Heparin Cofactor II Attenuates Vascular Remodeling in Humans and Mice

Aihara, Ken‐ichi

doi:10.1253/circj.cj-10-0577

Cited by 5 publications

(5 citation statements)

References 51 publications

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“…After one week of exposure to 4.1 mGy/h FERMT3 expression was increased (FC 1.80). Regarding complement and coagulation cascades, single gene expression analysis is supportive of anti-thrombotic actions as indicated by a signifi cantly increased expression of plasminogen activator tissue-type (PLAT) and serin peptidase inhibitor, clade D, member 1 (SERPIND1; FC 1.61 at week one with 1.4 mGy/h) (Ladenvall et al 2003, Vicente et al 2007, Aihara 2010. In particular, PLAT expression is greatly induced over time in HUVEC exposed to 4.1 mGy/h (FC 2.08 at week one, and FC 2.42 at week six).…”

Section: Candidate Genes Involved In Radiation-induced Premature Senementioning

confidence: 99%

Transcriptomic profiling suggests a role for IGFBP5 in premature senescence of endothelial cells after chronic low dose rate irradiation

Rombouts

Aerts

Quintens

et al. 2014

International Journal of Radiation Biology

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Section: Candidate Genes Involved In Radiation-induced Premature Senementioning

confidence: 99%

Transcriptomic profiling suggests a role for IGFBP5 in premature senescence of endothelial cells after chronic low dose rate irradiation

Rombouts

Aerts

Quintens

et al. 2014

International Journal of Radiation Biology

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“…Heparin cofactor II (HCII) is a serine protease inhibitor (SERPIN) that acts to neutralize thrombin’s activity within subendothelial layer of the blood vessel wall, thereby influencing the blood coagulation cascade. HCII plays a protective role against vascular remodeling, which includes atherosclerosis, and plasma HCII activity could serve as a predictive biomarker and a novel therapeutic target for preventing cardiovascular disease [ 28 ]. However, to the best of our knowledge, no association between this protein and PH has been reported yet.…”

Section: Discussionmentioning

confidence: 99%

Proteomic biomarkers for survival in systemic sclerosis-associated pulmonary hypertension

Mismetti,

Delavenne,

Montani

et al. 2023

Respir Res

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Background Interstitial lung disease (ILD) and pulmonary hypertension (PH) represent the major causes of mortality in systemic sclerosis (SSc). Patients with systemic sclerosis and combined PH and ILD (SSc-PH-ILD) generally have a poor prognosis. Predictors of survival and of potential benefit of treatment are lacking in patients with SSc-PH-ILD. Objective To identify specific plasma protein expression patterns associated with survival in patients with SSc-PH-ILD. Materials and methods Post-hoc analysis of a prospective multicenter French study in patients with PH-ILD. An untargeted proteomic analysis using mass spectrometry was performed to identify plasma protein changes associated with long-term overall survival in patients with SSc-PH-ILD. Results Thirty two patients were included in the analysis, of whom 13 died during follow-up (median survival: 76.5 months). At baseline, survivors had less severe hemodynamic impairment [pulmonary vascular resistance of 4.4 Wood Units (IQR 3–5.2) vs. 6.2 Wood Units (IQR 4.2–10.7)] and higher carbon monoxide diffusing capacity [median 39% (IQR 35–44%) vs. 25% (IQR 22–30.5%)], than the 13 patients who died. Seven proteins, associated with haemostasis and fibrosis, were differentially expressed according to patients’ survival. In the survivor group, two proteins were increased (ADAMTS13, SERPIND1) and five were decreased (PTGDS, OLFM1, C7, IGFBP7, FBN1) compared to the non-survivor groups. Conclusion The prognosis of SSc-PH-ILD patients is poor. This proteomic approach found 7 plasma proteins (involved in haemostasis and fibrosis pathways) associated with survival. These potential biomarkers may be good candidates to prognostic enrichment.

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“…NQO1 is an enzyme involved in the detoxification of mutagenic and carcinogenic quinones, by preventing electron transfer and the generation of free radicals and reactive oxygen species 28 and converting the intermediates to the less toxic hydroquinones 29 . SERPIND1 encodes the heparin cofactor II (HCII), which is an endogenous thrombin inhibitor that protects against vascular remodeling and atherosclerosis via its inhibition of thrombin in the vascular wall 30 . It may also play a role in enhancing cell motility and promoting metastasis in non-small cell lung cancer 31 .…”

Section: Discussionmentioning

confidence: 99%

The Overlap of Lung Tissue Transcriptome of Smoke Exposed Mice with Human Smoking and COPD

Obeidat

Dvorkin‐Gheva

et al. 2018

Sci Rep

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Genome-wide mRNA profiling in lung tissue from human and animal models can provide novel insights into the pathogenesis of chronic obstructive pulmonary disease (COPD). While 6 months of smoke exposure are widely used, shorter durations were also reported. The overlap of short term and long-term smoke exposure in mice is currently not well understood, and their representation of the human condition is uncertain. Lung tissue gene expression profiles of six murine smoking experiments (n = 48) were obtained from the Gene Expression Omnibus (GEO) and analyzed to identify the murine smoking signature. The “human smoking” gene signature containing 386 genes was previously published in the lung eQTL study (n = 1,111). A signature of mild COPD containing 7 genes was also identified in the same study. The lung tissue gene signature of “severe COPD” (n = 70) contained 4,071 genes and was previously published. We detected 3,723 differentially expressed genes in the 6 month-exposure mice datasets (FDR <0.1). Of those, 184 genes (representing 48% of human smoking) and 1,003 (representing 27% of human COPD) were shared with the human smoking-related genes and the COPD severity-related genes, respectively. There was 4-fold over-representation of human and murine smoking-related genes (P = 6.7 × 10−26) and a 1.4 fold in the severe COPD -related genes (P = 2.3 × 10−12). There was no significant enrichment of the mice and human smoking-related genes in mild COPD signature. These data suggest that murine smoke models are strongly representative of molecular processes of human smoking but less of COPD.

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Heparin Cofactor II Attenuates Vascular Remodeling in Humans and Mice

Cited by 5 publications

References 51 publications

Transcriptomic profiling suggests a role for IGFBP5 in premature senescence of endothelial cells after chronic low dose rate irradiation

Transcriptomic profiling suggests a role for IGFBP5 in premature senescence of endothelial cells after chronic low dose rate irradiation

Proteomic biomarkers for survival in systemic sclerosis-associated pulmonary hypertension

The Overlap of Lung Tissue Transcriptome of Smoke Exposed Mice with Human Smoking and COPD

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