Low dose radiation primed iNOS + M1macrophages modulate angiogenic programming of tumor derived endothelium.

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dc.contributor.authorNadella, Vinod
dc.contributor.authorSingh Sandhya
dc.contributor.authorJain, Aklank
dc.contributor.authorJain, Manju
dc.contributor.authorVasquez, Karen M.
dc.contributor.authorSharma, Ashok
dc.contributor.authorTanwar, Pranay
dc.contributor.authorRath, Goura Kishore
dc.contributor.authorPrakash Hridayesh.
dc.date.accessioned2019-03-26T09:01:38Z
dc.date.accessioned2024-08-13T10:34:40Z
dc.date.available2019-03-26T09:01:38Z
dc.date.available2024-08-13T10:34:40Z
dc.date.issued2018
dc.description.abstractSolid tumors are covered by stroma, which is hypoxic in nature and composed of various non‐malignant components such as endothelial cells, fibroblasts, and pericytes that support tumor growth. Tumor stroma represents a mechanical barrier for tumor infiltration of CD8+ effector T cells in particular. In this context, our previous studies have demonstrated the therapeutic impact of Low‐Dose Radiation (LDR)‐primed and M1‐retuned (iNOS+) peritumoral macrophages that produce inducible nitric oxide, have immunological roles on tumor infiltration of effector T cells, cancer‐related inflammation, and subsequent tumor immune rejection in a mouse model of pancreatic cancer. These findings suggested a possible modification of tumor endothelium by LDR‐primed macrophages. In line with these observations, here we demonstrate the influence of LDR in down‐modulating HIF‐1 in irradiated tumors in the course of polarization of irradiated tumor‐associated macrophages toward an M1 phenotype. Furthermore, we demonstrate that M1 macrophages which are primed by LDR can directly influence angiogenic responses in eNOS+ endothelial cells which produce nitric oxide having both vascular and physiological roles. Furthermore, we demonstrate that naïve macrophages, upon differentiating to an M1 phenotype either by Th1 stimuli or LDR, potentially modify sphingosine‐1‐phosphate/VEGF‐induced angiogenic signaling in tumor‐derived endothelial cells with tumorigenic potential, thus indicating the significance of iNOS+ macrophages in modulating signaling in eNOS+ tumor‐derived endothelium. Our study suggests that iNOS+ macrophages can activate tumor endothelium which may contribute to cancer‐directed immunotherapy in particular.en_US
dc.identifier.citationNadella, Vinod., Singh, Sandhya., Jain, Aklan and et. al. (2018) Low dose radiation primed iNOS + M1macrophages modulate angiogenic programming of tumor derived endothelium. Molecular Carcinogenesis. Vol. 57(11), PP. 1664-1671.https://doi.org/10.1002/mc.22879en_US
dc.identifier.doi10.1002/mc.22879
dc.identifier.issn1098-2744
dc.identifier.urihttp://10.2.3.109/handle/32116/2164
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pubmed/30035346
dc.language.isoenen_US
dc.publisherPLOSen_US
dc.subjectAngiogenesisen_US
dc.subjectEndotheliumen_US
dc.subjectGamma irradiationen_US
dc.subjectImmune cells infiltrationen_US
dc.subjectM1 macrophagesen_US
dc.subjectTumor therapyen_US
dc.titleLow dose radiation primed iNOS + M1macrophages modulate angiogenic programming of tumor derived endothelium.en_US
dc.title.journalMolecular Carcinogensisen_US
dc.typeArticleen_US
dc.type.accesstypeClosed Accessen_US

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