A recent study from the Cancer Immunology Branch, Department of System Cancer Science, National Cancer Center, 111 jungbalsan-ro, Kyunggi 410-769, Republic of Korea; and Department of Physiology, Development and Neuroscience, University of Cambridge, UK shows that “The HIF-1/glial TIM-3 axis controls inflammation-associated brain damage under hypoxia.” This study was published in the 20 March 2015 issue of the online Journal “Nature Communications” by Drs. Park EJ, Koh HS, Johnson RS, and others.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: MiRNA-based therapy for hypoxia/inflammation-associated brain damage: 17β-Estradiol (Estrogen or E2) decreases infarct size, edema formation, neutrophil infiltration and promotes neuronal survival via down regulation of TIM-3. This study suggests, for the first time, that 17β-Estradiol, by increasing the expression of its target gene, it may : (1) decrease infarct size, edema formation, neutrophil infiltration; and (2) promote neuronal survival. Together, pharmacological formulations encompassing “17β-Estradiol or its analogues” may be used to treat hypoxia/ischemia-associated brain diseases.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
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To cite: Boominathan, MiRNA-based therapy for hypoxia/inflammation-associated brain damage: 17β-Estradiol decreases infarct size, edema formation, neutrophil infiltration and promotes neuronal survival via down regulation of TIM-3, 22/March/2015, 23.48, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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* Research cooperation
Undisclosed information: How 17β-Estradiol decreases the expression of TIM-3
