scholarly journals Altered hypoxia-inducible factor-1α (HIF-1α ) signaling contributes to impaired angiogenesis in fetal lambs with persistent pulmonary hypertension of the newborn (PPHN)

2019 ◽  
Vol 7 (3) ◽  
pp. e13986 ◽  
Author(s):  
Kartikeya Makker ◽  
Adeleye J. Afolayan ◽  
Ru-Jeng Teng ◽  
Girija G. Konduri
Keyword(s):  
Pulmonary Hypertension ◽  
Hypoxia Inducible Factor ◽  
Persistent Pulmonary Hypertension ◽  
Hypoxia Inducible Factor 1Α ◽  
Impaired Angiogenesis

scholarly journals Contribution of inflammation and impaired angiogenesis to the pathobiology of chronic thromboembolic pulmonary hypertension

2015 ◽  
Vol 46 (2) ◽  
pp. 431-443 ◽  
Author(s):  
Rozenn Quarck ◽  
Marijke Wynants ◽  
Erik Verbeken ◽  
Bart Meyns ◽  
Marion Delcroix
Keyword(s):  
Pulmonary Hypertension ◽  
Systemic Inflammation ◽  
Inflammatory Cell ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Persistent Pulmonary Hypertension ◽  
Vascular Lesions ◽  
Poor Survival ◽  
Severity Scores ◽  
Thromboembolic Pulmonary Hypertension ◽  
Impaired Angiogenesis

Deficient angiogenesis and systemic inflammation could be involved in the pathophysiology of chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to characterise the histopathology of pulmonary vascular lesions from 52 CTEPH patients who underwent a pulmonary endarterectomy (PEA) and investigate a potential link between clinical, biological and morphometric parameters.Collagen, elastin, fibrin, lipid, endothelial, smooth muscle and inflammatory cell content was investigated using immunohistochemistry. Qualitative changes were evaluated using severity scores. Circulating levels of inflammatory mediators were measured using ELISA.Neointima, thrombotic, recanalised and atherosclerotic lesions were found. Accumulation of macrophages, T-lymphocytes and neutrophils was found mainly in atherosclerotic and thrombotic lesions. Angiogenesis was observed in all kinds of lesions; low-scored angiogenesis predicted adverse outcome, including persistent pulmonary hypertension post-PEA, start of medical therapy and poor survival. C-reactive protein (CRP), interleukin-10, monocyte chemotactic protein-1, macrophage inflammatory protein-1α and matrix metalloproteinase (MMP)-9 were significantly elevated in CTEPH patients. Plasma CRP and MMP-9 levels correlated with neutrophil and macrophage accumulation, respectively.Enhanced systemic inflammation parallels local inflammatory cell infiltration in major pulmonary arteries at advanced stages of CTEPH. Impaired neovascularisation is associated with poor survival, start of medical treatment and persistent pulmonary hypertension post-PEA. These findings suggest that inflammation and impaired angiogenesis could contribute to the progression of the disease.

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