Helena (Elena) Parfenova, Ph.D.
Department of Physiology
The University of Tennessee Health Science Center
894 Union Avenue
Memphis, TN 38163
Phone: (901) 448-8319
Fax: (901) 448-7126
Lab: 305 Nash Research Building
Email: Helena (Elena) Parfenova
- Ph.D. Institution: Institute of Cytology, Leningrad (St Petersburg), Russia.
Maintaining cerebral blood flow during cerebrovascular insults is critical for neuroprotection in the newborn. Our goal is to understand the endogenous mechanisms that protect neonatal brain from long-term effects of acute cerebrovascular insults caused by seizures. We investigate the roles of heme oxygenase (HO) and carbon monoxide (CO), the HO-derived endogenous gaseous mediator, in promoting survival of brain endothelial cells during cerebral vascular insult caused by seizures and oxidative stress. Seizures cause sustained cerebral vascular injury, reduction of brain endothelial dilator function, and subsequent loss of cerebral blood flow regulation. Activation of endogenous HO/CO system or pharmacological delivery of CO to the brain reduces brain oxidative stress, prevents cerebral vascular endothelial injury, and restores cerebral vascular endothelial function. We investigate the HO/CO system as a critical component of anti-apoptotic mechanisms involved in protecting the brain from cerebral vascular injury caused by seizures and oxidative stress. Our latest project is finding the correlation between the cerebral vascular injuries and circulating endothelial cells in the peripheral blood that may predict potential secondary neurological injury caused by cerebrovascular disease. The projects involve in vivo and in vitro studies in newborn pigs using intravital microscopy of cerebral resistance arterioles (closed cranial windows) for detection of cerebral blood flow responses, isolated cerebral microvessels, and primary cultures of cerebral microvascular endothelial and smooth muscle cells.
- Liu J, Fedinec AL, Leffler CW, Parfenova H. Enteral supplements of a carbon monoxide donor CORM-A1 protect against cerebrovascular dysfunction caused by neonatal seizures. J Cereb Blood Flow Metab. 2015 Feb;35(2):193-9. doi: 10.1038/jcbfm.2014.196. Epub 2014 Nov 5. PubMed PMID: 25370858.
- Nnorom CC, Davis C, Fedinec AL, Howell K, Jaggar JH, Parfenova H, Pourcyrous M, Leffler CW. Contributions of KATP and KCa channels to cerebral arteriolar dilation to hypercapnia in neonatal brain. Physiol Rep. 2014 Aug 28;2(8). pii: e12127. doi: 10.14814/phy2.12127. Print 2014 Aug 1. PubMed PMID: 25168876; PubMed Central PMCID: PMC4246596.
- Basuroy S, Leffler CW, Parfenova H. CORM-A1 prevents blood-brain barrier dysfunction caused by ionotropic glutamate receptor-mediated endothelial oxidative stress and apoptosis. Am J Physiol Cell Physiol. 2013 Jun 1;304(11):C1105-15. doi: 10.1152/ajpcell.00023.2013. Epub 2013 Apr 10. PubMed PMID: 23576575; PubMed Central PMCID: PMC3677176.
- Parfenova H, Tcheranova D, Basuroy S, Fedinec AL, Liu J, Leffler CW. Functional role of astrocyte glutamate receptors and carbon monoxide in cerebral vasodilation response to glutamate. Am J Physiol Heart Circ Physiol. 2012 Jun 1;302(11):H2257-66. doi: 10.1152/ajpheart.01011.2011. Epub 2012 Mar 30. PubMed PMID: 22467311; PubMed Central PMCID: PMC3378289.
- Parfenova H, Leffler CW, Basuroy S, Liu J, Fedinec AL. Antioxidant roles of heme oxygenase, carbon monoxide, and bilirubin in cerebral circulation during seizures. J Cereb Blood Flow Metab. 2012 Jun;32(6):1024-34. doi: 10.1038/jcbfm.2012.13. Epub 2012 Feb 22. PubMed PMID: 22354150; PubMed Central PMCID: PMC3367218.
- Xi Q, Tcheranova D, Basuroy S, Parfenova H, Jaggar JH, Leffler CW. Glutamate-induced calcium signals stimulate CO production in piglet astrocytes. Am J Physiol Heart Circ Physiol. 2011 Aug;301(2):H428-33. doi: 10.1152/ajpheart.01277.2010. Epub 2011 May 13. PubMed PMID: 21572018; PubMed Central PMCID: PMC3154668.