Amine-endcap PLGA from PolySciTech used in development of heart-attack treatment

Heart attack, or myocardial infarction, is the leading cause of death worldwide. One of the causes of tissue damage which occurs during a heart attack is excess calcium influx that occurs once blood-flow is reestablished (reperfusion). This calcium influx leads to cell death and massive tissue damage to the heart muscles rendering them inoperable which can be lethal for the patient. Recently, researchers working jointly at University of Iowa and Mahidol University (Thailand), utilized PLGA-NH2 from PolySciTech division of Akina, Inc. (www.polyscitech.com) (PolyVivo AI063) as a component in developing a targeted nanoparticle preparation which delivered an CaMKII inhibitor peptide to prevent heart-cell death during reperfusion. This research holds promise for the development of a medicine which can be used to prevent tissue damage during a heart-attack potentially aiding in life-saving therapy. Read more here: Wongrakpanich, Amaraporn, Angie S. Morris, Sean M. Geary, A. Joiner Mei-ling, and Aliasger K. Salem. “Surface-modified particles loaded with CaMKII inhibitor protect cardiac cells against mitochondrial injury.” International Journal of Pharmaceutics (2017). http://www.sciencedirect.com/science/article/pii/S0378517317300704

“Abstract: An excess of calcium (Ca2+) influx into mitochondria during mitochondrial re-energization is one of the causes of myocardial cell death during ischemic/reperfusion injury. This overload of Ca2+ triggers the mitochondrial permeability transition pore (mPTP) opening which leads to programmed cell death. During the ischemic/reperfusion stage, the activated Ca2+/calmodulin-dependent protein kinase II (CaMKII) enzyme is responsible for Ca2+ influx. To reduce CaMKII-related cell death, sub-micron particles composed of poly(lactic-co-glycolic acid) (PLGA), loaded with a CaMKII inhibitor peptide were fabricated. The CaMKII inhibitor peptide-loaded (CIP) particles were coated with a mitochondria targeting moiety, triphenylphosphonium cation (TPP), which allowed the particles to accumulate and release the peptide inside mitochondria to inhibit CaMKII activity. The fluorescently labeled TPP-CIP were taken up by mitochondria and successfully reduced ROS caused by Isoprenaline (ISO) in a differentiated rat cardiomyocyte-like cell line. When cells were treated with TPP-CIP prior ISO exposure, they maintained mitochondrial membrane potential. The TPP-CIP protected cells from ISO-induced ROS production and decreased mitochondrial membrane potential. Thus, TPP-CIP have the potential to be used in protection against ischemia/reperfusion injury.”

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