The relationship between endothelial progenitor cells and pulmonary hypertension in children with congenital heart disease

Abstract

Background: To assess the relationship between endothelial progenitor cells (EPCs) in peripheral blood and pulmonary hypertension (PH) in children with congenital heart disease (CHD) and explore the possibility of applying EPCs to treatment of PH in children with CHD. Methods: In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the right heart catheterization of mean pulmonary arterial pressure (mPAP) results, these cases were divided into PH groups (including high PH group, n=32, and the middle PH group, n=30) and non-PH group (n=111). We took their peripheral blood for flow cytometry, and counted the number of EPCs(CD133+/KDR+ cells). The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL =WBC /L × lymphocytes % × EPCs % × 10-6. Results: The median EPCs of the non-PH group, middle PH group and high PH group are 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P<0.05). After adjustment of gender, age and BMI, the EPCs was significantly associated with a decreased risk of high PH (OR=0.37, 95%CI: 0.16-0.87, P<0.05). However, EPCs was not significantly associated with middle PH (P>0.05). Conclusion: The findings revealed that the EPCs and high PH in CHD patients correlate significantly and EPCs may become an effective treatment for PH in CHD patients.EPCs may be a protective factor of high PH for children with CHD.

Research progress on astrocyte autophagy in ischemic stroke

“…circAkap7-modified adipose-derived mesenchymal stem cell-sourced exosomes can target ATG12, facilitating astrocyte autophagy and ameliorating ischemic brain injury, and are thus of clinical therapeutic value ( 137 ). Other pharmacological studies suggest that both anthocyanins ( 113 ) and delta-opioid peptide [D-Ala2, D-leu5] enkephalin ( 138 ) confer protection against hypoxia-ischemia injury by inducing autophagy in astrocytes, whereas breviscapine ( 139 ), nimodipine ( 140 ), and propofol ( 141 ) have protective effects on hypoxia-ischemia injury via suppression of astrocyte autophagy. Many experimental studies have demonstrated that astrocyte autophagy is a potentially important therapeutic target in cerebral ischemia by utilizing the dual effects of astrocyte autophagy, but how to develop targeted drug therapy based on the characteristics of astrocyte autophagy requires further research.…”