Cynthia Dharmawan

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Cynthia is a rising third year at UC Santa Barbara majoring in Pharmacology. At UCSB, she works in Dr. Weimbs’ lab, where she studies the mechanism of polycystic kidney disease.   As a UCLA Amgen Scholar, Cynthia works in Dr. Crosbie’s lab in the Integrative Biology and Physiology department studying muscular dystrophy. Duchenne muscular dystrophy (DMD) is an X-linked childhood onset degenerative disease caused by loss of function mutations in the DMD gene that encodes for dystrophin, affecting 1 in 5700 males. Patients with DMD have muscle weakness, leading to loss of ambulation as well as respiratory and cardiac dysfunction, ultimately leading to death. Dr. Crosbie has identified a transmembrane protein, sarcospan (SSPN), that associates with major adhesion complexes that provide stability to the cell during muscle contraction. Overexpression of SSPN in dystrophin-deficient mdx mice (murine model of DMD), improved skeletal muscle pathology and cardiac physiology. Previous studies have taken a targeted approach to determine which proteins are important for SSPN to ameliorate dystrophic pathology in mdx mice. To identify the global molecular mechanisms underlying SSPN’s cardioprotective effect, the Crosbie lab performed proteomics analysis on 1-year old wild-type, mdx, and mdxTG (transgenically overexpressing SSPN) hearts. Cynthia’s project will involve identifying the pathways of interest that could be contributing to the rescue of DMD by SSPN in cardiac tissue and to confirm the proteomics data by immunofluorescence analysis and western blots.   Cynthia would like to thank the Amgen Foundation, Dr. Crosbie, and mentor Hafsa Mamsa for supporting her interest in research.  

Cynthia is a rising third year at UC Santa Barbara majoring in Pharmacology. At UCSB, she works in Dr. Weimbs’ lab, where she studies the mechanism of polycystic kidney disease.

 

As a UCLA Amgen Scholar, Cynthia works in Dr. Crosbie’s lab in the Integrative Biology and Physiology department studying muscular dystrophy. Duchenne muscular dystrophy (DMD) is an X-linked childhood onset degenerative disease caused by loss of function mutations in the DMD gene that encodes for dystrophin, affecting 1 in 5700 males. Patients with DMD have muscle weakness, leading to loss of ambulation as well as respiratory and cardiac dysfunction, ultimately leading to death. Dr. Crosbie has identified a transmembrane protein, sarcospan (SSPN), that associates with major adhesion complexes that provide stability to the cell during muscle contraction. Overexpression of SSPN in dystrophin-deficient mdx mice (murine model of DMD), improved skeletal muscle pathology and cardiac physiology. Previous studies have taken a targeted approach to determine which proteins are important for SSPN to ameliorate dystrophic pathology in mdx mice. To identify the global molecular mechanisms underlying SSPN’s cardioprotective effect, the Crosbie lab performed proteomics analysis on 1-year old wild-type, mdx, and mdxTG (transgenically overexpressing SSPN) hearts. Cynthia’s project will involve identifying the pathways of interest that could be contributing to the rescue of DMD by SSPN in cardiac tissue and to confirm the proteomics data by immunofluorescence analysis and western blots.

 

Cynthia would like to thank the Amgen Foundation, Dr. Crosbie, and mentor Hafsa Mamsa for supporting her interest in research.