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Pcb153-Induced Overexpression Of Id3 Contributes To The Development Of Microvascular Lesions, Jayanta K. Das, Quentin Felty

Jayanta Das

Microvascular lesions resulting from endothelial cell dysfunction are produced in the brain, lung, kidney, and retina of patients of complex chronic diseases. The environmental and molecular risk factors which may contribute in the development of microvascular damage are unclear. The mechanism(s) responsible for initiating microvascular damage remain poorly defined, although several inciting factors have been proposed, including environmental toxicants-induced oxidative stress. Enhanced neovascularization has been implicated in either the development or progression of proliferative vascular lesions. Here, we present evidence for how PCB-induced ROS may contribute to the development of a neovascular phenotype with the aim of elucidating the role …

Redox Signalling To Nuclear Regulatory Proteins By Reactive Oxygen Species Contributes To Oestrogen-Induced Growth Of Breast Cancer Cells, Victor Okoh, N. A. Garba, Jayanta K. Das, Alok Deoraj, K. P. Singh, S. Sarkar, Quentin Felty, Changwon Yoo, R. M. Jackson, Deodutta Roy

Jayanta Das

Background:

17β-Oestradiol (E2)-induced reactive oxygen species (ROS) have been implicated in regulating the growth of breast cancer cells. However, the underlying mechanism of this is not clear. Here we show how ROS through a novel redox signalling pathway involving nuclear respiratory factor-1 (NRF-1) and p27 contribute to E2-induced growth of MCF-7 breast cancer cells.

Methods:

Chromatin immunoprecipitation, qPCR, mass spectrometry, redox western blot, colony formation, cell proliferation, ROS assay, and immunofluorescence microscopy were used to study the role of NRF-1.

Results:

The major novel finding of this study is the demonstration of oxidative modification of phosphatases PTEN and …

Microvascular Lesions By Estrogen-Induced Id3: Its Implications In Cerebral & Cardiorenal Vascular Disease, Jayanta K. Das, Quentin Felty

Jayanta Das

Severe symptoms of cerebral and cardiorenal vascular diseases can be triggered when cerebral, coronary, or glomerular arterioles grow inappropriately as a result of abnormal cell proliferation. The risk factor(s) and molecular mechanisms responsible for microvascular lesion formation are largely unknown. Although controversial, both animal and epidemiological studies have shown that estrogen increases the risk of stroke which may be due to microvascular lesions. Since microvascular diseases are characterized by excessive vessel growth, it is plausible that estrogen-induced neovascularization contributes to the growth of microvascular lesions. We present evidence for how ID3 overexpression in endothelial cells contributes to the development of …

Id3 Contributes To The Acquisition Of Molecular Stem Cell-Like Signature In Microvascular Endothelial Cells: Its Implication For Understanding Microvascular Diseases, Jayanta K. Das, Norbert F. Voelkel, Quentin Felty

Jayanta Das

While significant progress has been made to advance our knowledge of microvascular lesion formation, yet the investigation of how stem-like cells may contribute to the pathogenesis of microvascular diseases is still in its infancy. We assessed whether the inhibitor of DNA binding and differentiation 3 (ID3) contributes to the acquisition of a molecular stem cell-like signature in microvascular endothelial cells. The effects of stable ID3 overexpression and SU5416 treatment — a chemical inducer of microvascular lesions, had on the stemness signature was determined by flow cytometry, immunoblot, and immunohistochemistry. Continuous ID3 expression produced a molecular stemness signature consisting of CD133+ …