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Biological Sciences Colloquium     

 

March 17, 2016
Dr. Uday Bandyopadhyay, IICB

Local Host: Siddhartha S. Jana
Venue & Time: C V Raman Hall at 3:00 PM

Mitochondria: A subcellular target to prevent non-steroidal anti-inflammatory drug (NSAID) -induced gastric ulcer

Non-steroidal anti-inflammatory drugs (NSAIDs) develop gastropathy, the cause for the induction of gastropathy is not yet clear. We have investigated the role of mitochondria on the development of indomethacin (a non-steroidal anti-inflammatory drug)-induced gastropathy in rat. Indomethacin, develops gastropathy by inducing mitochondrial pathology and reactive oxygen species (ROS) generation. Indomethacin damages mitochondrial ultrastructure and causes mitochondrial dysfunction as documented by transmission electron microscopic studies, decreased stage-3 respiration, dehydrogenase activity and transmembrane potential (Dym). Upregulation of proapoptotic Bax, Bak and downregulation of antiapoptotic Bcl-2, BclxL are found to occur in NSAID-induced gastric mucosal apoptosis, which favors mitochondrial translocation of Bax to open mitochondrial permeability transition pores (MPTP). Opening of MPTP releases apoptosis promoting factor, cytochrome c, which then activates caspase-9 and active caspase-9 further activates caspase-3. Mitochondrial pathology is associated with increased generation of intramitochondrial ROS, such as O2·-, H2O2 and ·OH leading to oxidative stress. O2·- is the most effective to damage mitochondrial aconitase, leading to the release of iron from its iron-sulfur cluster. Immunoprecipitation of mitochondrial aconitase and subsequent westernimmunoblotting indicate carbonylation of aconitase along with the loss of activity in vivo after indomethacin treatment. The release of iron has been documented by fluorescence imaging of mucosal cells by using Phen Green SK, a specific probe for chelatable iron. Interestingly, intra-mitochondrial ·OH generation is crucial for the development of mitochondrial pathology and activation of mitochondrial death pathway by indomethacin. Scavenging of ·OH by dimethyl sulfoxide or α-phenyl-n-tert-butyl-nitrone, a spin-trap, prevents indomethacin-induced mitochondrial ultrastructural changes, oxidative stress, collapse of Dym, and mitochondrial dysfunction. Scavenging of ·OH also prevents the activation of NSAID-induced gastric mucosal cell death and gastropathy.

February 29, 2016
Dr. Arabinda Chaudhuri, IICT

Local Host: Prof. P. K. Das

Fighting Cancer with Fatty Bubbles

Liposomes, the fatty bubbles containing an aqueous interior, are finding widespread uses in directing potent anti-cancer drugs selectively to tumor vasculature in anti-angiogenic cancer therapy. To this end, recently we have developed efficient integrin receptor selective liposomal systems for delivering potent anti-cancer drugs/genes to tumor vasculature and have demonstrated their significant tumor growth inhibition properties in syngeneic mouse tumor model. In the emerging field of dendritic cell (DC) based genetic immunization, previously we showed that immunization with autologous DCs ex-vivo pre-transfected with electrostatic complexes (lipoplexes) of a plasmid DNA encoding melanoma tumor associated antigen (DNA vaccine) and liposomes of cationic amphiphiles with mannose-mimicking quinoyl- & shikimoyl head-groups induces long-lasting immune responses against melanoma tumor. However, there are a number of time-consuming and cost-ineffective steps to be followed in such ex-vivo DC-transfection based cancer immunotherapy. One needs to painstakingly isolate the autologous DCs from the recipients. The isolated DCs then need to be ex vivo pre-transfected with DNA vaccines of interest and finally the ex-vivo transfected DCs needs to be re-implanted back into recipient’s body. Stated differently, the currently practiced ex vivo DC-transfection based genetic immunization procedures are labor-intensive and are likely to be prohibitively costly for large scale applications. We have now succeeded in designing efficient liposomal DNA vaccine carriers for direct in vivo targeting of tumor antigen encoded DNA vaccines to dendritic cells. Importantly, this newly developed liposomal DNA vaccine carriers are capable of inducing long-lasting immune response including strong memory response against melanoma tumors in a syngeneic mouse tumor model. Most recently, we have succeeded in developing a platform technology for eradicating/regressing established tumors through a combination of in vivo DC-transfection based cancer immunotherapy and targeted chemotherapy. My presentation will be centered around discussing these translationally important recent findings from our laboratory.

January 18, 2016

Dr. Roop Mallik, TIFR

Local Host: Dr. Deepak Sinha

Lipid Rafts as Force Generating Platforms for Motor Proteins

Liposomes, the fatty bubbles containing an aqueous interior, are finding widespread uses in directing potent anti-cancer drugs selectively to tumor vasculature in anti-angiogenic cancer therapy. To this end, recently we have developed efficient integrin receptor selective liposomal systems for delivering potent anti-cancer drugs/genes to tumor vasculature and have demonstrated their significant tumor growth inhibition properties in syngeneic mouse tumor model. In the emerging field of dendritic cell (DC) based genetic immunization, previously we showed that immunization with autologous DCs ex-vivo pre-transfected with electrostatic complexes (lipoplexes) of a plasmid DNA encoding melanoma tumor associated antigen (DNA vaccine) and liposomes of cationic amphiphiles with mannose-mimicking quinoyl- & shikimoyl head-groups induces long-lasting immune responses against melanoma tumor. However, there are a number of time-consuming and cost-ineffective steps to be followed in such ex-vivo DC-transfection based cancer immunotherapy. One needs to painstakingly isolate the autologous DCs from the recipients. The isolated DCs then need to be ex vivo pre-transfected with DNA vaccines of interest and finally the ex-vivo transfected DCs needs to be re-implanted back into recipient’s body. Stated differently, the currently practiced ex vivo DC-transfection based genetic immunization procedures are labor-intensive and are likely to be prohibitively costly for large scale applications. We have now succeeded in designing efficient liposomal DNA vaccine carriers for direct in vivo targeting of tumor antigen encoded DNA vaccines to dendritic cells. Importantly, this newly developed liposomal DNA vaccine carriers are capable of inducing long-lasting immune response including strong memory response against melanoma tumors in a syngeneic mouse tumor model. Most recently, we have succeeded in developing a platform technology for eradicating/regressing established tumors through a combination of in vivo DC-transfection based cancer immunotherapy and targeted chemotherapy. My presentation will be centered around discussing these translationally important recent findings from our laboratory.

   
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 Last Modified March 03, 2016

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