Differential effects of recombinant human endostatin treatment on differentiated and undifferentiated blood vessels in Lewis lung cancer

Abstract

In the present study, we evaluated the effects of recombinant human (rh-)endostatin treatment on differentiated and undifferentiated tumor vasculature in Lewis lung cancer for the first time. Lewis lung carcinoma models were established. The animals were treated daily with varying doses of rh-endostatin or physiological saline for 14 days. Intravital microscopy was performed following treatment. The expression of CD31 and CD34 was determined by immunohistochemical staining, and microvessel density (MVD) was determined. Rh-endostatin treatment significantly decreased the tumor volume compared with the control group. Rh-endostatin treatment normalized the architecture of the vascular network. CD31+ cells decreased following rh-endostatin treatment, whereas CD34+ cells were unaffected by the treatment. Accordingly, the MVD value of CD31+ cells in rh-endostatin treatment groups significantly decreased (P<0.01), and the MVD value of CD34+ cells in the rh-endostatin treatment groups did not decrease. Undifferentiated tumor blood vessels were significantly inhibited by rh-endostatin treatment. In conclusion, the normalization of the tumor vasculature by endostatin may be related to the differential effects of endostatin on differentiated and undifferentiated blood vessels.

Temperature‐sensitive hydrogel releasing pectolinarin facilitate scarless wound healing

“…During angiogenesis, a balance between the activation of pro‐angiogenic genes and the inhibition of inhibitory factors stimulates angiogenesis 44 . The von Willebrand factor (vWF) gene is involved in coagulation and assists in platelet adhesion, promoting haemostasis 45 .…”

“…During angiogenesis, a balance between the activation of proangiogenic genes and the inhibition of inhibitory factors stimulates angiogenesis. 44 The von Willebrand factor (vWF) gene is involved in coagulation and assists in platelet adhesion, promoting haemostasis. 45 As shown in Figure 4D, the expression of the vWF gene was elevated by more than 1.7-fold in the PF-127@P50 hydrogel extract group compared to the group without pectolinarin, and enhanced expression of the vWF gene was observed in all pectolinarin-treated groups except for PF-127 hydrogels alone.…”

Engineering a photosensitizer nanoplatform for amplified photodynamic immunotherapy via tumor microenvironment modulation

“…Vascular normalization is accompanied by CD31 (a sensitive marker of blood vessels, expressed in all blood vessels) downregulation. [51][52][53] For the tumors treated with free Ce6based PDT, the blood vessel density based on anti-CD31 immunohistochemistry (IHC) increased significantly compared to that of the NS group (Fig. 3f and Fig.…”

Predictive value of microvascular density for response to anlotinib in advanced NSCLC

“…[6] Another study found that recombinant human vascular endothelial growth inhibitor significantly reduced the number of CD31+ but not CD34+ vessels in a mouse model of lung cancer, suggesting that the immature microvessels can be inhibited by endostatin. [27] Our study analyzed the clinical data of 30 patients with advanced NSCLC who were treated with anlotinib. The tumoral vasculature was stained for CD31 and CD34.…”

“…Patients with lung adenocarcinoma of high undifferentiated-vessel MVD were more sensitive to bevacizumab [6] . Another study found that recombinant human vascular endothelial growth inhibitor significantly reduced the number of CD31+ but not CD34+ vessels in a mouse model of lung cancer, suggesting that the immature microvessels can be inhibited by endostatin [27] …”