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"A Novel Role For Telomere Dysfunction In Myofibroblast Transdifferentiation"

Neetu Razdan
B.S., University of Delhi, 2002, New Delhi, India
M.S., 2004, Banasthali Vidyapith, Rajasthan, India

Thesis Advisor: Utz Herbig, Ph.D.
Associate Professor
Department of Microbiology, Biochemistry and Molecular Genetics

Thursday, October 6, 2016
11:00 A.M., Rutgers NJMS Cancer Center, room G1196


Proper telomere maintenance is critical for the proliferation of normal cells and disruption of telomeric function in normal human cells leads to accelerated entry into a proliferative arrest called cellular senescence. Cellular senescence plays an important role in diverse physiological processes such as promoting aging, preventing tumor progression and facilitating tissue repair during wound healing. The role of telomere dysfunction induced senescence, or TDIS, in suppressing cancer development is well defined, however, whether TDIS is important for other physiologic processes is unknown. In this proposal, we have discovered that telomere dysfunction can be triggered by paracrine signals. We demonstrate that molecules secreted from senescent cells can cause telomere dysfunction in neighboring cells that lack high telomerase activity. Significantly, we show that the generation of such dysfunctional telomeres is essential for fibroblast to myofibroblast transdifferentiation. Expression of telomerase suppresses telomere dysfunction caused by paracrine signals and suppresses myofibroblast transdifferentiation. Thus, our data demonstrate that telomere function can be regulated by paracrine signals and provide insights into a novel role for telomere dysfunction induced senescence in tissue repair during wound healing.

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