Event Title

Inhibition Of Il-6/Jack/Stat Pathway Decreases Fibrosis In Tgf Beta-Treated Fibroblasts

Location

Lobby in front of Auditorium

Start Date

19-4-2019 11:00 AM

Department

Biology

Description

Systemic sclerosis is an autoimmune disease that causes abnormal inflammation and overproduction of collagen in tissues, causing fibrosis in vital organs such as lungs, liver, and skin. As of today, there is no treatment to prevent or treat the disease. Understanding the mechanisms of the activation of this disease is pivotal to develop a possible treatment to ameliorate fibrosis. Several cell-signaling pathways are implicated in fibrosis. One of them is the IL6/Jak/Stat pathway that activates the overproduction of inflammatory and fibrotic genes in fibroblasts. The purpose of my research is to repurpose an FDA-approved drug (tofacitinib), currently used for rheumatoid arthritis and psoriasis treatment to inhibit the IL6/Jak/Stat pathway and fibrotic gene expression. To accomplish this goal, I will test the activation of the IL6/Jak/Stat pathway by collecting neonatal foreskin fibroblasts, pre-treating them with a lower and higher dose Tofacitinib for 30 minutes and then treating them with a pro-inflammatory cytokine (IL6). I will use Western Blot analysis to examine if the phosphorylation levels were inhibited by Tofacitinib. Secondly, I will use qPCR on treated foreskins to look at levels of inflammatory and fibrotic gene expression in the presence and absence of Tofacitinib. The results of the Western Blot analysis showed a decrease phosphorylation levels in the foreskin fibroblasts treated with tofacitinib. The results of the qPCR analysis were a decrease in the expression of inflammatory and fibrotic genes in the presence of Tofacitinib. The next experimental approach would be to test the activation of the IL6/Jak/Stat pathway in vivo on a murine model and determining an effective dosage (either the low or high dose) of Tofacitinib. Together, these data will provide evidence for the feasibility of using tofacitinib to treat fibrosis and systemic sclerosis.

Comments

Cindy Voisine is the faculty sponsor of this poster.

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Apr 19th, 11:00 AM

Inhibition Of Il-6/Jack/Stat Pathway Decreases Fibrosis In Tgf Beta-Treated Fibroblasts

Lobby in front of Auditorium

Systemic sclerosis is an autoimmune disease that causes abnormal inflammation and overproduction of collagen in tissues, causing fibrosis in vital organs such as lungs, liver, and skin. As of today, there is no treatment to prevent or treat the disease. Understanding the mechanisms of the activation of this disease is pivotal to develop a possible treatment to ameliorate fibrosis. Several cell-signaling pathways are implicated in fibrosis. One of them is the IL6/Jak/Stat pathway that activates the overproduction of inflammatory and fibrotic genes in fibroblasts. The purpose of my research is to repurpose an FDA-approved drug (tofacitinib), currently used for rheumatoid arthritis and psoriasis treatment to inhibit the IL6/Jak/Stat pathway and fibrotic gene expression. To accomplish this goal, I will test the activation of the IL6/Jak/Stat pathway by collecting neonatal foreskin fibroblasts, pre-treating them with a lower and higher dose Tofacitinib for 30 minutes and then treating them with a pro-inflammatory cytokine (IL6). I will use Western Blot analysis to examine if the phosphorylation levels were inhibited by Tofacitinib. Secondly, I will use qPCR on treated foreskins to look at levels of inflammatory and fibrotic gene expression in the presence and absence of Tofacitinib. The results of the Western Blot analysis showed a decrease phosphorylation levels in the foreskin fibroblasts treated with tofacitinib. The results of the qPCR analysis were a decrease in the expression of inflammatory and fibrotic genes in the presence of Tofacitinib. The next experimental approach would be to test the activation of the IL6/Jak/Stat pathway in vivo on a murine model and determining an effective dosage (either the low or high dose) of Tofacitinib. Together, these data will provide evidence for the feasibility of using tofacitinib to treat fibrosis and systemic sclerosis.