d 5 ′ -GACTTCCGGAAAGCTCTGCT-3′, Reverse 5′-ACCAGCATCGTAGAGGGTCT-3′, Beclin1 Forward 5′-GCCTCTGAAACTGGACACGA-3′ Reverse 5′ -CTTCCTCCTGGCTCTCTCCT-3′. Reaction conditions were as follows: 95°C modification for 5 min; 95°C modification for 30 s, 30 s 50°C annealing, extension at 72°C for 30 s, a total of 30 cycles.…”

Section: Real-time Pcr Analysis For Lc3 and Beclinmentioning

confidence: 99%

The Effect of Autophagy on Inflammation Cytokines in Renal Ischemia/Reperfusion Injury

et al. 2015

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Acute kidney injury (AKI) is characterized by a rapid loss of kidney function and an antigen-independent inflammatory process that causes tissue damage, which was one of the main manifestations of kidney ischemia/reperfusion (I/R). Recent studies have demonstrated autophagy participated in the pathological process of acute kidney injury. In this study, we discuss how autophagy regulated inflammation response in the kidney I/R. AKI was performed by renal I/R. Autophagy activator rapamycin (Rap) and inhibitor 3-methyladenine (MA) were used to investigate the role of autophagy on kidney function and inflammation response. After the experiment, kidney tissues were obtained for the detection of autophagy-related protein microtubule-associated protein light chain 3(LC3)II, Beclin1, and Rab7 and lysosome-associated membrane protein type (LAMP)2 protein by reverse transcription-polymerase chain reaction (PT-PCR) and Western blotting, and histopathology and tissue injury scores also. The blood was harvested to measure kidney function (creatinine (Cr) and blood urea nitrogen (BUN) levels) after I/R. Cytokines TNF-α, IL-6, HMGB1, and IL-10 were measured after I/R. I/R induced the expression of LC3II, Beclin1, LAMP2, and Rab7. The activation and inhibition of autophagy by rapamycin and 3-MA were promoted and attenuated histological and renal function in renal I/R rats, respectively. Cytokines TNF-α, IL-6, and HMGB1 were decreased, and IL-10 was further increased after activation of autophagy treated in I/R rats, while 3-MA exacerbated the pro-inflammatory cytokines TNF-α, IL-6, HMGB1, and anti-inflammatory cytokine IL-10 in renal I/R. I/R can activated the autophagy, and autophagy increase mitigated the renal injury by decreasing kidney injury score, levels of Cr and BUN after renal I/R, and inflammation response via regulating the balance of pro-inflammation and anti-inflammation cytokines.

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“…The association of PAI-1 with a wide spectrum of inflammatory diseases indicates that PAI-1 may play a fundamental role during inflammation. While a positive association between PAI-1 and inflammation has been well established [9,10], the functional consequence of PAI-1 in inflammation is as yet undefined, and remains an area of extensive research. Since macrophages are essential cells in both the innate and adaptive immune responses, and they are the primary cell type that significantly influences the duration and magnitude of most inflammatory responses, the effects of PAI-1 on macrophage activation were examined.…”

Section: Introductionmentioning

confidence: 99%

Plasminogen activator inhibitor-1 stimulates macrophage activation through Toll-like Receptor-4

Gupta

Castellino

et al. 2016

Biochemical and Biophysical Research Communications

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Plasminogen Activator Inhibitor-1 Regulates LPS Induced Inflammation in Rat Macrophages through Autophagy Activation

Cited by 34 publications

References 37 publications

Activation of Coagulation and Fibrinolysis in Acute Respiratory Distress Syndrome: A Prospective Pilot Study

Activation of Coagulation and Fibrinolysis in Acute Respiratory Distress Syndrome: A Prospective Pilot Study

The Effect of Autophagy on Inflammation Cytokines in Renal Ischemia/Reperfusion Injury

Plasminogen activator inhibitor-1 stimulates macrophage activation through Toll-like Receptor-4

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