Department of Pathology and Laboratory Medicine
Su-Hua Sha is an Associate Professor in the Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC. She received her undergraduate degree from Tongji Medical School in Wuhan, China, and an MD degree from the University of Essen Medical School in Germany. Her research training began in biochemistry and molecular biology at the Kresge Hearing Research Institute in the University of Michigan in 1994, first as a post-doctoral research fellow under the supervision of Dr. Jochen Schacht and then as a junior faculty member. In 2010, she established her own laboratory at the Medical University of South Carolina.
Drawing from this background, her research interest lies in the mechanisms underlying cochlear pathologies and in translating research findings into clinical therapies to prevent or ameliorate acquired hearing loss. Over the last twenty years, her research projects have been focused on molecular and cellular mechanisms of acquired hearing loss and its prevention. She has identified and characterized molecular pathways of acquired hearing loss, those involved with ototoxicity, noise trauma, and age-related hearing loss. While her research projects provide valuable insights into basic molecular events responsible for causing inner ear damage, she is also addressing translational questions with the goal of designing rational pharmacological or molecular/genetic therapeutic interventions to ameliorate acquired induced hearing loss.
On a broader scale, her lab has investigated the interactions of oxidative stress, autophagy, and cell death signaling pathways in both noise- and aminoglycoside-induced hearing loss. Her lab first demonstrated that autophagy is upregulated in sensory hair cells in CBA/J mice after noise exposure that induces temporary hearing loss. These results led to the novel concept that autophagy is an initial intrinsic cellular response that protects against inner ear damage by attenuating oxidative stress. Her lab also identified interactions between apoptotic and necrotic cell death pathways in noise-induced hair cell death, showing that inhibition of apoptotic cell death shifts hair cells to necrotic-like cell death. These results have proven to be very important for translational efforts of prevention. Currently, her research focuses on transient-cellular-energy depletion-induced changes in the activity of small GTPases in sensory hair cells and resultant actin cytoskeleton rearrangements after exposure to noise and ototoxic drugs. She is fortunate to be able to lead an excellent and productive research team of postdoctoral fellows and graduate students. Her research is funded by an R01 grant from NIH/NIDCD.
Age-related changes in expression of CTL2/SLC44A2 and its isoforms in the mouse inner ear.
Hearing research Dec, 2011 | Pubmed ID: 21986210
Antioxidant-enriched diet does not delay the progression of age-related hearing loss.
Neurobiology of aging May, 2012 | Pubmed ID: 22154190
Activation of apoptotic pathways in the absence of cell death in an inner-ear immortomouse cell line.
Hearing research Feb, 2012 | Pubmed ID: 22240458
Traumatic noise activates Rho-family GTPases through transient cellular energy depletion.
The Journal of neuroscience : the official journal of the Society for Neuroscience Sep, 2012 | Pubmed ID: 22956833
Intra-tympanic delivery of short interfering RNA into the adult mouse cochlea.
Hearing research Feb, 2013 | Pubmed ID: 23183031
Mitochondrial peroxiredoxin 3 regulates sensory cell survival in the cochlea.
PloS one , 2013 | Pubmed ID: 23626763
Tumor necrosis factor-alpha-mutant mice exhibit high frequency hearing loss.
Journal of the Association for Research in Otolaryngology : JARO Dec, 2013 | Pubmed ID: 23996384
Noise-induced cochlear F-actin depolymerization is mediated via ROCK2/p-ERM signaling.
Journal of neurochemistry Jun, 2015 | Pubmed ID: 25683353
Autophagy attenuates noise-induced hearing loss by reducing oxidative stress.
Antioxidants & redox signaling May, 2015 | Pubmed ID: 25694169
Increased Sensitivity to Noise-Induced Hearing Loss by Blockade of Endogenous PI3K/Akt Signaling.
Journal of the Association for Research in Otolaryngology : JARO Jun, 2015 | Pubmed ID: 25790950
MEKK4 Signaling Regulates Sensory Cell Development and Function in the Mouse Inner Ear.
The Journal of neuroscience : the official journal of the Society for Neuroscience Jan, 2016 | Pubmed ID: 26818521
Inhibitors of Histone Deacetylases Attenuate Noise-Induced Hearing Loss.
Journal of the Association for Research in Otolaryngology : JARO 08, 2016 | Pubmed ID: 27095478
Noise-Induced Loss of Hair Cells and Cochlear Synaptopathy Are Mediated by the Activation of AMPK.
The Journal of neuroscience : the official journal of the Society for Neuroscience 07, 2016 | Pubmed ID: 27413159
Emerging therapeutic interventions against noise-induced hearing loss.
Expert opinion on investigational drugs Jan, 2017 | Pubmed ID: 27918210
Histone Deacetylase Inhibitors Are Protective in Acute but Not in Chronic Models of Ototoxicity.
Frontiers in cellular neuroscience , 2017 | Pubmed ID: 29114207
Mitochondrial Calcium Transporters Mediate Sensitivity to Noise-Induced Losses of Hair Cells and Cochlear Synapses.
Frontiers in molecular neuroscience , 2018 | Pubmed ID: 30670946
Inhibition of Histone Methyltransferase G9a Attenuates Noise-Induced Cochlear Synaptopathy and Hearing Loss.
Journal of the Association for Research in Otolaryngology : JARO Jun, 2019 | Pubmed ID: 30710318
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