Publication Date


Document Type


Committee Members

Hongmei Ren, Ph.D. (Advisor); Weiwen Long, Ph.D. (Committee Member); Michael Leffak, Ph.D. (Committee Member)

Degree Name

Master of Science (MS)


Duchenne muscular dystrophy (DMD) is a genetic disorder leading to progressive muscle degeneration and weakness due to mutation in dystrophin gene, which is very important for maintaining muscle membrane integrity. Dystrophin is the largest gene in the human genome therefore more prone to mutation. There is currently no cure for DMD. Our lab recently found that Lipin1 deficient myofibers showed upregulation of necroptosis correlated with the loss of muscle membrane integrity. Our primary approach for ameliorating dystrophic phenotype in DMD is through reduction of necroptosis using drugs which can potentially upregulate Lipin1 expression. In this study, we identified two drugs i.e., dexamethasone which is a glucocorticoid and rosiglitazone which is PPARγ agonist, can elevate Lipin1 mRNA and protein expression levels in vivo and in vitro. Mdx mice treated with dexamethasone for two weeks and rosiglitazone for one week had elevated Lipin1 expression level and downregulated necroptotic markers including RIPK1, RIPK3, and MLKL. Rosiglitazone treatment in mdx mice also downregulated apoptotic markers including BAX, BAK and cleaved caspase-3. Our future study will identify whether the effects of dexamethasone and rosiglitazone on the inhibition of necroptotic markers and the improvement of membrane integrity of dystrophic muscles are through the upregulation of Lipin1 expression.

Page Count


Department or Program

Department of Biochemistry and Molecular Biology

Year Degree Awarded