Sreejani Kanuri
Pronouns: She/Her
Research Mentor(s): Dibyendu Bhattacharyya
Research Mentor School/College/Department: Internal Medicine / Medicine
Program:
Authors: Sreejani Kanuri, Dibyendu Bhattacharyya
Session: Session 2: 10:00 am – 10:50 am
Poster: 79
Abstract
The present study aims to investigate the role of microtubule polymerization and actin polymerization, processes involved in cell growth and shape, in fibrotic disorders. It is hypothesized that enhancing microtubule polymerization should act as an effective anti-fibrotic measure through the concurrent reduction of actin polymerization. Prior research has found that increased levels of microtubule polymerization factor TPPP3 are associated with decreased levels of ASMA and COL1A1, gene markers that signal actin polymerization, in transcription growth factor beta (TGF-B1) treated skin fibroblast cells. The down regulation of ASMA is associated with increased levels of TPPP3 which results in a decrease of actin stress fiber assembly and actin polymerization. This study predicts that the expression of TPPP3, and therefore microtubule polymerization, is decreased in fibrotic conditions such as diseased Systemic Sclerosis (SSc) cell lines. This study also investigates the effect that the drug Nocodazole has on microtubule polymerization and actin polymerization. Previous research has found that Nocodazole treatment inhibits microtubule regrowth, so it is expected that Nocodazole will act as an effective fibrotic factor which increases actin stress fiber formations. To examine the effect of Nocodazole, both preventative and reversal in vitro experiments were performed through cell culture to test the effect that various concentrations of Nocodazole had on TGF-B1 treated and untreated skin fibroblasts. These cell samples were ran through the immunofluorescence staining and qPCR procedures to examine the expression levels of genes COL1A1, and ASMA. The western blot procedure was also conducted in order to do a protein analysis of the protein ?-SMA. It is expected that Nocodazole will act as a fibrotic factor by down regulating microtubule polymerization, thereby proving that microtubule depolymerization promotes fibrosis while microtubule polymerization is anti-fibrotic in nature. The results of this study will be applicable to potentially designing a therapeutic treatment for fibrotic diseases through regulating microtubule polymerization.
